Cardiovascular & Renal · Full case

Chronic Kidney Disease

NICE NG203 CKS 2026 KDIGO 2024 📄 Patient leaflets

eGFR <60CKD if sustained >3 months

ACR ≥3 mg/mmolSignificant albuminuria — start ACEi/ARB

eGFR <30CKD G4 — nephrology referral threshold

BP <130/80Target in CKD with diabetes or ACR ≥70

K⁺ <6.0 mmol/LHyperkalaemia threshold — review ACEi/ARB

Hb <100 g/LCKD anaemia — consider ESA/iron

DapagliflozinSlows CKD progression — eGFR ≥25

Annual eGFRMonitor every 6–12m depending on stage

📋 Clinical Stem — Chronic Kidney Disease Presentation

A patient with newly identified or established CKD attends for review — incidental finding, progressive disease, or complication management

"Mrs Amara Patel, 64, attends following a routine blood test showing eGFR 34 mL/min/1.73m² and ACR 42 mg/mmol. She has known hypertension and type 2 diabetes managed with metformin and amlodipine. She is asymptomatic but worried — her brother is on dialysis. She was not previously told her kidneys were a concern."

CKD affects 1 in 7 adults in the UK, with the majority unaware of their diagnosis. Most CKD is identified incidentally on blood or urine testing. The leading causes are diabetes (40%) and hypertension (25%). The key clinical task: stage accurately, identify the cause, slow progression, prevent complications, and refer at the right time — while supporting a frightened patient who may assume the worst.

Scenario A — New diagnosis (SCA)eGFR 34, ACR 42, T2DM + hypertension. Not previously told about CKD. Brother on dialysis. Worried she will also need dialysis. On metformin — needs urgent review.

Scenario B — Progressive CKDKnown CKD G3b. eGFR declining: 48 → 41 → 34 over 3 years. Now G4. On ACEi. K⁺ 5.8. Haemoglobin 99 g/L. When to refer to nephrology?

Scenario C — HyperkalaemiaCKD G3a on ramipril 10mg. K⁺ 6.2 mmol/L on repeat. Not on patiromer. Diet high in bananas, potatoes, tomatoes. Needs urgent management to prevent cardiac arrhythmia.

Scenario D — CKD anaemiaCKD G4. Hb 87 g/L. Ferritin 18, TSAT 16%. Fatigue, breathlessness. Iron-deficient anaemia + ESA eligibility. When to start erythropoietin stimulating agent?

Scenario E — Medication reviewCKD G4. On NSAIDs (prescribed by rheumatology for OA). On metformin 1g BD. Also on spironolactone. Multiple nephrotoxic drugs — needs urgent medication rationalisation.

Key variableseGFR + ACR (CGA staging) · Rate of decline · Cause (DM/HTN/GN/PKD) · BP control · K⁺ · Haemoglobin · Drug nephrotoxicity · Referral threshold · Patient's understanding of prognosis

Your character

Amara Patel, 64. Retired secondary school teacher. You attended for a routine diabetes check and the nurse said the blood results showed "a kidney problem." You have known diabetes and high blood pressure — you take metformin and amlodipine. Your brother Raj, 68, has been on dialysis for 2 years after kidney failure. You are frightened this is the start of the same path.

ICE — open only if asked

Ideas: You think CKD means you will end up on dialysis like your brother. You have heard dialysis is three times a week and ruins your quality of life. You are not sure why your kidneys are affected if you "take all your tablets."
Concerns: Terrified of dialysis — it has severely restricted your brother's life, travel, and independence. Also worried about whether your metformin needs to stop and what that means for your diabetes.
Expectations: Understand what this result means, whether dialysis is inevitable, what you can do to slow it down, and whether your current tablets are safe.

"The nurse said something about my kidneys when she rang with my blood results. My brother Raj is on dialysis — he has been for two years. Is that what's going to happen to me? I take all my tablets every day. I thought my diabetes was under control."

Resist reassurance unless the doctor gives a specific reason why Amara's situation differs from her brother's. Push back if not asked about her brother: "Do you know what happened with my brother — is it the same thing?" Become anxious if told metformin needs to stop without explanation. Agree to the management plan only once: (1) dialysis risk is contextualised honestly, (2) metformin situation explained clearly, (3) specific follow-up named. Volunteer her diet (high fruit and vegetable intake — including bananas and tomatoes) only if asked about potassium sources.

Steps:

Step 1

History Taking — Open Question First · Symptoms · ICE · Psychosocial Context

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Two parallel agendas in CKD history: the clinical (stage, cause, rate of progression, complications, nephrotoxic drugs) and the patient's (does this mean dialysis? will I end up like my brother? is my metformin safe?). Both must be explored. The open question is the most efficient tool — Amara's first response will reveal the dialysis fear, the brother's story, and the medication anxiety simultaneously.

🎓 SCA opener — use what you already know

"I can see from your notes that your kidney function came up on your recent blood test and you've been asked to come in. Before I go through the results, I'd like to hear from you first — what's been going through your mind since you got that call?"

Acknowledge the result from the notes. Open the floor. Amara's first response will surface the brother's dialysis story, the fear of the same outcome, and the metformin worry — all three ICE elements in one reply, without any direct questions.

1A — Open question first, then targeted history

Question to ask	Why it matters clinically	Changes what?
🟢 OPEN QUESTION — always start here"Tell me in your own words what the nurse said, and what's been going through your mind since that call?"	Surfaces the hidden agenda immediately. Patients with incidental CKD diagnoses carry enormous unexpressed fears — dialysis, death, loss of independence, family history mirroring. Amara will volunteer the brother's story, the dialysis fear, and the medication worry in one response if given space. Rigid symptom-led questioning misses all of this and damages rapport.In SCA: the first minute is scored for open questioning and note use. Both are lost if you dive straight into "How is your breathing?" or "Any swelling in your legs?"	Reveals hidden agendaICE in one response
Symptom screen — uraemia and complications"Have you noticed any changes in your energy levels, appetite, sleep, or concentration? Any swelling in your ankles, breathlessness, or foamy urine?"	Most CKD is asymptomatic until stage G4–G5. Uraemic symptoms (fatigue, anorexia, nausea, pruritis, cognitive slowing, restless legs) indicate significant uraemia requiring urgent nephrology. Fluid overload (peripheral oedema, orthopnoea) suggests haemodynamic compromise. Foamy urine = significant proteinuria.Absence of symptoms does not exclude significant CKD — eGFR 34 can be entirely asymptomatic. The bloods matter more than the symptoms at this stage.	Urgency of referralDiuretic / ESA need
Cause identification"Do you know why your kidneys might be affected? Have you had diabetes or high blood pressure for a long time? Any kidney problems in the family — like polycystic kidneys?"	Identifying the cause of CKD is essential for targeting the correct intervention. Diabetic nephropathy (40%): microalbuminuria → macroalbuminuria → declining eGFR — tight glycaemic and BP control are the intervention. Hypertensive nephrosclerosis (25%): BP control + ACEi/ARB. PKD: genetic, referral, blood pressure. Glomerulonephritis: haematuria + proteinuria, urgent nephrology. IgA nephropathy: most common GN, often presents with haematuria.Without knowing the cause, the management plan may be non-specific and miss the most impactful intervention.	Cause-specific treatmentReferral pathway
Rate of decline"Has your kidney function been tested before? Do you know if it has been changing over time?"	Rate of eGFR decline is as important as the absolute value. eGFR decline >5 mL/min/year is significant and warrants nephrology referral regardless of absolute stage. Rapid decline (>10 mL/min in 5 years) suggests active process requiring investigation. Stable eGFR over years is more reassuring. Check the trajectory from the records before the consultation.NICE NG203: refer if eGFR declines by >25% or >15 mL/min within 12 months.	Referral decisionRepeat bloods urgency
Drug history — nephrotoxic agents"Can I go through all the tablets and medicines you take? Including anything you buy over the counter or take occasionally — like ibuprofen, naproxen, or any herbal remedies?"	Nephrotoxic drugs are a major reversible cause of CKD progression. NSAIDs (especially ibuprofen/naproxen): reduce renal blood flow → accelerate CKD. Metformin: contraindicated eGFR <30 (lactic acidosis), use with caution eGFR 30–45. ACEi/ARB: protective but can acutely reduce eGFR 10–15% on initiation and cause hyperkalaemia — do not stop unless K⁺ >6 or eGFR falls >25% on initiation. Contrast agents: hold before procedures. Aminoglycosides, vancomycin: avoid if possible.Over-the-counter NSAIDs are the most commonly missed nephrotoxic agent — patients rarely mention them unless specifically asked.	Stop nephrotoxinsReversible cause?
Cardiovascular risk — the dominant cause of death in CKD"Have you ever had a heart attack, stroke, or heart failure? Do you smoke? Do you know your cholesterol levels?"	The majority of patients with CKD die from cardiovascular disease before reaching dialysis. CKD is an independent CV risk factor equivalent to established cardiovascular disease. CV risk reduction is therefore the single most impactful intervention in most CKD patients: statin, ACEi/ARB, BP control, smoking cessation, aspirin (if established CVD).A patient with CKD G3 has a higher 10-year CV mortality than lifetime risk of dialysis. This reframes the conversation.	Statin, aspirin, BP targetCV risk stratification
Family history and psychosocial impact"You mentioned your brother — can you tell me about what happened with him? And how has this diagnosis been affecting you day to day?"	Brother's dialysis story shapes Amara's entire understanding of her prognosis. Her mental model is: CKD → dialysis → restricted life. This must be directly addressed with accurate personalised risk information — not generic reassurance. Family history of PKD is clinically important (autosomal dominant — 50% inheritance). Psychosocial impact of CKD diagnosis includes anxiety, depression, lifestyle restriction fear, and occupational concerns.In SCA: using the brother's story in the management plan is a high-quality shared decision-making marker (equivalent to T2DM "uncle's blindness"). Not using it is a domain deduction.	PKD family history?Shapes management framing

1B — Red flags: act before continuing history

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Red Flags in CKD — Features Requiring Immediate Action

Red flag	Why dangerous	Action
Hyperkalaemia: K⁺ >6.5 mmol/L or K⁺ 5.5–6.5 with ECG changes (tall T waves, wide QRS, sine wave)	Life-threatening cardiac arrhythmia. Hyperkalaemia is the most acutely dangerous complication of CKD. Any K⁺ >6.5 = emergency; K⁺ 6.0–6.5 = urgent same-day review. ACEi/ARB must be reviewed immediately. Diet restriction insufficient alone above 6.5.	999 if ECG changes
Acute-on-chronic kidney injury: eGFR drop >25% within days (intercurrent illness, dehydration, new drug)	AKI on CKD has a poor prognosis. Triggers: sepsis, dehydration, NSAIDs, contrast. "Sick day rules" — stop nephrotoxins and hold ACEi/ARB/diuretics when acutely unwell. Failure to hold during illness = preventable AKI.	Hospital if oliguric or vomiting
Uraemic emergency: pericarditis, encephalopathy, pulmonary oedema, bleeding	End-stage features requiring immediate renal replacement therapy initiation. Uraemic pericarditis (friction rub + pleuritic chest pain): dialysis indication. Encephalopathy: altered consciousness, asterixis, myoclonus.	Emergency nephrology
Haematuria + proteinuria + rapid eGFR decline in a non-diabetic patient (rapidly progressive GN)	Crescentic GN, vasculitis (ANCA-associated), anti-GBM disease. Can lose 50% of renal function in days to weeks. Dialysis-dependent if untreated within days. Requires urgent biopsy + immunosuppression.	Urgent same-day nephrology
Haemoglobin <80 g/L in CKD (severe symptomatic anaemia)	Severe CKD anaemia causing symptomatic compromise — breathlessness, chest pain, high-output cardiac failure. Iron studies + ESA eligibility assessment urgent. Transfusion may be required as bridge if severely symptomatic.	Urgent haematology/nephrology
Obstructive nephropathy: bilateral hydronephrosis on USS, loin pain, anuria	Post-renal AKI — obstruction by prostate, retroperitoneal mass, ureteric stone bilateral, or pelvis pathology. Relief of obstruction = recovery of function. Untreated → irreversible. Bladder scan bedside: post-void residual >300mL = retention.	Catheterise + urology

🛡️

Safeguarding Considerations — Consider in Every CKD Consultation

CKD is a disease of social inequality. It disproportionately affects people from South Asian, Black African, and Caribbean backgrounds, those in socioeconomic deprivation, and those with limited healthcare access. Many patients reach CKD G4–G5 without prior awareness. The safeguarding lens in CKD includes carer capacity, health literacy, medication safety, and end-of-life planning.

