Proteinuria is usually a chronic marker, but a handful of presentations are emergencies hiding behind a dipstick result. Nephrotic and nephritic syndromes, and proteinuria accompanying acute kidney injury, need same-day nephrology because the kidney is being actively damaged. The examiner-critical point is myeloma: standard urine dipsticks detect albumin, not the monoclonal free light chains (Bence Jones protein) of myeloma, so an older patient with bone pain, anaemia, hypercalcaemia or a high ESR needs a deliberate myeloma screen under NG12 — the proteinuria may be "overflow", and the dipstick can be falsely reassuring.

The first decision in proteinuria is whether it is real and persistent. Fever, urinary infection, strenuous exercise and decompensated heart failure all produce transient proteinuria that resolves, so a single positive result is repeated once the patient is well. In younger people, orthostatic proteinuria — present on standing, absent in the first-morning sample — is benign and needs only reassurance. The history then sorts the persistent causes into the common metabolic ones (diabetes, hypertension) and the glomerular and systemic ones that change the urgency and the work-up.

Quantification matters because the number drives both staging and referral. The albumin:creatinine ratio on a first-morning urine is the standard, removing the variability of a dipstick and the inconvenience of 24-hour collections. A mismatch — dipstick-positive but ACR low — is an important clue, because it points away from albumin (glomerular) proteinuria towards tubular or overflow light-chain proteinuria, and should prompt a PCR and a myeloma screen rather than reassurance.

Sorting proteinuria by mechanism keeps the dangerous overflow cause visible alongside the common glomerular ones. Glomerular proteinuria (diabetes, hypertension, the glomerulonephritides) is albumin-predominant and well captured by ACR. Tubular and overflow proteinuria are not — and overflow proteinuria is the footprint of myeloma. Holding these categories in mind prevents the two classic errors: investigating benign orthostatic proteinuria as if it were renal disease, and reassuring an older patient with overflow proteinuria whose ACR looks unremarkable.

Investigation is tiered by what the history and ACR suggest. Everyone gets the core panel — eGFR, HbA1c, FBC, lipids and a confirmed ACR — that stages CKD and identifies the common drivers. A glomerulonephritis picture (haematuria, casts, systemic features, falling eGFR) triggers the immunology screen and prompt referral, while an older patient or a non-albumin pattern triggers the myeloma screen. Renal ultrasound checks structure and obstruction. The recurring rule is confirmation: neither CKD nor proteinuria is diagnosed on a single reading.

The referral thresholds are deliberately concrete: an ACR of 70 or above, or 30 or above with haematuria, defines the renal disease that benefits from nephrology, as does any sustained fall in eGFR. Around these sit the two cancer pathways — a positive myeloma screen to haematology, and visible or qualifying non-visible haematuria to urology under NG12 — and the emergencies (nephrotic, nephritic, AKI) that bypass all of this for same-day assessment. In pregnancy, new proteinuria with hypertension is pre-eclampsia until proven otherwise.

For most proteinuric kidney disease the disease-modifying treatment is a bundle, not a single drug. Blocking the renin–angiotensin system with an ACE inhibitor or ARB titrated to the maximum tolerated dose reduces proteinuria and slows progression, and an SGLT2 inhibitor added on top now has strong evidence for protecting the kidney and the heart. Around these sit blood-pressure and lipid targets, glycaemic control in diabetes, and removal of nephrotoxins. The safety rule is the post-initiation U&E: a modest eGFR dip is expected and acceptable, but it must be checked.

Lifestyle in proteinuric CKD is genuinely disease-modifying rather than supportive. Salt restriction unlocks the full antiproteinuric benefit of RAS blockade, smoking cessation slows progression and protects the heart, and weight loss lowers both proteinuria and blood pressure. Equally important is what to avoid — routine NSAIDs and unregulated herbal products — and sick-day rules for the renoprotective drugs, which should be paused during significant dehydrating illness to prevent acute kidney injury.

Follow-up does two things: it tracks the trajectory of the kidney (serial ACR and eGFR, with monitoring frequency scaled to CKD stage) and it keeps the dangerous causes under review. The myeloma safety-net never fully closes in older patients with unexplained proteinuria, and any drift towards nephrotic features, visible haematuria or a rising creatinine warrants same-day reassessment. Each change to a renoprotective drug — and every dehydrating illness — is a cue to recheck renal function.