Synopsis
Recognise the nephrotic phenotype, identify a treatable glomerular cause, and prevent thrombosis, infection, acute kidney injury and harmful over-diuresis while specialist assessment proceeds.
- Adult nephrotic syndrome combines heavy glomerular protein loss, hypoalbuminaemia and oedema; hyperlipidaemia and lipiduria are supportive consequences rather than essential diagnostic criteria.
- Quantify urine protein with a laboratory protein:creatinine ratio because albumin-only measurement can underestimate non-albumin proteins and a dipstick is concentration-dependent.
- Primary causes include minimal change disease, focal segmental glomerulosclerosis and membranous nephropathy; diabetes, lupus, amyloid, infection, medicines and malignancy are important secondary causes.
Key red flags
Sudden dyspnoea, pleuritic pain, syncope, tachycardia, hypoxaemia or asymmetric leg swelling is not explained away by nephrotic oedema and requires an urgent VTE pathway.
Investigation priorities
Confirm and characterise glomerular protein loss while looking for haematuria or infection.
Management branches
Heavy proteinuria with hypoalbuminaemia, oedema or an otherwise convincing nephrotic presentation.
- Assess ABCDE, perfusion and true fluid state; look actively for sepsis, VTE, pulmonary oedema, oliguria and other reasons for immediate admission.
- Quantify total urine protein, establish kidney-function and albumin trends, review systemic disease, infection, malignancy and medicine exposures, and send focused secondary-cause tests.
Key medicines
Loop diureticDose and route are individualised to congestion, kidney function and prior exposure; follow the local renal prescription.
ACE inhibitor or ARBStart one agent at a low licensed dose after stabilisation, then titrate with specialist-agreed biochemical checks.