💊 Medication safety and health literacy

Many patients with CKD are on complex multi-drug regimens. Check: can the patient read the labels? Do they know what each tablet is for? Are they taking nephrotoxic OTC drugs they haven't mentioned?
Patients with cognitive impairment or literacy barriers may be unable to implement sick day rules without carer support — identify and document this.
ACEi/ARB + SGLT2i + diuretic = triple therapy with significant AKI risk when unwell — explicit written sick day rules are a safety-critical requirement, not optional.

🏠 Social circumstances and carer involvement

Elderly patients with CKD G4–G5 may lack capacity to manage the dietary and fluid restrictions that become necessary. Is there a carer? Are they involved in the consultation?
Dialysis preparation requires significant social support — transport to dialysis three times weekly, home adaptations for PD, carer education. Begin this conversation early at G4, not G5.
Financial impact: CKD-related sick leave, dialysis travel costs, and the cost of recommended low-potassium diets disproportionately affect low-income patients.

🌍 Ethnic background and health inequity

South Asian patients (including Amara): higher rates of diabetic nephropathy, lower eGFR thresholds for complications, culturally specific dietary factors affecting potassium and phosphate.
Black African/Caribbean patients: APOL1 gene variants confer significantly higher risk of hypertensive nephrosclerosis and focal segmental glomerulosclerosis — higher progression rate.
Do not assume language or health literacy. Use an interpreter for complex consultations — CKD staging, dialysis planning, and sick day rule discussions are too important to be lost in translation.

🕊️ End-of-life and conservative management

Not all patients with CKD G5 should be referred for dialysis — frail, elderly patients with multiple comorbidities may have better quality of life with conservative management (symptom control, dietary support, palliative care).
ReSPECT / DNACPR conversations should begin at G4 for those with significant frailty or multimorbidity — not as the first conversation, but planned and structured.
Family involvement in end-stage planning requires patient consent — do not share prognosis with family without the patient's explicit agreement.

If a safeguarding concern is identified: Document clearly. Identify carer involvement and capacity. For medication safety issues: written sick day rules + pharmacy medication use review. For frailty/end-of-life: involve the GP-led frailty team + renal supportive care service. For social needs: social prescribing + social work referral. Do not let the clinical CKD agenda override immediate safety needs.

1C — PMH · FH · Drug history · Social history

🧬 PMH / FH — changes management and urgency

Factor	Why it matters	Management impact
Type 2 diabetes	Leading cause of CKD. Tight HbA1c control slows progression (UKPDS, ADVANCE). Dapagliflozin licensed for CKD with T2DM — renal and CV protective independent of glucose lowering.	ACEi/ARB + dapagliflozin + tight HbA1c + BP <130/80. Review metformin dose at eGFR <45, stop at <30.
Hypertension	Second most common cause and major accelerant of CKD progression. BP <130/80 target in CKD with diabetes or ACR ≥70. ACEi/ARB first-line — antiproteinuric effect independent of BP lowering.	ACEi/ARB first-line regardless of race. Add CCB or thiazide if needed. Review at every CKD consultation.
PKD (polycystic kidney disease)	Autosomal dominant — 50% first-degree relative risk. Presents with hypertension, haematuria, flank pain, large palpable kidneys. Tolvaptan licensed for ADPKD with rapidly progressive disease (TEMPO trial).	USS for first-degree relatives. Refer nephrology early. Aggressive BP control. Tolvaptan if eligible.
Glomerulonephritis / haematuria + proteinuria	Non-diabetic, non-hypertensive CKD with haematuria + proteinuria = primary glomerular disease until proven otherwise. IgA nephropathy most common. Lupus nephritis, vasculitis, anti-GBM require rapid diagnosis.	Urgent nephrology referral. Renal biopsy required. Immunosuppression may be indicated.
Cardiovascular disease (IHD, HF, stroke)	CKD is an independent CV risk factor. CV disease is the commonest cause of death in CKD G3–G4. Statin indicated regardless of lipid levels in CKD (SHARP trial — 25% CV event reduction). ACEi/ARB have dual CV + renal benefit.	Statin for all CKD regardless of lipids. Aspirin if established CVD. BP <130/80. Stop smoking.
Recurrent UTIs / obstructive uropathy	Recurrent pyelonephritis → reflux nephropathy → CKD. Obstructive uropathy (BPH, pelvic mass, ureteric stone) causes post-renal AKI superimposed on CKD. USS is essential to exclude structural cause in all new CKD diagnoses.	USS kidneys mandatory in all new CKD. Treat obstruction urgently. UTI prophylaxis if recurrent.

💊 Drug history · Social history — nephrotoxins and lifestyle factors

Factor	Why it matters	Management impact
NSAIDs (ibuprofen, naproxen, diclofenac)	Inhibit prostaglandin-mediated renal afferent arteriole dilation → reduce GFR → accelerate CKD. Even short courses cause measurable eGFR reduction in CKD patients. OTC use is the most commonly missed nephrotoxin.	STOP all NSAIDs in CKD G3b and above. Paracetamol for analgesia. Document in records. Alert pharmacist.
Metformin (eGFR-dependent dosing)	Safe in CKD G3a (eGFR 45–59). Reduce dose at eGFR 30–44. Stop at eGFR <30 — lactic acidosis risk. Amara: eGFR 34 = review dose urgently. Do not stop without replacing diabetes management plan.	Reduce to metformin 500mg BD if eGFR 30–44. Stop if <30. Add/review alternative diabetes agent.
ACEi/ARB — the most important renoprotective drugs	Reduce intraglomerular pressure → slow progression, reduce proteinuria (30–40% ACR reduction). eGFR may drop 10–15% on initiation — acceptable and expected. Stop if K⁺ >6.0 or eGFR drops >25% on initiation.	Start if not already on (ACR ≥3 + DM or ACR ≥30). Monitor K⁺ + eGFR at 1–2 weeks after any dose change.
Potassium-raising drugs (ACEi/ARB + spironolactone + trimethoprim)	Triple combination ACEi + ARB + spironolactone is high-risk in CKD — severe hyperkalaemia. Trimethoprim raises K⁺ — avoid in CKD G4+. Heparins, beta-blockers, and digoxin also raise K⁺.	Avoid dual RAAS blockade. Review spironolactone if K⁺ rising. Use nitrofurantoin instead of trimethoprim for UTI in CKD (<eGFR 45: neither).
Dietary potassium intake	High-potassium foods (bananas, tomatoes, potatoes, dried fruit, nuts, chocolate) can precipitate hyperkalaemia in CKD G4–G5. Dietary restriction is the first-line intervention for K⁺ 5.5–6.0. Patiromer (potassium binder) for persistent K⁺ >5.5 on ACEi/ARB.	Dietary assessment + low-potassium diet counselling. Dietitian referral. Patiromer if K⁺ >5.5 persists.
Smoking and alcohol	Smoking accelerates CKD progression (endothelial damage, BP elevation). Alcohol in excess impairs BP control and contributes to nephrotoxicity. Both are independent CV risk amplifiers in CKD — the dominant cause of death.	QUIT referral for smoking. Alcohol advice <14 units/week. Frame as protecting both kidneys and heart.

1D — ICE: Ideas · Concerns · Expectations

Amara has a concrete, frightening mental model of CKD based on her brother's experience of dialysis. Unless the doctor actively explores and addresses this model, she will hear the management plan through the filter of "this is just the beginning of what happened to Raj." All three ICE elements — ideas (CKD = dialysis), concerns (dialysis restriction + metformin safety), expectations (honest prognosis + safety of current tablets) — must be directly addressed before the management plan has any chance of being accepted.

💭 Ideas

"When you think about this kidney result — what does it mean to you? What do you think is going to happen?"

Amara's mental model: CKD → dialysis → restricted life (her brother). This must be surfaced and directly corrected with honest, personalised risk information. "Most people with CKD G3b never need dialysis" is not the same as dismissing the concern — it is an evidence-based, emotionally respectful reframe.

😟 Concerns

"You mentioned your brother Raj — can you tell me what happened with him? And what worries you most about your own situation?"

Two layered concerns: (1) dialysis — concrete, vivid, terrifying based on personal witness; (2) metformin safety — a rational medication concern that must be addressed with specific eGFR-related guidance, not generic reassurance. Both require a specific plan, not vague comfort.

🎯 Expectations

"What were you hoping we could sort out today — and what would make this appointment feel helpful rather than frightening?"

Amara expects: an honest explanation of what this result means, a clear statement about her dialysis risk, clarity on her metformin, and a specific plan. Address expectation BEFORE the management plan — this is an SCA scoring criterion. A patient who leaves without clarity on her brother's relevance will not engage with the management plan.

1E — Psychosocial context: the person living with CKD

For Amara, CKD is not just an abnormal number — it is a potential life sentence modelled on her brother's experience. The consultation has two jobs: first, deliver accurate prognostic information that is honest but not catastrophising; second, establish a management plan that gives Amara agency rather than passivity. "There's nothing more we can do" is never the right message — there is always an intervention that slows progression, reduces complications, or improves quality of life.

🫀 Dialysis fear — contextualise, don't dismiss

Amara's brother's dialysis is real, present, and formative. Do not dismiss it — engage with it directly. Use the brother's story to explain why early intervention matters, what is different about Amara's situation, and what can be done now that was not done early enough for Raj.

"Your brother's situation helps me understand why this feels so frightening. What I want to explain is how your situation is different — and what we can do now that could change the outcome significantly."

💊 Metformin — address directly, not vaguely

Amara's eGFR 34 sits in the "reduce dose" zone for metformin. She needs a specific answer: what happens to her metformin, why, and what replaces it. Vague reassurance ("we'll keep an eye on it") without a specific plan is not acceptable — it generates anxiety rather than confidence.

"Your metformin needs to be reviewed because at your current kidney level, the full dose could accumulate. I'm going to adjust it today — and here is what I'm adding to keep your diabetes controlled."

🧠 Anxiety and health fatigue

Patients with CKD who also have diabetes and hypertension carry a complex multi-tablet regimen and multiple clinic appointments. Health fatigue is real — acknowledge the burden before adding to it. Prioritise the two or three highest-impact changes rather than overwhelming with every possible intervention at once.

"You are already doing a lot to manage your health. I don't want to add ten things today. Let me tell you the two that will make the biggest difference to your kidneys."

🌍 Ethnicity and CKD risk

South Asian patients have a 3–5× higher risk of diabetic nephropathy and CKD from hypertension. This is not a reason for fatalism — it is a reason for more intensive early intervention. Dietary factors (high potassium in traditional South Asian diets) are relevant and require culturally competent dietary advice, not generic "eat less salt" instructions.

"Some foods in traditional cooking are higher in potassium — I'd like to refer you to a dietitian who can give you specific guidance that works for the way you cook at home."

🏃 Exercise and lifestyle agency

Patients with CKD often become physically inactive due to fatigue and fear of worsening their condition. Regular moderate exercise is evidence-based in CKD — it improves CV outcomes, reduces fatigue, and improves quality of life without accelerating kidney decline. Framing exercise as protective and achievable reduces learned helplessness.

"Staying active is actually one of the most protective things you can do for your heart and kidneys — you don't need to avoid exercise. 30 minutes of walking five times a week is exactly what we'd recommend."

📋 Information needs and health literacy

CKD staging, eGFR, ACR, and proteinuria are concepts unfamiliar to most patients. Avoid all jargon unless explained. Use analogies: "Your kidneys are working at about half their ideal capacity" is clearer than "eGFR 34 represents stage G3b CKD." Written information (Kidney Care UK leaflets) and structured follow-up are essential.

"I'm going to give you a leaflet today that explains this in plain English. And I'd like you to come back in [X weeks] so we can go through your questions together — this is a lot to take in at once."

🎓 SCA Checkpoint — Step 1TasksRelating to OthersGlobal Skills

Key phrases that score

"I can see from your notes your kidney function came up on your blood test. Before I explain the result, what has been going through your mind since the nurse called?"

"You mentioned your brother Raj is on dialysis — that must make this feel very frightening. Can you tell me what happened with him?"

"Your metformin — I do need to talk to you about that. At your current kidney level I want to adjust the dose. Let me explain why and what we're going to do instead."

"The good news is: most people with your level of kidney function never need dialysis. What matters is what we do now."

