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.
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.
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.
Key medicines
PrednisoloneKDIGO high-dose daily or alternate-day treatment is specialist prescribed for up to the response limit, then tapered after remission.
RituximabUse a specialist intravenous induction schedule with screening, premedication and any re-dosing based on the renal plan.