Synopsis
Recognise minimal change disease as a biopsy-defined cause of nephrotic syndrome, manage adult glucocorticoid response and complications safely, and identify relapse, secondary triggers and alternative diagnoses.
- Minimal change disease causes a selective or predominantly albuminuric nephrotic syndrome through podocyte foot-process injury without immune-complex deposition.
- Light microscopy is normal or nearly normal, immunofluorescence is negative or nonspecific, and electron microscopy shows diffuse podocyte foot-process effacement.
- Children with a typical steroid-sensitive nephrotic presentation may be treated without initial biopsy, whereas adults usually need tissue confirmation before immunosuppression.
- Adults can develop abrupt anasarca, severe hypoalbuminaemia, venous thrombosis and acute kidney injury; AKI is especially recognised in older adults with marked oedema.
- Primary disease is often idiopathic, but NSAIDs, lithium, interferon, immune checkpoint inhibitors, infection, allergy and Hodgkin lymphoma are notable secondary associations.
- NSAID-associated minimal change may coexist with acute interstitial nephritis, so rash, eosinophilia and pyuria are helpful but often absent.
- Initial adult treatment is high-dose oral glucocorticoid under nephrology care, continued until remission or a maximum exposure window before gradual taper.
- Adult response can take substantially longer than childhood response; failure to remit by the specialist-defined treatment limit triggers adherence and pathology review, not endless steroid escalation.
- Frequent relapse or steroid dependence can be treated with cyclophosphamide, rituximab, a calcineurin inhibitor or a mycophenolic-acid analogue chosen around toxicity and patient priorities.
- Thrombotic prophylaxis is individualised from albumin, histology-independent risks, bleeding and planned biopsy; oedema alone is not an indication for anticoagulation.
- Supportive care includes careful sodium restriction and diuresis, infection prevention, blood-pressure and lipid assessment, vaccination and avoidance of the triggering medicine.
- Relapse is detected through renewed quantitative proteinuria and falling albumin; isolated ankle swelling or a home dipstick should be confirmed and alternative causes considered.
Key red flags
Oliguria and rising creatinine can accompany severe nephrosis through underfilling, tubular or interstitial oedema, sepsis, thrombosis or nephrotoxic exposure and require urgent cause assessment.
New pleuritic pain, hypoxia, asymmetric swelling, flank pain or haematuria can represent pulmonary, limb or renal-vein thrombosis and demands an urgent VTE pathway.
Investigation priorities
Quantify protein loss, assess albumin predominance and identify inflammatory or glomerular mimics.
Management branches
An adult has new heavy proteinuria, hypoalbuminaemia and oedema with a possible minimal-change phenotype.
- Assess fluid and perfusion, infection, VTE and AKI, quantify protein and review NSAIDs, cancer therapies, allergy, infection and malignancy clues.
- Send focused secondary tests and arrange native kidney biopsy with adequate immunofluorescence and electron microscopy, correcting blood pressure and bleeding risk.
- Begin cause-specific and glucocorticoid treatment only after nephrology integrates biopsy and clinical context; stop a plausible trigger safely with the prescribing team.
Key medicines
PrednisoloneKDIGO high-dose daily or alternate-day treatment is specialist prescribed for up to the response limit, then tapered after remission.Infection, diabetes, mood disturbance, hypertension, osteoporosis, cataract and adrenal suppression require proactive prevention and a defined taper rather than repeated unreviewed courses.
RituximabUse a specialist intravenous induction schedule with screening, premedication and any re-dosing based on the renal plan.Infusion reaction, hepatitis B reactivation, hypogammaglobulinaemia and infection require vaccine timing, viral screening, immunoglobulins and blood-count review.