Deductions

Asking "Do you have swollen ankles?" when the notes document this was not a concern — failing to use notes before asking
Not exploring the brother's dialysis as a specific concern — generic reassurance without engaging with the family history
Failing to address metformin with a specific plan — vague "we'll keep an eye on it" generates anxiety
Not asking about NSAIDs and OTC analgesic use — the most commonly missed nephrotoxin
Going straight to management without surfacing ICE

🔴 Red

Notes not used · No open Q · Brother's story not explored · Metformin not addressed specifically · No ICE · NSAIDs not asked about · Goes straight to management

🟠 Amber

Open Q attempted then rigid · Brother collected not used in plan · Metformin mentioned not dose-adjusted · NSAIDs not systematically asked · ICE incomplete

🟢 Green

Notes used first · Open Q yields full ICE · Brother used to frame management · Metformin specifically addressed with dose plan · NSAIDs explicitly asked · Drug history complete · History done by 6–7 min

Step 2

Triage Engine — Emergency · Urgent · Routine

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CKD triage is complication-first, stage-second. The first question is never "what stage is this?" — it is "is there a complication that needs immediate management?" Hyperkalaemia, uraemia, AKI on CKD, and rapidly progressive GN can all present in a routine CKD review and require immediate action. Assess K⁺, eGFR trend, and BP before any management decision.

🔴 Emergency — 999 / same day

Immediate Threat to Life

Emergency

K⁺ >6.5 mmol/L or ECG changesCardiac arrhythmia risk — 999, IV calcium gluconate, insulin/dextrose
Uraemic emergency: pericarditis, encephalopathy, pulmonary oedemaDialysis initiation required — emergency nephrology
AKI on CKD: oliguric, vomiting, eGFR fall >25% from baselineHospital for IV fluids, hold nephrotoxins, renal support
Obstructive nephropathy: bilateral hydronephrosis, anuriaCatheterise + urology same day
Rapidly progressive GN: haematuria + proteinuria + rapid eGFR declineEmergency nephrology — biopsy + immunosuppression

🟠 Urgent — within days

Significant Complication

Within days

K⁺ 5.5–6.5 mmol/L (without ECG changes)Stop ACEi/ARB if K⁺ >6.0 — review diet, add patiromer
eGFR <30 (G4) — first identificationNephrology referral within 4 weeks + full complication screen
eGFR decline >25% in 12 monthsNephrology referral regardless of absolute stage — active process
Haemoglobin <100 g/L in CKDIron studies + ESA eligibility + haematology/nephrology review
BP >160/100 despite treatment in CKDUrgent medication review — accelerated hypertension risk

🟢 Routine — planned review

Stable CKD Management

Planned

New CKD G3a/G3b — stable, no complicationsFull assessment: cause, rate, ACR, complications screen, drug review
Annual CKD revieweGFR + ACR + K⁺ + Hb + BP + medication review + smoking
Medication review (metformin, NSAIDs, dose adjustment)eGFR-guided dose adjustment + stop nephrotoxins
CKD mineral bone disease (phosphate, PTH, vitamin D)G4+: check phosphate, PTH, vitamin D annually

🎓 SCA Checkpoint — Step 2TasksGlobal Skills

Safety screen — verbalise before management

"Before we go through the plan I want to check a few things — have you had any dizziness, muscle weakness, or heart palpitations? Do you know what your potassium level is? Any significant changes in how much you're passing water?"

Deductions

Going straight to management without checking K⁺ level — hyperkalaemia is acutely life-threatening
Not assessing eGFR trend — absolute value alone is insufficient without trajectory
Missing obstructive symptoms (poor stream, nocturia, loin pain) in a patient with unexplained CKD

🔴 Red

K⁺ not checked · No eGFR trend assessment · No symptom screen for uraemia · Goes to management without safety screen

🟠 Amber

K⁺ mentioned not acted on · Trend assessed but not interpreted · Uraemic symptoms not screened · Triage category not assigned

🟢 Green

K⁺ checked and acted on · eGFR trend interpreted · Uraemic symptoms screened · Triage category assigned and explained to patient · Complication screen before management plan

Step 3

Do I Need This Examination?

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"Will this examination change management?" CKD examination findings must link directly to a clinical decision. BP measurement is mandatory at every CKD consultation. Oedema assessment determines fluid management. Fundoscopy or eye examination links to diabetic nephropathy staging. Explaining each finding to Amara is a domain 3 opportunity.

Examination	Why it matters in CKD	What finding changes management	Changes management?
Blood pressure — both arms, sitting and standing	BP control is the single most impactful modifiable factor in slowing CKD progression. Target <130/80 in CKD with diabetes or ACR ≥70; <140/90 otherwise. Postural hypotension in elderly CKD = over-treatment risk — especially on ACEi + diuretics.Every 10 mmHg reduction in SBP reduces CKD progression rate by ~25% and CV events by similar magnitude.	BP >130/80 → intensify antihypertensives. Postural drop >20 mmHg → reduce diuretics. New hypertension in previously normotensive CKD → screen for renal artery stenosis.	YES — every visit
Fluid status — JVP, peripheral oedema, ascites, lung bases	Fluid overload in CKD G4–G5 indicates failing cardiac or renal compensation. Bilateral pitting oedema + crackles = pulmonary oedema → urgent hospital. Peripheral oedema alone may be postural or nephrotic. Hypovolaemia in CKD → AKI risk — avoid overdiuresis.In nephrotic syndrome: hypoalbuminaemia causes oedema despite relatively preserved eGFR. Treatment targets albumin, not diuretics alone.	Pulmonary oedema → hospital. Peripheral oedema → diuretic + fluid restriction. Hypovolaemia → reduce diuretics, ensure adequate hydration.	YES — urgency
Abdominal examination — kidneys, bladder, masses	Large palpable kidneys bilaterally = PKD until proven otherwise. Unilateral enlarged kidney = obstructed or dysplastic. Distended bladder = urinary retention → obstructive nephropathy. Loin tenderness = pyelonephritis or ureteric colic — exclude in unexplained AKI on CKD.PKD kidneys can be enormous — easily palpable in thin patients. Always examine the abdomen in a first CKD presentation.	Large palpable kidneys → USS urgent (PKD). Bladder distension → catheterise, urology same day. Loin tenderness + fever → septic screen, urine MC&S, antibiotics.	YES — diagnosis
Cardiovascular examination — heart sounds, pulse, JVP	CKD is the dominant cause of death from CV disease. Pericardial friction rub = uraemic pericarditis → dialysis indication. Irregular pulse = AF (common in CKD + hypertension) → anticoagulation decision. Signs of heart failure → fluid management and ACEi/spironolactone review.Uraemic pericarditis: scratchy friction rub + pleuritic chest pain. This is a dialysis emergency, not an outpatient cardiac referral.	Pericardial rub → emergency nephrology. AF → anticoagulation (CKD increases bleeding risk — DOAC preferred). Heart failure signs → diuretics + ACEi + specialist review.	YES — urgency
Fundoscopy / eye examination	Diabetic retinopathy closely parallels diabetic nephropathy severity. Background retinopathy coexisting with CKD confirms diabetic aetiology. Hypertensive retinopathy (AV nipping, cotton wool spots, papilloedema) indicates target organ damage from BP. Papilloedema = malignant hypertension → emergency.NICE: offer annual diabetic eye screening (NDESP). Finding retinopathy in a patient with CKD strongly supports diabetic nephropathy as the cause.	Retinopathy + CKD → confirms diabetic nephropathy. Papilloedema → malignant hypertension → emergency. No retinopathy in diabetic CKD → reconsider whether CKD is truly diabetic in aetiology.	YES — cause
Skin — pallor, pruritis, pigmentation	Pallor = anaemia (CKD → EPO deficiency + iron deficiency). Uraemic pruritis (generalised itching without rash) = uraemic toxin accumulation — CKD G4–G5 feature indicating insufficient clearance. Hyperpigmentation = chronic uraemia in advanced CKD. Bruising = platelet dysfunction.Uraemic pruritis is a significant quality-of-life burden — responds to dialysis initiation or improved uraemic control. Ask about it specifically in G4–G5 patients.	Pallor → Hb check → iron studies + ESA eligibility. Pruritis → uraemic toxin load → expedite nephrology referral + consider dialysis timing.	YES — complication

🎓 SCA Checkpoint — Step 3Tasks

How to propose examination

"I'd like to check your blood pressure — keeping that controlled is the single most important thing we can do for your kidneys. I also want to feel your tummy to check the kidneys directly, listen to your heart, and look at your ankles for any swelling. Then I can give you a much more complete picture of where we are."

Deductions

Not measuring BP at a CKD review — mandatory at every visit
Not examining the abdomen in a first CKD presentation — PKD and obstructive uropathy may be missed
Not linking each examination to a management decision when explaining to the patient
Missing signs of fluid overload — peripheral oedema and crackles require active assessment

🔴 Red

No BP measurement · No abdominal exam at first presentation · No fluid status assessment · Examinations not explained · Uraemic pericarditis not on differential

🟠 Amber

BP measured · Abdomen not examined · Fluid status not assessed · Examinations done silently without explanation · Eye exam not linked to cause

🟢 Green

BP + fluid status + abdomen + CV exam + skin · Each explained with rationale · Findings linked to specific management decision · Eye exam discussed and NDESP documented

Step 4

Do I Need This Investigation?

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Every CKD investigation must answer a specific clinical question. The minimum dataset at new CKD diagnosis: eGFR + ACR + K⁺ + Hb + USS kidneys. Additional tests are ordered based on suspected cause and stage. Explain each test in plain language — "this blood test tells me if your kidneys are leaking protein, which helps me choose the right medicine to protect them."

Investigation	Clinical question it answers	What result changes management?
eGFR (estimated GFR) — repeated ×2 at least 3 months apart to confirm CKD	Staging and trajectory — the diagnostic cornerstone. CKD is defined as eGFR <60 mL/min/1.73m² OR markers of kidney damage (ACR ≥3, haematuria) for >3 months. Single low eGFR ≠ CKD — confirm with repeat. Track the trend: rate of decline >5 mL/min/year = significant. eGFR also guides drug dosing for metformin, SGLT2i, ACEi, and contrast agents.	eGFR <30 → nephrology referral. Decline >25% in 12 months → urgent referral. Stable for years → more reassuring prognosis.
ACR (albumin:creatinine ratio) — first morning urine sample	Quantifies proteinuria — the most powerful independent predictor of CKD progression and CV risk. ACR <3 = normal. 3–30 = microalbuminuria (A2). >30 = macroalbuminuria (A3). >70 = significantly elevated — most aggressive ACEi/ARB therapy + BP <130/80 mandatory. CGA staging uses both G (eGFR) and A (ACR) — G3bA3 has a very different prognosis to G3bA1.	ACR ≥3 + DM or ACR ≥30 → start ACEi/ARB. ACR >70 → BP target <130/80. ACR rising → progression marker → intensify treatment.
Urine dipstick + MC&S (microscopy, culture, sensitivity)	Haematuria + proteinuria without UTI = primary glomerular disease — urgent nephrology referral. Isolated haematuria in CKD >age 40 = urology referral (bladder cancer exclusion). Persistent haematuria after UTI treatment = renal cause. Sterile pyuria = tubulointerstitial nephritis, TB.	Haematuria + proteinuria (non-infective) → urgent nephrology. Isolated haematuria >40 → urology. UTI confirmed → treat and repeat ACR after clearance.
Full blood count — Hb, MCV, platelets	Normochromic normocytic anaemia of CKD = EPO deficiency (reduced renal production). Microcytic anaemia = iron deficiency (reduced absorption, GI loss, dialysis-related). Both can coexist. Hb <100 g/L in CKD with Transferrin saturation <20% or ferritin <100 = iron-deficient → IV iron before ESA. Thrombocytopenia: consider TTP/HUS in rapidly progressive CKD + anaemia + low platelets.	Hb <100 g/L → iron studies + ESA eligibility assessment. Hb <80 g/L symptomatic → urgent haematology. Thrombocytopenia + AKI → exclude TTP urgently.
U&E (urea, electrolytes, creatinine), calcium, phosphate	K⁺: hyperkalaemia risk on ACEi/ARB in CKD — must monitor at baseline and after any dose change. Bicarbonate: metabolic acidosis (HCO3⁻ <22) in CKD G4–G5 = oral sodium bicarbonate supplementation (slows progression, reduces muscle catabolism). Phosphate: elevated in G4–G5 → renal osteodystrophy → phosphate binders. Calcium: hypocalcaemia in G4–G5 → active vitamin D (alfacalcidol).	K⁺ >5.5 → review ACEi/ARB + diet + add patiromer. HCO3⁻ <22 → sodium bicarbonate. Phosphate elevated → phosphate binders + dietary restriction.
PTH (parathyroid hormone) and vitamin D — in G4–G5	CKD mineral bone disease (CKD-MBD): reduced 1-alpha hydroxylation of vitamin D in CKD → low active vitamin D → secondary hyperparathyroidism → bone resorption → renal osteodystrophy + vascular calcification. PTH and vitamin D should be checked annually from G4. 25-OH vitamin D: replace if deficient. Active vitamin D (alfacalcidol): for secondary hyperPTH.	PTH elevated >2× upper normal in G4 → active vitamin D. PTH >9× upper normal in G5 = tertiary hyperparathyroidism → parathyroidectomy consideration.
USS kidneys and urinary tract — all new CKD diagnoses	Structural diagnosis: small scarred kidneys (chronic disease), large hyperechoic kidneys (diabetic/HTN), multiple cysts (PKD), hydronephrosis (obstruction). Asymmetric kidney size: consider renal artery stenosis (especially in hypertensive CKD resistant to treatment — Doppler USS). Absence of both kidneys on USS = technical failure or horseshoe kidney — CT required. First USS in all new CKD is mandatory per NICE NG203.	Hydronephrosis → obstruction → urology same day. PKD-pattern → genetics + tolvaptan eligibility. Asymmetric size → renal artery stenosis screen. Small bilateral scarred → chronic irreversible disease.
Renal biopsy — in specialist settings for unexplained CKD	Indicated when: proteinuria + haematuria without clear cause (diabetic/hypertensive aetiology unconfirmed), rapidly progressive GN, systemic disease with renal involvement (lupus, vasculitis, amyloid), or treatment-altering diagnosis is suspected. Not indicated in: clearly diabetic CKD with retinopathy + albuminuria, bilateral small scarred kidneys (too high risk), single functioning kidney, or uncorrected coagulopathy.	Specific diagnosis (IgA, FSGS, lupus, vasculitis) → targeted immunosuppression. Amyloid → underlying cause treatment. Normal biopsy → reconsider systemic cause.

