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.
- Generalised oedema does not prove intravascular excess: low oncotic pressure, diuretics, diarrhoea and sepsis can leave a visibly oedematous patient hypotensive and kidney under-perfused.
- Urinary antithrombin loss, increased hepatic procoagulant synthesis and immobility produce substantial venous thromboembolism risk, especially with profound hypoalbuminaemia and membranous nephropathy.
- Fever, abdominal pain or subtle deterioration may represent serious infection because immunoglobulin and complement losses, oedematous tissue and immunosuppression impair defence.
- Acute kidney injury may reflect hypovolaemia, sepsis, interstitial oedema, renal-vein thrombosis, drug toxicity or the underlying glomerular lesion; do not label every creatinine rise as disease progression.
- Salt restriction and carefully titrated loop diuresis treat symptomatic oedema, but daily weights, blood pressure, creatinine and electrolytes must guide the pace of fluid removal.
- ACE inhibition or ARB therapy can reduce proteinuria after haemodynamic stability is established; never combine the two, and review potassium and kidney function after initiation or titration.
- Prophylactic anticoagulation is not automatic: nephrology weighs albumin, histology, bleeding risk, mobility, previous thrombosis and anticipated biopsy or procedures.
- Kidney biopsy usually defines non-diabetic adult disease, but the indication and timing depend on phenotype, diabetes history, serology, bleeding risk and whether histology will alter treatment.
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.
Flank pain, macroscopic haematuria, abrupt kidney dysfunction or unexplained worsening proteinuria can signal renal-vein thrombosis, but presentation may be silent and imaging choice depends on kidney function.
Fever, abdominal tenderness, cellulitis, cough, confusion or an unexplained fall in blood pressure may indicate bacterial infection and warrants cultures and prompt sepsis assessment.
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.
- Discuss early with nephrology for biopsy planning, complication-risk assessment and disease-specific treatment; avoid empirical glucocorticoids in an undiagnosed adult unless a specialist directs them.