🎓 SCA Checkpoint — Step 4TasksRelating to Others

How to explain investigations in plain language

"I need to check two main things: a blood test to see how well your kidneys are filtering, and a urine test to see if they are leaking any protein — because that tells me how much they are being stressed and helps me pick the right medicine to protect them. I also want to do an ultrasound scan to look at the shape and size of the kidneys."

Deductions

Not ordering ACR — staging without ACR is incomplete (CGA system requires both G and A)
Not ordering USS kidneys at first CKD presentation — NICE NG203 mandatory
Not checking K⁺ before or shortly after starting/reviewing ACEi/ARB
Not explaining investigations in lay language — jargon without explanation is a domain 3 deduction

🔴 Red

ACR not ordered · USS not requested · K⁺ not checked · Investigations not explained · Metformin not reviewed against eGFR

🟠 Amber

eGFR + ACR ordered · USS not mentioned · K⁺ checked but not acted on · Investigations mentioned not explained in plain language

🟢 Green

eGFR + ACR + K⁺ + Hb + USS + urine dipstick all addressed · Each test explained with reason in plain language · Metformin dose reviewed against eGFR · ACEi/ARB monitoring plan stated · Results timeline given

Step 5

Reaching a Diagnosis — CKD Classification · Lay Language · DDx · Prognosis

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CKD diagnosis has two components: accurate CGA staging (eGFR G-stage + ACR A-stage + cause) and communicating the diagnosis in a way that directly addresses the patient's specific fears. For Amara, the diagnosis communication must include: what CKD means in plain language, what the realistic dialysis risk is for her specifically, what is different from her brother's situation, and what the management plan is going to do.

🗣️ Explaining CKD in plain language

"Your kidneys are working at about half the level we would ideally like — they are filtering your blood more slowly than normal. This does not mean your kidneys are failing right now, or that dialysis is inevitable. What it means is that we need to protect them carefully — by controlling your blood pressure, adjusting your diabetes tablets, and removing anything that could stress them further. Most people with your level of kidney function never need dialysis, especially when we catch it at this stage and take action."

🫂 Addressing the brother — the most important conversation in this consultation

"Will I end up on dialysis like my brother Raj?"
"That is exactly the question I want to answer directly. Your brother's situation is very real and understandably frightening for you. What I can tell you is this: your kidney function is at a level where we can still do a significant amount to slow or even stop any further decline. The fact that you are here, that we have caught this now, and that your kidneys are still working at half capacity — these are all reasons for measured optimism, not despair. Your brother's journey was different — we don't know exactly when his kidneys were first identified as a concern, or what the cause was. What I can control is what happens from today onwards for you."

Why this matters: Honest, specific, compassionate engagement with the brother's story is the central domain 3 marker in this consultation. Generic reassurance ("try not to worry") is actively harmful. Specific engagement with personalised risk information is the only approach that builds therapeutic trust.

5A — KDIGO CGA Staging

G-Stage (eGFR)

Stage	eGFR	Description	Action
G1	≥90	Normal or high	CKD only if ACR ≥3 or haematuria
G2	60–89	Mildly decreased	CKD only if ACR ≥3 or haematuria
G3a	45–59	Mild-moderate decrease	Annual monitoring. ACEi/ARB if ACR ≥3. Review drugs.
G3b	30–44	Moderate-severe ← Amara	6-monthly review. Reduce metformin. Complication screen.
G4	15–29	Severely decreased	Nephrology referral. CKD-MBD screen. Dialysis planning.
G5	<15	Kidney failure	Renal replacement therapy or conservative management.

A-Stage (ACR)

Stage	ACR mg/mmol	Action
A1	<3	Normal. Annual check if CKD risk factors.
A2	3–30	Microalbuminuria. Start ACEi/ARB if DM. 6-monthly ACR.
A3 ← Amara (42)	>30	Macroalbuminuria. ACEi/ARB mandatory. BP <130/80.

Amara's staging: G3b A3 — eGFR 34 + ACR 42. High-risk cell on KDIGO heat map. 6-monthly review. ACEi/ARB mandatory. Dapagliflozin eligible. Nephrology referral not yet mandatory (G4 threshold) but consider given ACR >30.

5B — Differential Diagnosis

Diabetic nephropathy — Most common DDx

T2DM + hypertension + ACR ≥3 + retinopathy = diabetic nephropathy confirmed clinically. No biopsy needed. Proteinuria precedes eGFR decline by years. ACEi/ARB + tight glycaemia + BP <130/80 are the treatment.

Hypertensive nephrosclerosis

Long-standing hypertension + small kidneys on USS + moderate proteinuria (ACR 30–300) without diabetic retinopathy. Pathological small vessel disease. ACEi/ARB + strict BP control <130/80.

IgA nephropathy — Most common GN

Microscopic haematuria + proteinuria, often following URTI. Macroscopic haematuria episodes. Progressive in 30–40% over 20 years. Biopsy required. SGLT2i + ACEi/ARB. Sparsentan emerging.

Polycystic Kidney Disease (ADPKD)

Family history, bilateral large kidneys on USS, multiple cysts, hypertension. ADPKD1/2 mutations. Tolvaptan slows progression in rapidly progressive disease (licensed in UK). Refer nephrology early.

ANCA vasculitis / anti-GBM disease

Haematuria + heavy proteinuria + rapidly progressive eGFR decline. Systemic features: sinusitis, haemoptysis (GPA), rash. Emergency nephrology — immunosuppression within days. PR3-ANCA, MPO-ANCA, anti-GBM antibodies.

Renovascular disease / renal artery stenosis

Resistant hypertension + asymmetric kidney size + flash pulmonary oedema. ACEi causes significant eGFR drop. Doppler USS or MRA. Atherosclerotic most common. Revascularisation rarely beneficial except progressive loss.

🎓 SCA Checkpoint — Step 5TasksRelating to Others

Communicating diagnosis + brother in lay language

"Your kidneys are working at about half the level we'd ideally like — and this has likely been going on for some time, because of your diabetes and blood pressure. The honest answer about dialysis is: most people at your stage never need it, especially when we act now. Your brother's situation was different, and what we can control is what happens from today."

Deductions

Giving a vague prognosis without engaging specifically with the brother's story
Using CKD staging jargon (G3b, A3) without translating it into plain language
Not distinguishing diabetic nephropathy from other causes — affects treatment decision
False reassurance ("don't worry about dialysis") rather than honest, evidence-based framing

🔴 Red

Jargon throughout · Brother's story not engaged with · Dialysis risk not contextualised · No lay language translation · Cause not identified

🟠 Amber

Diagnosis communicated · Brother acknowledged but not used in plan · Stage explained without cause · Dialysis risk mentioned not personalised

🟢 Green

Lay language · Brother's story used to frame management · Honest personalised prognosis · CGA stage explained as "half capacity" · Cause identified (diabetic nephropathy) · What we can do now framed as actionable agency

Step 6

If Referral Is Needed — What the GP Does Before & During

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Most CKD G1–G3b is managed entirely in primary care. Referral is targeted to specific indications — eGFR <30, rapid decline, unexplained cause, complications beyond primary care management, or dialysis planning. The GP must not stop treatment while awaiting referral — ACEi/ARB, BP control, and drug review continue in parallel. Explain to the patient why referral is happening and what the specialist will add.

Scenario	Urgency	What GP does before/during referral	What GP must NOT do
Rapidly progressive GN: haematuria + proteinuria + rapid eGFR decline	Same day	Urgent bloods: ANCA, anti-GBM, ANA, ASOT, complement, blood film. Urine for casts. Discuss with on-call nephrologist. Do not start immunosuppression without specialist guidance.	Do NOT give high-dose steroids in primary care without nephrology guidance. Do NOT delay referral — hours matter in crescentic GN.
Hyperkalaemia: K⁺ >6.5 with ECG changes	999 immediately	ECG immediately. IV calcium gluconate if available. Call 999. Hold all potassium-raising agents. IV insulin/dextrose in hospital. Monitor continuously.	Do NOT wait for repeat bloods if ECG changes. Do NOT continue ACEi/ARB/spironolactone until K⁺ controlled. Do NOT discharge from primary care if K⁺ >6.5.
eGFR <30 (G4) — first identification or transition	Within 4 weeks	Full complication screen: Hb, K⁺, phosphate, PTH, vitamin D, bicarbonate. Adjust drug doses. Start CKD-MBD management. Pre-dialysis education referral. USS if not done. Dietitian referral. Ensure ACEi/ARB optimised.	Do NOT stop ACEi/ARB unless K⁺ >6.0 or eGFR drop >25% on initiation. Do NOT start patient on pre-dialysis pathway without nephrology confirmation.
eGFR decline >25% in 12 months or >15 mL/min in 5 years	Within 4 weeks	Check for AKI trigger (infection, drug, dehydration). Review all nephrotoxins. Optimise BP. Optimise ACEi/ARB. Repeat USS. Send referral with full investigation summary and eGFR trend graph.	Do NOT assume decline is inevitable — always look for reversible cause. Do NOT refer without full investigation set completed.
Unexplained CKD: no diabetes, no hypertension, or atypical features	Routine	USS kidneys. Urine dipstick. ANA, ANCA, complement, immunoglobulins, serum protein electrophoresis, Bence Jones protein. HIV, hepatitis B/C screen. Refer with investigation results.	Do NOT label as idiopathic without investigation. Do NOT delay — unexplained CKD may be treatable GN.
CKD anaemia: Hb <100 g/L in CKD G4–G5	Routine via nephrology	Iron studies (ferritin, TSAT). If iron-deficient: IV iron (not oral — poor absorption in CKD). If iron-replete + Hb <100: ESA eligibility referral. Exclude other causes: haemolysis, blood loss, B12/folate deficiency.	Do NOT start ESA in primary care — nephrology-initiated. Do NOT give oral iron alone in CKD G4–G5 (absorption inadequate).

🎓 SCA Checkpoint — Step 6TasksGlobal Skills

How to explain referral to Amara

"At your current kidney level, I am managing this in primary care — that is completely appropriate. If your kidney function drops further, I would refer you to a kidney specialist who can assess whether there are additional treatments. That is not the situation today — but I want you to know the plan at every stage."

Deductions

Referring to nephrology at G3b without the NICE NG203 indications met — not necessary at this stage
Not referring at G4 or with rapid decline — a serious safety failure
Stopping ACEi/ARB before specialist review without clinical justification
Starting ESA in primary care — nephrology-initiated only

🔴 Red

Refers at G3b without indication · Does not refer at G4 · Stops ACEi/ARB without reason · Starts ESA in primary care · Rapidly progressive GN not recognised as emergency

🟠 Amber

Referral decision correct · Investigation set incomplete at referral · Patient not told what specialist will add · Referral threshold criteria not explained

🟢 Green

Correct referral thresholds · Investigations completed before referral · Patient told reason for referral and what to expect · GP management continues during wait · "Do NOT" actions explicitly avoided

Step 7

Management — Expectation · Goals · Non-Medication · Prescribing Guide · Drug Selector · Drug Reference · Psychosocial · Follow-Up · Safety-Netting

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7A — Address the patient's expectation first: validate → explain → negotiate

🤝

Never dismiss the expectation — acknowledge it, share your reasoning, then agree a shared plan

Validate — name their expectation

Amara has two specific fears: dialysis (her brother's experience) and metformin safety. Both are rational. Acknowledge them explicitly before any management plan — not after.

"Before I go through the plan — can I come back to the two things you mentioned at the start? Your brother's situation, and your worry about your metformin. Let me address both of those directly."

Explain — share your clinical reasoning

Give honest, specific, personalised prognostic information. Do not say "don't worry." Say "here is what the evidence shows about people at your stage" and "here is what is different about your situation compared to Raj's."

"Most people with a kidney level like yours — eGFR of 34 — never need dialysis, especially when we act at this point. Your brother's situation was different and I can't change what happened there. What I can do is make sure we do everything right from today."

Negotiate — offer something today

Name one specific action agreed today. Adjust metformin, start or optimise ACEi/ARB, order USS and bloods — give Amara something concrete and actionable. Use the brother's story as motivational framing, not a source of dread.

"The goal I want for you is that your kidneys stay stable — and that in five years you are nowhere near needing dialysis. The things we are doing today are the things that make that difference. Let's agree what we are starting now."

7B — Why treatment matters: goals tailored to this patient

Treatment goals

Slow eGFR declineReduce proteinuria (ACR <30) BP <130/80Prevent hyperkalaemia Prevent CV eventsAvoid dialysis Stop nephrotoxinsMaintain quality of life

Motivational language — tailored to Amara

"The goal isn't just to stop the number getting worse — it's to protect your kidney function so that five years from now dialysis is still just a worry, not a reality. Every BP reading we control, every tablet we get right, is a step in that direction."

"You came in today worried. I want you to leave today with a plan. There is a lot we can do — and we are starting it today, not next month."

7C — Non-medication management: mechanism + evidence + tailored advice

Never give generic lifestyle advice. Each intervention below has a specific mechanism, a quantified effect on eGFR decline or CV risk, and a measurable outcome. Present each as a real treatment — and tailor it to Amara's specific situation. For Amara: her South Asian background, traditional cooking, and diabetic comorbidity make generic advice inadequate.

🧂

Salt Restriction

Target: <5g NaCl/day (2g sodium)

Mechanism

High dietary sodium → volume expansion → elevated BP → increased intraglomerular pressure → accelerates proteinuria and eGFR decline. Sodium also directly activates RAAS independent of BP, increasing angiotensin II-mediated fibrosis in the kidney.

Evidence

Each 1g/day reduction in sodium intake reduces systolic BP by ~3–4 mmHg. In CKD, salt restriction potentiates ACEi/ARB antiproteinuric effect by 30–40% (COMBINE trial). Dietary salt reduction alone can reduce ACR significantly within weeks.

Tailored — Amara

South Asian cooking often uses salt, soy sauce, and pickles. Tailor: "Avoid adding salt at the table. Use herbs and lemon instead. Ask your dietitian about low-sodium substitutes for specific dishes." Refer to dietitian with South Asian dietary expertise.

↓ BP + ↓ ACR — potentiates ACEi/ARB by up to 40%

🍌

Potassium Restriction (G3b–G5)

Target: K⁺ <5.5 mmol/L; dietary K⁺ <3g/day

Mechanism

As eGFR declines, renal potassium excretion falls. ACEi/ARB further impairs K⁺ excretion via aldosterone suppression. High-potassium foods can precipitate dangerous hyperkalaemia in CKD G3b+, especially in patients on RAAS agents.

Evidence

Dietary potassium restriction effectively reduces K⁺ by 0.5–1.0 mmol/L in CKD, allowing continuation of ACEi/ARB (which are renoprotective). Abrupt stopping of ACEi/ARB due to hyperkalaemia accelerates CKD progression — preventing this with diet + patiromer is the preferred approach.

Tailored — Amara

Amara may be eating bananas, tomatoes, and potatoes daily — all high potassium. Tailor: "Switch bananas for apples. Boil potatoes and discard the water — that removes up to 50% of the potassium. Avoid tomato-based sauces and dried fruit." Specific, not generic.

↓ K⁺ by 0.5–1.0 mmol/L → enables ACEi/ARB continuation

🥩

Protein Restriction (G4–G5)

Target: 0.6–0.8g/kg/day in G4–G5

Mechanism

High dietary protein → increased urea production → elevated intraglomerular pressure → hyperfiltration → accelerated nephron loss. Protein restriction reduces urea load, phosphate intake, and intraglomerular pressure — slowing CKD progression in G4–G5.

Evidence

MDRD trial: moderate protein restriction (0.58g/kg/day) slowed GFR decline in CKD G4–G5. Not recommended in G1–G3 — insufficient evidence and risk of malnutrition. In G3b (Amara): avoid very high protein diet; no need for formal restriction yet.

Practical

Dietitian referral for CKD G4+. Avoid excessive protein supplementation (gym supplements, protein shakes). Plant-based protein (lentils, beans) may be preferred — lower phosphate content vs animal protein. Do not restrict to the point of malnutrition.

↓ Hyperfiltration + ↓ phosphate load in G4–G5

🏃

Exercise

Target: 150 min moderate exercise/week

Mechanism

Regular aerobic exercise reduces BP, improves insulin sensitivity (reducing diabetic nephropathy progression), reduces CV risk (dominant cause of death in CKD), and improves fatigue and quality of life. Does not accelerate eGFR decline in stable CKD.

Evidence

Cochrane review (2019): regular exercise in CKD reduces BP by 3–5 mmHg, improves physical function, and reduces fatigue without adverse renal effects. Particularly important given CV mortality dominates over dialysis risk in CKD G3.

Tailored

"Walking 30 minutes five times a week is exactly right — and it is actively protective for both your kidneys and your heart. You do not need to avoid exercise because of your kidneys. The opposite is true."

↓ BP + ↓ CV risk — does not accelerate CKD

🚭

Smoking Cessation

Target: complete cessation

Mechanism

Smoking causes endothelial dysfunction → vasoconstriction → reduced renal perfusion + accelerated progression of both diabetic and hypertensive nephropathy. Smoking doubles the rate of eGFR decline in CKD. Also the single most modifiable CV risk factor — CKD patients die predominantly from CV disease.

Evidence

Multiple cohort studies: smoking associated with 2× faster eGFR decline and 3× higher rate of ESRD in CKD G3. Cessation slows this trajectory within 1 year. CO breath test at every review — objective feedback motivates change more than verbal advice alone.

Practical

QUIT referral. Varenicline most effective. NRT as alternative. Frame as: "Stopping smoking is the single most powerful thing you can do for both your kidneys and your heart today." Use CO breath test as motivational feedback.

↓ eGFR decline rate by up to 50% + dominant CV risk reduction

⚖️

Weight Management

Target: BMI <30; 5–10% weight loss

Mechanism

Obesity drives CKD through multiple pathways: hypertension, insulin resistance, glomerular hyperfiltration (increased single-nephron GFR in obese patients → early nephron loss), and pro-inflammatory adipokines. Obesity also worsens proteinuria directly — adipocytokines increase glomerular permeability.

Evidence

Weight loss of 5kg in obese CKD patients reduces proteinuria by 30% and BP by 5 mmHg within 3 months (Kidney International, 2017). SGLT2i (dapagliflozin) provide modest additional weight loss in CKD with T2DM — dual benefit.

Practical

NHS structured weight management programme referral. Frame as: "Losing even 5kg reduces the stress on your kidneys and directly reduces the protein leak we saw in your urine test." SGLT2i adds modest weight reduction alongside renoprotection.

↓ Proteinuria 30% + ↓ BP 5 mmHg with 5kg loss

7D — Prescribing Guide: what to start, in what order, and why

Three decisions, in this order, every time: (1) Is there a contraindication or safety check required before this drug — confirm eGFR, K⁺, and BP trend before any RAAS agent or SGLT2i. (2) Which intervention is most urgent and impactful for this patient's CKD stage and cause? (3) Within that decision, which drug and dose fits this patient's comorbidities, eGFR, and tolerability? For Amara: ACEi/ARB is the single most urgent new prescription — she has ACR 42, T2DM, and hypertension and is not yet on a RAAS agent.

Before prescribing anything — confirm these safety checks first

🔬 Check K⁺ and eGFR before starting ACEi/ARB

ACEi/ARB are the cornerstone of CKD management — but must not be started into unknown electrolytes. Baseline K⁺ must be <5.5 mmol/L before initiation. eGFR drop of 10–15% in the first 2 weeks is expected and acceptable — it reflects haemodynamic change, not nephrotoxicity. Recheck K⁺ + eGFR at 1–2 weeks after starting or any dose change.

"Before I start your blood pressure tablet, I need to check a blood test today to make sure your potassium level is safe to start it."

💊 Review all nephrotoxins before adding new agents

Stop NSAIDs (the most commonly missed accelerant). Review metformin dose: eGFR 30–44 = reduce to 500mg BD; eGFR <30 = stop. Review contrast agent plans. Identify any herbal or OTC nephrotoxins. Do not add a renoprotective drug on top of an ongoing nephrotoxin — the benefit is negated.

"Are you taking any painkillers occasionally — like ibuprofen — even ones you buy yourself? These can stress the kidneys significantly."

🩺 Confirm eGFR eligibility before dapagliflozin

Dapagliflozin is licensed for CKD renal benefit from eGFR ≥25 (DAPA-CKD trial). Glycaemic benefit requires eGFR ≥45 but renal/CV protection continues to eGFR 25. Confirm eGFR ≥25 before starting. Sick day rules are mandatory — hold if unwell, vomiting, or pre-procedure. UTI risk: ensure no active infection before starting.

"This tablet protects your kidneys independently of your diabetes control — it reduces the stress on them directly. But we need to hold it if you become unwell."

Only once K⁺ confirmed <5.5 + eGFR confirmed + all nephrotoxins stopped → proceed to drug selection below

Step-by-step prescribing order — NICE NG203 / KDIGO 2024

Priority 1

All CKD + ACR ≥3

START: ACEi or ARB — ramipril 2.5mg OD → titrate to 10mg OD

Ramipril 2.5mg OD (or losartan 50mg OD if ACEi cough). Titrate to maximum tolerated dose over 4–8 weeks. Check K⁺ + eGFR at 1–2 weeks after every dose increase. Expected: eGFR drop 10–15% = acceptable. Do not combine ACEi + ARB (increased hyperkalaemia and AKI risk — ONTARGET trial).

WHY ACEi/ARB first

Dual mechanism: BP lowering + intraglomerular pressure reduction via efferent arteriole dilation. Reduces ACR by 30–40% independently of BP. Reduces CKD progression risk by 25–30% (REIN, RENAAL, IDNT trials). Reduces CV events. The single most evidence-based intervention in CKD with proteinuria.

→ Recheck K⁺ + eGFR at 1–2 weeks. Stop if K⁺ >6.0 or eGFR drops >25% from baseline.

Priority 2

CKD + T2DM or ACR ≥25

ADD: Dapagliflozin 10mg OD

Dapagliflozin 10mg OD — licensed for CKD with or without T2DM (eGFR ≥25). Continue alongside ACEi/ARB. Sick day rules mandatory (hold if vomiting, dehydration, or pre-surgery — euglycaemic DKA risk). Genital hygiene counselling. Minor eGFR dip on initiation expected — do not stop.

WHY dapagliflozin at priority 2

DAPA-CKD trial: 39% reduction in sustained eGFR decline ≥50%, ESRD, or renal/CV death vs placebo across CKD G2–G4 with ACR ≥200 (with or without T2DM). Benefit is additive to ACEi/ARB. Also reduces HF hospitalisation and CV mortality. For Amara: ACR 42 + T2DM + eGFR 34 = ideal candidate.

→ Check eGFR 2–4 weeks after starting. Expected minor dip — do not stop unless eGFR drops >25%.

Priority 3

All CKD

OPTIMISE: BP to target — add CCB or thiazide if ACEi alone insufficient

Target BP <130/80 in CKD with diabetes or ACR ≥70; <140/90 otherwise. Add amlodipine 5mg OD (CCB — first add-on) if ACEi alone insufficient. Thiazide-like diuretic (indapamide 1.25mg) as third-line. Avoid thiazides if eGFR <30 (reduced efficacy). Loop diuretic (furosemide) for fluid overload in G4–G5.

WHY BP control is priority 3

Each 10 mmHg reduction in SBP reduces CKD progression by ~25% and CV events by a similar magnitude. BP control after ACEi/ARB adds incremental benefit. CCB preferred over beta-blocker as add-on in CKD (less metabolic effect, no hyperkalaemia risk). Avoid beta-blocker unless there is a specific cardiac indication.

→ Measure BP at every consultation. Review add-on agents at 4–6 weeks. Postural BP in elderly patients.

Priority 4

All CKD — statin

ADD: Statin — atorvastatin 20mg OD (dose-adjust in severe CKD)

Atorvastatin 20mg OD for all CKD regardless of cholesterol level. In CKD G4–G5: rosuvastatin preferred (less hepatic metabolism → lower systemic exposure). Avoid simvastatin >10mg in CKD G4–G5 (myopathy risk). Do not stop statin in dialysis patients unless started before ESRD — evidence limited once established on dialysis.

WHY statin for all CKD

SHARP trial (9270 CKD patients): simvastatin/ezetimibe reduced major atherosclerotic events by 25% in CKD regardless of baseline LDL. CKD is an independent CV risk equivalent to established CVD — statin is indicated on this basis alone, not just cholesterol level. Most CKD patients die from CV events before reaching dialysis.

→ Annual lipid profile. LDL target <1.8 mmol/L in CKD + established CVD. CK if myalgia develops.

Priority 5

K⁺ >5.5 on ACEi/ARB

ADD: Patiromer (potassium binder) — 8.4g OD sachet with food

Patiromer 8.4g OD (titrate up to 25.2g OD). Taken with food, not within 3 hours of other medicines. Reduces K⁺ by 0.5–1.0 mmol/L. Allows continuation of ACEi/ARB in hyperkalaemic CKD — enabling renoprotection that would otherwise need to be stopped. Alternative: sodium zirconium cyclosilicate (ZS-9, Lokelma).

WHY patiromer rather than stopping ACEi/ARB

AMBER trial: patiromer enabled 80% of patients with CKD + hyperkalaemia to continue ACEi/ARB (vs 40% placebo). ACEi/ARB stopping due to hyperkalaemia accelerates CKD progression significantly. Patiromer is the pharmacological bridge that maintains renoprotection. NICE approved for persistent hyperkalaemia on RAAS therapy in CKD and HF.

→ Recheck K⁺ at 1 week after starting. Titrate dose until K⁺ <5.0. Do not crush or heat sachets.

G4–G5

Complications

ADD: CKD-MBD management + anaemia management — specialist input

CKD-MBD: phosphate binders (calcium carbonate or sevelamer) if phosphate elevated. Active vitamin D (alfacalcidol 0.25–1 mcg OD) for secondary hyperPTH. Sodium bicarbonate 500mg TDS if HCO3⁻ <22 mmol/L. CKD anaemia: IV iron if TSAT <20% or ferritin <100. ESA (darbepoetin / epoetin) if Hb <100 after iron optimisation — nephrology-initiated.

WHY these matter at G4–G5

Metabolic acidosis (HCO3⁻ <22) independently accelerates CKD progression and muscle catabolism — sodium bicarbonate slows both (BICAR-ICU, Goraya trials). Secondary hyperPTH causes renal osteodystrophy and vascular calcification — active vitamin D suppresses PTH. CKD anaemia worsens quality of life and CV outcomes — IV iron + ESA reduces hospitalisation and transfusion need.

→ ESA and phosphate binders are initiated by nephrology — GP role: monitor, ensure compliance, report side effects.

Within the priority — choose the right agent for this patient's phenotype

ACEi vs ARB — when to choose which

Scenario	Choose	Why
Standard CKD + proteinuria	Ramipril (ACEi)	First-line. REIN trial evidence. Titrate to max tolerated.
ACEi dry cough intolerance	Losartan / Irbesartan (ARB)	No cough. RENAAL/IDNT trials — equivalent renoprotection.
CKD + HFrEF	ACEi (or ARB) + empagliflozin	CV mortality + HF hospitalisation benefit added from SGLT2i.
ACEi + ARB combination	⛔ Do NOT combine	ONTARGET trial: dual RAAS blockade → excess AKI + hyperkalaemia. No added renal benefit.
K⁺ >6.0 mmol/L	Hold ACEi/ARB + patiromer	Hold until K⁺ <5.5, then restart. Patiromer bridges the gap.

Drug choice by CKD complication / phenotype

Complication / phenotype	Preferred drug
CKD + T2DM + ACR ≥25	Dapagliflozin 10mg
CKD + HFrEF	Empagliflozin + ACEi
Hyperkalaemia on RAAS	Patiromer 8.4g OD
Metabolic acidosis (HCO3⁻ <22)	Sodium bicarbonate 500mg TDS
CKD anaemia (iron-deficient)	IV iron (ferric carboxymaltose)
Secondary hyperPTH (G4–G5)	Alfacalcidol 0.25–1 mcg OD

⛔ Absolute prescribing rules — never broken: (1) Check K⁺ and eGFR before starting ACEi/ARB — do not prescribe blind. (2) Never combine ACEi + ARB — dual RAAS blockade causes excess AKI and hyperkalaemia (ONTARGET). (3) SGLT2i sick day rules are mandatory — hold if unwell, vomiting, or pre-surgery (euglycaemic DKA risk). (4) ESA and phosphate binders are nephrology-initiated — primary care role is monitoring, not initiation. (5) Stop all NSAIDs in CKD G3b+ — no exceptions, even short courses. (6) Metformin: reduce at eGFR 30–44, stop at <30 — document the change.

⚙ Interactive Medication Chooser — tick the patient profile, options re-tier live against NICE / BNF

A live, topic-scoped version of the standalone Medication Chooser. The static selector and reference cards below are unchanged.

7E — Medication selection tool — choose patient characteristics for tailored recommendations

7F — Drug reference cards

ACEi / ARB — RAAS Blockade

Ramipril · Lisinopril · Losartan · Irbesartan

✓ Priority 1 — all CKD + ACR ≥3

Priority 1Ramipril 2.5→10mg OD

✓ Indications

CKD + ACR ≥3 (any stage) — renoprotective + antiproteinuric

CKD + hypertension — first-line antihypertensive

CKD + heart failure — mortality benefit (ACEi)

⚠ Rules and monitoring

K⁺ + eGFR at 1–2 weeks after every dose increase

Stop if K⁺ >6.0 or eGFR drops >25% from baseline on initiation

NEVER combine ACEi + ARB (dual RAAS blockade — ONTARGET)

Expected eGFR dip 10–15% on starting — do not stop for this

⚠ Side effects

ACEi dry cough (10–15%): switch to ARB. Angioedema: stop permanently.

💬 Counselling phrase

"This tablet reduces the pressure inside your kidneys and reduces the protein leak we saw in your urine test — it is the single most important tablet for protecting your kidneys. Your kidney level may drop slightly at first, and your potassium may rise — that is why we check blood tests 1–2 weeks after starting."

In SCA: starting or optimising ACEi/ARB in CKD + ACR ≥3 is a mandatory Tasks domain item. Not doing so is a significant deduction. The expected eGFR dip must be explained to the patient — otherwise they will stop it when the blood test comes back.

SGLT2 Inhibitor — Dapagliflozin

Dapagliflozin (Forxiga) 10mg OD · Empagliflozin (Jardiance) for HF

✓ Priority 2 — CKD + T2DM or ACR ≥25

Priority 2Dapagliflozin 10mg OD

✓ Indications in CKD

CKD G2–G4 (eGFR ≥25) with T2DM — DAPA-CKD trial

CKD without T2DM with ACR ≥25 — renal benefit independent of glucose

CKD + HFrEF — empagliflozin preferred for HF indication

⚠ Sick day rules — mandatory

HOLD if vomiting, dehydration, pre-surgery, or severe illness (euglycaemic DKA)

Stop if eGFR <25 (glycaemic benefit lost; renal benefit reduced)

Minor eGFR dip on initiation expected — do not stop for this

⚠ Side effects

Genital mycotic infections — hygiene counselling. UTI risk: ensure no active infection before starting.

💬 Counselling phrase

"This tablet protects your kidneys directly — it reduces the stress inside them and slows the decline, independent of your sugar levels. The most important rule: if you become unwell and cannot keep fluids down, stop it that day and contact us. It is safe at all other times."

DAPA-CKD is a landmark trial — dapagliflozin reduces ESRD/renal death by 39% in CKD G2–G4 with ACR ≥200. In SCA, prescribing or recommending dapagliflozin for Amara (G3b, ACR 42, T2DM) is a high-scoring Tasks domain action. Sick day rules must be counselled.

Statin — Atorvastatin / Rosuvastatin

Atorvastatin 20mg · Rosuvastatin 10mg (G4–G5)

✓ All CKD — regardless of cholesterol

All CKDAtorvastatin 20mg OD

✓ Indications

All CKD G1–G5 — SHARP trial evidence regardless of LDL level

CKD = independent CVD risk equivalent — statin indicated on this basis alone

⚠ Rules

Avoid simvastatin >10mg in CKD G4–G5 (myopathy risk)

Rosuvastatin preferred in severe CKD (less hepatic metabolism)

Do not stop statin once started in CKD (de-prescribing not evidence-based)

⚠ Side effects

Myalgia — check CK. Hepatitis — check LFTs at 3 months. Statin-associated muscle symptoms: switch to different statin or reduce dose.

💬 Counselling phrase

"Patients with kidney disease have a higher risk of heart attacks and strokes — this tablet protects your heart as much as your cholesterol level does. We prescribe it regardless of your cholesterol reading because the kidney disease itself increases the risk."

SHARP trial is the key evidence: statin + ezetimibe in CKD → 25% reduction in major atherosclerotic events. In SCA: prescribing statin for CKD without needing a high cholesterol reading to justify it demonstrates understanding of CKD as an independent CV risk factor.

Patiromer — Potassium Binder

Veltassa (patiromer) 8.4g sachets · Lokelma (ZS-9) alternative

✓ K⁺ >5.5 on ACEi/ARB in CKD

Add-on8.4g OD sachet with food

✓ Indications

K⁺ >5.5 mmol/L in CKD on ACEi/ARB — enables continuation of renoprotective therapy

CKD + HF on RAAS + MRA (spironolactone) — prevents K⁺ accumulation

⚠ Rules

Do NOT take within 3 hours of other medicines — chelates drugs

Recheck K⁺ at 1 week and adjust dose

Target K⁺ 3.8–5.0 mmol/L on patiromer

⚠ Side effects

Constipation, hypomagnesaemia. GI discomfort. Do not crush or heat sachets.

💬 Counselling phrase

"This sachet binds potassium in your gut before it is absorbed — it keeps your potassium at a safe level so we can keep you on the blood pressure tablet that protects your kidneys. Take it with food, not within 3 hours of your other tablets."

AMBER trial key evidence. In SCA: knowing that patiromer enables ACEi/ARB continuation in hyperkalaemic CKD (rather than stopping the RAAS agent) demonstrates a sophisticated understanding of the risk-benefit trade-off in CKD management.

Sodium Bicarbonate — Metabolic Acidosis

Sodium bicarbonate 500mg tablets

✓ HCO3⁻ <22 mmol/L in CKD G4–G5

G4–G5500mg TDS with meals

✓ Indications

CKD G4–G5 with HCO3⁻ <22 mmol/L — slows CKD progression + reduces muscle catabolism

Target serum bicarbonate 22–26 mmol/L

⚠ Rules

Avoid in fluid overload or hypertension poorly controlled (sodium load)

Monitor bicarbonate and BP at 4–6 weeks after starting

⚠ Side effects

Bloating, belching. Worsens hypertension if high sodium intake. Alkalosis if overdosed.

💬 Counselling phrase

"Your blood is slightly too acidic — this is a side effect of reduced kidney function. These tablets gently correct that, which helps slow the kidney decline and protect your muscles."

Metabolic acidosis is often overlooked in CKD. In SCA: recognising HCO3⁻ <22 in a G4 patient and recommending sodium bicarbonate demonstrates completeness of CKD complication management.

IV Iron + ESA (Nephrology-Initiated)

Ferric carboxymaltose (Ferinject) · Darbepoetin alfa (Aranesp) · Epoetin

✓ Hb <100 + iron-deficient in CKD G4–G5

G4–G5Specialist-initiated

✓ Indications

Hb <100 g/L in CKD — iron studies first (TSAT, ferritin)

IV iron: TSAT <20% or ferritin <100 — correct iron deficiency before ESA

ESA: Hb <100 after iron optimised — reduce transfusion dependency

⚠ Primary care rules

ESA is nephrology-initiated only — GP role: monitor Hb, ferritin, BP on ESA

Do NOT use oral iron in CKD G4–G5 — absorption inadequate, use IV iron

Target Hb 100–120 g/L on ESA — avoid >130 g/L (CV events)

💬 Counselling phrase

"Your kidneys normally produce a hormone that tells your body to make red blood cells — when the kidneys are struggling, this hormone is reduced. We can replace it with an injection, but we need to check your iron levels first and get the kidney team involved."

CKD anaemia mechanism (reduced EPO production) is a classic exam question. In SCA: recognising Hb <100 in CKD, ordering iron studies, and stating that ESA needs nephrology initiation (not GP) demonstrates appropriate referral knowledge.

7G — Psychosocial context: integrate into the plan

💛

Psychosocial Factors — Shape Every Management Decision in CKD

🫀

Dialysis fear — brother's story

Amara's mental model of CKD is entirely shaped by watching her brother go through dialysis. Engage with this directly, honestly, and compassionately — not with generic reassurance. Use it as a motivational frame: "What we do today is what makes your outcome different from Raj's."

"Your brother's situation is very real and I understand why it scares you. Let me explain what is different about your situation — and what we can change from today."

💊

Metformin — address specifically

Amara needs a specific answer about her metformin — not "we'll monitor." At eGFR 34, the dose needs reducing. Explain why, what changes, and what replaces it for diabetes management. Vague answers generate anxiety; specific answers generate trust.

"Your metformin needs to be adjusted — at your current kidney level the normal dose can accumulate. I'm reducing it today to a safer amount and adding a new tablet to support your diabetes."

🍽️

Dietary restrictions

Salt and potassium restrictions in South Asian diets require culturally competent dietitian advice — not generic "avoid salt." Specific guidance for traditional cooking (boiling potatoes, avoiding dried fruit, low-sodium alternatives) is far more likely to be followed than generic instruction.

"I'd like to refer you to a dietitian who can give you specific advice that works with the way you cook at home — not generic advice that doesn't fit your life."

🧠

Anxiety and prognostic uncertainty

CKD G3b is a life-altering diagnosis for many patients. PHQ-9 and GAD-7 should be offered at diagnosis. Depression in CKD independently worsens outcomes — it reduces adherence, increases hospitalisation, and worsens quality of life. Acknowledge the emotional weight before the clinical plan.

"Being told your kidneys aren't working as well as they should be is a significant thing to hear. How has it been sitting with you since the nurse called?"

🏃

Exercise and activity

Many CKD patients reduce activity fearing it will worsen their kidneys. The opposite is true — regular moderate exercise reduces CV risk (the dominant cause of death), improves fatigue, and does not accelerate eGFR decline. Specifically correcting this misconception is a quality-of-life intervention.

"Walking 30 minutes five times a week actively protects your kidneys and your heart — you should not avoid exercise because of this diagnosis. Staying active is part of the treatment."

👨‍👩‍👧

Family context and carer needs

Amara's brother's experience means her family may have strong views about her care — and may become over-involved or under-supportive. Explore who is in her support network, whether she wants family involved in the consultation, and whether she has been discussing her diagnosis with them.

"Would you like to bring anyone — a family member or friend — to the next appointment? Sometimes it helps to have someone who can help remember everything we discuss."

7H — Follow-up timeline

Diagnosis / initiation visit — today

eGFR + ACR confirmed · K⁺ checked · Metformin dose adjusted · ACEi/ARB initiated (if K⁺ <5.5) · Statin started if not on one · NSAIDs stopped · Dapagliflozin considered · USS kidneys requested · Urine dipstick · Dietitian referral · Written information (Kidney Care UK) · Sick day rules given · Follow-up booked 1–2 weeks for post-ACEi bloods

ACEi/ARB startedMetformin adjustedSick day rulesUSS requested

1–2w

1–2 weeks — post-ACEi/ARB check

K⁺ + eGFR mandatory after any new RAAS agent or dose increase. Expected: eGFR dip 10–15% (acceptable), K⁺ may rise slightly. Stop ACEi/ARB only if K⁺ >6.0 or eGFR drops >25% from baseline. Reassure patient about expected changes before they see the result.

6 weeks — medication review and BP check

BP to target (<130/80 if DM or ACR ≥70) · ACEi/ARB dose titration · Dapagliflozin check (eGFR, UTI symptoms) · Statin LFTs at 3 months · Dietitian feedback · Patient questions from written information · PHQ-9 / GAD-7

6-monthly — CKD G3b review

eGFR + ACR + K⁺ + Hb + U&E · BP measurement · Medication review · Smoking / weight / exercise update · HbA1c (if T2DM) · eGFR trend assessment: is it stable, declining, or improving? · Refer to nephrology if eGFR <30 or decline >25% in 12 months

Mandatory G3beGFR trend

On reaching G4 (eGFR <30) — nephrology referral and complication screen

Nephrology referral within 4 weeks · Full CKD-MBD screen: phosphate, PTH, vitamin D, bicarbonate · Anaemia screen: Hb, iron studies · Dialysis modality education begins (pre-dialysis education service) · Dietitian for protein restriction guidance · ReSPECT/DNACPR conversation in appropriate patients · 3-monthly bloods from G4 onwards

7I — Monitoring targets and thresholds

Measure	Timing	Action threshold
eGFR	6-monthly (G3a/G3b); 3-monthly (G4)	Decline >5 mL/min/year = significant. >25% decline in 12 months → urgent nephrology.
ACR (albumin:creatinine ratio)	6-monthly (G3+)	Rising ACR = progression marker → intensify RAAS blockade + BP. ACR >70 → BP <130/80.
Potassium K⁺	1–2 weeks post ACEi/ARB change; then 6-monthly	K⁺ >5.5 → diet review + patiromer. K⁺ >6.0 → hold ACEi/ARB + urgent review. K⁺ >6.5 → emergency.
Blood pressure	Every consultation	>130/80 (if DM or ACR ≥70) or >140/90 → intensify antihypertensives. Check for postural hypotension.
Haemoglobin Hb	6-monthly (G3b+)	Hb <110 g/L → iron studies. Hb <100 g/L → IV iron if iron-deficient; ESA eligibility referral.
Bicarbonate HCO3⁻	Annually (G3b); 6-monthly (G4)	HCO3⁻ <22 → sodium bicarbonate 500mg TDS. Target 22–26 mmol/L.
Phosphate + PTH + vitamin D	Annually from G4	Phosphate >1.5 → dietary restriction + phosphate binders. PTH >2× upper normal → active vitamin D.
HbA1c (if T2DM)	Every 3–6 months	Target <53 mmol/mol in CKD (avoid hypoglycaemia). Review metformin dose at every eGFR change.

Key CKD targets

BP target: <130/80 if DM or ACR ≥70. <140/90 otherwise.

K⁺ targets: <5.5 to continue ACEi/ARB. <5.0 on patiromer. >6.5 = emergency.

eGFR triggers: <30 → nephrology. Decline >25% in 12 months → urgent nephrology regardless of stage.

Metformin: Reduce at 30–44. Stop at <30. Review at every eGFR result.

Emergency: K⁺ >6.5 + ECG changes · Uraemic pericarditis · AKI on CKD (oliguric) · Rapidly progressive GN · Pulmonary oedema

Safeguarding: Medication complexity + low literacy · Carer capacity · Dialysis social planning · End-of-life in frail G5

Urgent: K⁺ 5.5–6.5 (no ECG changes) · eGFR <30 new · eGFR decline >25% · Hb <100 g/L · BP >160/100 resistant

Drug review: Stop NSAIDs · Adjust metformin · Hold SGLT2i if unwell · Review contrast agents · No dual RAAS blockade

7J — Safety-netting: exact phrases for every CKD patient

⚠ Three scenario-specific phrases — use these verbatim

Why safety-netting is especially critical in CKD

Sick day rules for ACEi/ARB + SGLT2i + diuretics are NICE-mandated and must be given in writing — omission is a medico-legal risk and QOF quality failure

Hyperkalaemia on ACEi/ARB is the most commonly missed acutely life-threatening CKD complication — patients must know the cardiac symptoms

Euglycaemic DKA from SGLT2i during illness is a well-recognised but under-counselled risk — patients can be severely ill with normal glucose

AKI prevention in CKD requires patient education — 30–40% of all AKI admissions are avoidable with adequate sick day rule knowledge

eGFR decline thresholds for urgent review must be communicated — patients should know that a significant change in their blood result warrants a phone call, not a wait for the annual review

Metformin review obligations: failure to adjust dose as eGFR declines has medico-legal consequences — document every dose review and eGFR at time of review

1–2 weeksK⁺ + eGFR post-ACEi/ARB · Reassure about expected eGFR dip

6 weeksBP check · Medication titration · Dapagliflozin review · PHQ-9

6-monthlyFull CKD panel: eGFR + ACR + K⁺ + Hb + BP + medication review

📋 SCA Consultation Scorecard — self-assess your CKD consultation

🏥

Clinic Quick Reference

CKD — Diagnostic Pathway & Management Summary

NICE NG203 · KDIGO 2024 · Numbers · Drug priorities · Safety netting · Monitoring

▼expand

🔬 1 — Diagnostic Pathway & Triage Algorithm

eGFR <60 or ACR ≥3 sustained >3 months — confirm with repeat, then stage using CGA

↓

🚨 Emergency / same day

K⁺ >6.5 + ECG changes (arrhythmia)
Uraemic pericarditis / encephalopathy
AKI on CKD (oliguric, vomiting)
Rapidly progressive GN
Bilateral hydronephrosis + anuria

999 / emergency nephrology

⚠ Urgent — within days/weeks

K⁺ 5.5–6.5 without ECG changes
eGFR <30 (G4) first identification
eGFR decline >25% in 12 months
Hb <100 g/L in CKD
BP >160/100 resistant

Urgent nephrology / review

✓ Routine — GP management

G3a/G3b stable — 6-monthly review
New diagnosis assessment (cause + ACR + USS)
Drug review (NSAIDs, metformin, doses)
ACEi/ARB initiation + monitoring

NICE NG203 pathway

🔢 2 — Key Numbers to Know

eGFR thresholds

30–44

G3b — Amara

<30

G4 — refer nephrology

<15

G5 — RRT or conservative

ACR significant albuminuria	≥3 mg/mmol → start ACEi/ARB (if DM)
ACR macroalbuminuria	>30 mg/mmol → ACEi/ARB mandatory
K⁺ — hold ACEi/ARB	>6.0 mmol/L
K⁺ — emergency	>6.5 mmol/L + ECG changes
Metformin — reduce	eGFR 30–44
Metformin — stop	eGFR <30

Targets and referral triggers

BP target — DM or ACR ≥70	<130/80 mmHg
BP target — other CKD	<140/90 mmHg
Nephrology referral	eGFR <30 or decline >25%/year
Dapagliflozin eligibility	eGFR ≥25 + CKD (±T2DM)
ESA initiation	Hb <100 after IV iron — nephrology
Metabolic acidosis treatment	HCO3⁻ <22 → NaHCO3 500mg TDS

💊 3 — Drug Priority Ladder

Priority	Drug	Indication	Key rule
1	ACEi / ARB	All CKD + ACR ≥3 or hypertension	Check K⁺ + eGFR at 1–2 weeks. Never combine ACEi + ARB.
2	Dapagliflozin 10mg	CKD + T2DM or ACR ≥25, eGFR ≥25	Sick day rules mandatory. Hold if unwell.
3	Antihypertensives (CCB/thiazide)	BP not at target on ACEi alone	Amlodipine first add-on. Avoid thiazides if eGFR <30.
4	Statin (atorvastatin 20mg)	All CKD regardless of cholesterol	SHARP trial evidence. Rosuvastatin in G4–G5.
5	Patiromer (potassium binder)	K⁺ >5.5 on ACEi/ARB	Enables ACEi/ARB continuation. Not within 3h of other drugs.
G4–G5	NaHCO3 · IV iron · ESA · Phosphate binders	CKD-MBD + anaemia complications	ESA nephrology-initiated. IV iron not oral in G4–G5.

⛔ Never combine ACEi + ARB · ⛔ SGLT2i sick day rules mandatory · ⛔ Stop NSAIDs in G3b+ · ⛔ Adjust metformin at eGFR <45, stop at <30 · ⛔ ESA = nephrology only

⚠ 4 — Safety Netting & Follow-Up

Follow-up schedule

Diagnosis: ACEi/ARB initiated · Metformin adjusted · NSAIDs stopped · Dapagliflozin considered · USS + urine dipstick · Dietitian referral · Sick day rules written · 1–2 week bloods booked

1–2w

1–2 weeks: K⁺ + eGFR post-ACEi/ARB mandatory. Expected dip 10–15% = acceptable. Stop if K⁺ >6.0 or eGFR drops >25%.

6 weeks: BP to target · Medication titration · Dapagliflozin check · Statin LFTs · PHQ-9

6-monthly G3b: eGFR + ACR + K⁺ + Hb + BP + medication review + HbA1c + smoking

📌 eGFR <30 or decline >25% in 12 months → nephrology referral within 4 weeks

🔬 5 — Monitoring Targets

Measure	Timing	Action threshold
eGFR	6-monthly (G3); 3-monthly (G4)	Decline >25% in 12 months → urgent nephrology. <30 → nephrology referral.
ACR	6-monthly (G3b+)	Rising ACR = progression → intensify RAAS. ACR >70 → BP <130/80.
K⁺	1–2w post-ACEi change; then 6-monthly	>5.5 → patiromer + diet. >6.0 → hold ACEi/ARB. >6.5 → emergency.
BP	Every consultation	>130/80 (if DM/ACR ≥70) → intensify. Check postural drop in elderly.
Hb	6-monthly (G3b+)	<110 → iron studies. <100 → IV iron; ESA eligibility referral (nephrology).
HCO3⁻	Annually G3b; 6-monthly G4	<22 → sodium bicarbonate 500mg TDS.
Metformin dose	At every eGFR result	eGFR 30–44 → reduce dose. eGFR <30 → stop. Document every review.

Emergency: K⁺ >6.5 + ECG changes · Uraemic pericarditis · AKI oliguric · Rapidly progressive GN · Pulmonary oedema in CKD

Safeguarding: Medication complexity + low literacy · Sick day rule understanding · Dialysis social planning · End-of-life in frail G5

🛡️ 6 — Nephrotoxin Checklist & Drug Rules

Stop immediately in G3b+

NSAIDs (all — OTC and prescribed) · Aminoglycosides (if avoidable) · Contrast agents (hold ACEi/SGLT2i/metformin) · Lithium monitoring intensified · Herbal nephrotoxins (aristolochic acid)

Dose-adjust by eGFR

Metformin: reduce at eGFR <45, stop at <30 · Sitagliptin: reduce at eGFR <45 · Gabapentin/pregabalin: reduce at eGFR <30 · Direct anticoagulants: dose-adjust by eGFR

Sick day rules — hold when unwell

SGLT2i · ACEi/ARB · Diuretics (loop + thiazide) · Metformin · NSAIDs. Resume once eating/drinking and clinically well. Written card mandatory at every CKD consultation.

🎓

SCA Exam Quick Reference

SCA Consultation Blueprint

Tasks · Relating to Others · Global Skills · RAG guide

▼expand

🕐 12-Minute Consultation Flow

0–2 min

Open & ICE

"I can see from your notes that your kidney function came up on your blood test and you've been asked to come in. Before I go through the result, what has been going through your mind since the nurse called?"

"You mentioned your brother Raj is on dialysis — that must make this feel very frightening. Can you tell me what happened with him?"

Relating to OthersGlobal Skills

✗ Notes not used · Repeating documented info · No open Q · Going straight to symptoms · Brother's story not explored

2–4 min

Safety Screen

"Before we go through the plan — any muscle weakness, palpitations, or feeling very unwell recently? Do you know what your potassium level was? Any change in how much you're passing water?"

Red flags: K⁺ level · Uraemic symptoms (fatigue, nausea, pruritis) · Fluid overload · eGFR trend · Drug history (NSAIDs, metformin dose)

TasksGlobal Skills

✗ No K⁺ check · No eGFR trend assessment · Not asking about NSAIDs · No uraemic symptom screen

4–7 min

Context & Risk

Metformin: "Your metformin dose needs to be reviewed — at eGFR 34 I need to reduce it. Let me explain why and what changes."

Cause: T2DM + hypertension + ACR 42 = diabetic nephropathy. USS requested. Dietitian referral for potassium + salt restriction.

Prognosis: most G3b patients never reach dialysis — honest, specific, not falsely reassuring.

TasksRelating to Others

✗ Metformin vague ("we'll keep an eye on it") · Prognosis falsely reassuring · Cause not identified · Dietary advice generic

7–10 min

Explain & Address ICE

"Your kidneys are working at about half capacity — and most people at this stage never need dialysis, especially when we act now. What we do today is what makes your outcome different from your brother's."

"The expected eGFR dip after starting the new tablet is normal — please don't stop it when the blood test comes back slightly lower."

TasksRelating to Others

✗ Generic reassurance without engaging with brother · Jargon (G3b, ACR, RAAS) without translation · Not explaining expected eGFR dip

10–12 min

Plan & Close

"If you feel a fast heartbeat, muscle weakness, or you become very unwell and can't keep fluids down — go straight to A&E. Stop the dapagliflozin tablet when you're unwell."

ACEi/ARB started · Metformin adjusted · NSAIDs stopped · Dapagliflozin discussed · Statin started · USS + dietitian referral · 1–2 week bloods booked · Sick day rules written · "Is there anything else?"

TasksRelating to OthersGlobal Skills

✗ No sick day rules · No K⁺ emergency symptoms stated · Vague follow-up · No 1–2 week bloods booked · NSAIDs not stopped

🔴🟠🟢 RAG — All 3 Domains

Tasks

🟢

K⁺ checked · ACEi/ARB initiated (K⁺ <5.5 confirmed) · Metformin dose adjusted · NSAIDs stopped · Dapagliflozin discussed (eGFR ≥25 confirmed) · Statin started · USS + urine dipstick ordered · Sick day rules given in writing · 1–2 week bloods booked · Nephrology threshold communicated · eGFR trend interpreted

🟠

ACEi/ARB initiated but K⁺ not checked first · Metformin mentioned not dose-adjusted · Dapagliflozin not discussed · USS not ordered · Sick day rules verbal not written · Follow-up vague · eGFR trend not interpreted

🔴

K⁺ not checked · ACEi/ARB not started despite ACR ≥3 · Metformin not reviewed · NSAIDs not stopped · No sick day rules · No bloods booked · Goes to generic management without safety screen

Relating to Others

🟢

Notes used first · Brother's story engaged with directly and used to frame management · Metformin specifically addressed with dose plan · Honest personalised prognosis (not "don't worry") · Expected eGFR dip explained before blood result · Dietary advice culturally tailored · Expectation addressed before plan · Chunk-and-check · "Anything else?"

🟠

Brother's story collected but not used in plan · Prognosis vague ("hopefully won't need dialysis") · Metformin mentioned not addressed specifically · Dietary advice generic · Expectation after plan

🔴

Generic reassurance on dialysis · Brother not engaged with · Metformin not addressed · Jargon throughout · Straight to prescribing · No shared decision-making

Global Skills

🟢

Notes used first · Open Q yields full ICE in first response · Data gathering by 6–7 min · Lay language throughout · eGFR trend assessed · CGA staging explained as "half capacity" · Responsive to brother cue · Structured · Expectation before management

🟠

Some jargon · Overruns data gathering · eGFR trend not interpreted · CGA staging not explained · Expectation after plan

🔴

Notes not used · Jargon throughout · No open Q · Data gathering incomplete · Cues missed · No structure · Goes to management without ICE

💬 Key Phrases

💭 Ideas — dialysis fear

"When you think about this kidney result and your brother's situation — what do you think is going to happen to you?"

😟 Concerns — brother + metformin

"I want to come back to two things — your brother Raj, and your metformin. Let me address both of those directly before we go through the plan."

🎯 Honest prognosis

"Most people with your level of kidney function never need dialysis — especially when we catch it at this stage and act now. Your brother's situation was different. What we do today is what changes your outcome."

💊 Metformin specific

"Your metformin needs to be adjusted — at eGFR 34 the normal dose can accumulate. I'm reducing it to a safer amount today and adding a new tablet to support your diabetes at the same time."

🩸 ACEi/ARB expected dip

"After starting the new blood pressure tablet, your kidney number may drop slightly in the first 2 weeks — that is completely expected and normal. Please don't stop the tablet if you see that."

✅ Sick day rules + close

"If you feel palpitations, muscle weakness, or you're very unwell and can't keep fluids down — go straight to A&E. Stop the dapagliflozin when unwell. Here are the rules in writing. Is there anything else?"

🚫 9 Danger Zones

✗

Generic reassurance on dialysis without engaging with the brother's story
→ Engage directly and specifically. "Your brother's situation was different — here is what we can do now."

✗

Not checking K⁺ before starting ACEi/ARB
→ K⁺ must be <5.5 before initiation. Prescribing blind into unknown K⁺ is dangerous.

✗

Not addressing metformin with a specific dose plan
→ eGFR 34 = reduce to 500mg BD. Vague "we'll monitor" is not acceptable.

✗

Not stopping NSAIDs in CKD G3b
→ NSAIDs must be stopped. OTC ibuprofen must be specifically asked about.

✗

Combining ACEi + ARB (dual RAAS blockade)
→ ONTARGET trial: excess AKI + hyperkalaemia. Always one or the other.

✗

Not explaining the expected eGFR dip after ACEi/ARB initiation
→ Patients who see the dip stop the tablet. Explain before the blood result arrives.

✗

Not giving sick day rules for SGLT2i + ACEi/ARB in writing
→ NICE-mandated, medico-legal requirement, QOF indicator. Must be written.

✗

Starting ESA in primary care
→ ESA is nephrology-initiated only. GP role: iron studies + referral + monitoring on ESA.

✗

Not referring at eGFR <30 or with rapid decline
→ NICE NG203 mandatory referral thresholds. Failing to refer at G4 is a serious safety failure.

💊 Drug Quick-Pick

CKD + ACR ≥3 — all stages

→

ACEi (ramipril)

Check K⁺ + eGFR at 1–2w

ACEi cough intolerance

→

ARB (losartan)

Equivalent renoprotection

CKD + T2DM + eGFR ≥25

→

Dapagliflozin 10mg

Sick day rules mandatory

K⁺ >5.5 on ACEi/ARB

→

Patiromer 8.4g OD

Not within 3h of other drugs

All CKD — CV risk

→

Statin (atorvastatin)

Regardless of cholesterol (SHARP)

HCO3⁻ <22 mmol/L in G4–G5

→

NaHCO3 500mg TDS

Target HCO3⁻ 22–26

⛔ Never ACEi + ARB combined · ⛔ Stop NSAIDs in G3b+ · ⛔ Adjust metformin at eGFR <45, stop at <30 · ⛔ ESA = nephrology only · ⛔ SGLT2i sick day rules mandatory

Chronic Kidney Disease · GP Clinical Reasoning Framework · NICE NG203 · KDIGO 2024 · CKS 2023 · DAPA-CKD · SHARP · REIN · RENAAL · AMBER · ONTARGET

Includes: Clinical stem · Open Q first · ICE (dialysis fear + brother's story + metformin) · Safeguarding · CGA staging · Drug priority ladder · Prescribing guide · ACEi/ARB monitoring · Dapagliflozin sick day rules · Patiromer · Statin for all CKD · CKD-MBD · SCA RAG checkpoints · Dual collapsible summaries · SCA Scorecard /33

Teaching clinicians why each step matters — not just what to do · Always consult current BNF/SPC/NICE/KDIGO guidelines · Clinical judgement takes precedence over any framework