Steroid-responsive nephrotic syndrome with normal light microscopy and diffuse foot-process effacement.
Also known as: MCD, minimal change disease, nil disease, lipoid nephrosis
Overview
A podocytopathy characterized by nephrotic syndrome with normal-appearing glomeruli on light microscopy, absent immune deposits on immunofluorescence, and diffuse podocyte foot-process effacement on electron microscopy. The most common cause of nephrotic syndrome in children.
Epidemiology
Causes ~90% of nephrotic syndrome in children under age 10 and ~10-15% in adults. Peak childhood incidence age 2-6, with a male predominance in pediatrics that disappears in adults. Strong association with atopy and recent upper respiratory infections.
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MCD is felt to be a T-cell–mediated podocytopathy. A circulating factor (possibly anti-nephrin antibodies, IL-13, or hemopexin) alters the podocyte cytoskeleton, neutralizes the negatively charged glomerular filtration barrier, and produces selective loss of albumin into the urine. Foot-process effacement is diffuse but reversible, explaining the rapid response to corticosteroids and the absence of structural damage on light microscopy.
Clinical presentation
Symptoms
Abrupt onset (often within days) of periorbital and dependent edema
Foamy urine, weight gain, decreased urine output
Children may present with abdominal pain from ascites or peritonitis
Symptoms often follow a viral illness or allergen exposure
IgA nephropathy — Nephritic features (hematuria) usually dominate; mesangial IgA deposits
Diagnostic workup
Diagnostic criteria
In children with classic presentation (age 1-10, no hematuria, no hypertension, normal complement, normal renal function), empiric corticosteroid therapy is initiated without biopsy. Adults and steroid-resistant children require kidney biopsy showing normal LM, negative IF, and diffuse foot-process effacement on EM.
Labs
Spot urine protein-to-creatinine ratio or 24-hour urine — nephrotic range (>3.5 g/day adult; >40 mg/m²/h child)
Serum albumin (low, often <2.5 g/dL), lipid panel (elevated)
BMP — usually normal Cr; AKI can occur from intravascular volume depletion
C3, C4 — both normal (helps distinguish from membranoproliferative or lupus nephritis)
Hepatitis B, hepatitis C, HIV, ANA, anti-PLA2R (in adults) to exclude other causes
Consider age-appropriate malignancy screening in adults (lymphoma history, exam)
Imaging
Renal ultrasound only if AKI, hematuria, or suspicion of obstruction — usually normal-sized kidneys
Diagnostic algorithm
Feature
Minimal change disease
FSGS
Most common age
Children 2-6
Adults, especially Black patients
Hematuria
Rare
Common
Hypertension
Uncommon
Common
Light microscopy
Normal
Focal segmental sclerosis
EM foot-process effacement
Diffuse
Diffuse (primary) or segmental (secondary)
Steroid response
~90% in children
~30-50% in adults
Progression to ESKD
Rare
Common in untreated primary
MCD vs FSGS — overlapping presentations distinguished by biopsy and steroid response.
Treatment
First-line
Corticosteroids — prednisone 60 mg/m²/day (max 60 mg) in children for 4-6 weeks, then taper; 1 mg/kg/day (max 80 mg) in adults for up to 16 weeks
Dietary sodium restriction, fluid management
Loop diuretic (furosemide, torsemide, bumetanide) for symptomatic edema — use cautiously to avoid intravascular volume depletion
Albumin infusion before IV diuretic if severe hypoalbuminemia and refractory edema (controversial)
Pneumococcal vaccination and consideration of penicillin prophylaxis in children with hypogammaglobulinemia
Steroid-sensitive (most pediatric cases)
Remission within 4 weeks of steroid therapy
Taper over additional 2-5 months once urine protein negative
Progression to FSGS in steroid-resistant cases on repeat biopsy
PANCE pearls
Classic pediatric presentation does not require biopsy — empiric prednisone is both diagnostic and therapeutic.
Hodgkin lymphoma is the classic paraneoplastic association in adults.
Severe edema with hypoalbuminemia can precipitate intravascular volume depletion and prerenal AKI; diurese cautiously.
Children with relapse should be screened for SBP if abdominal pain develops.
Anti-nephrin antibodies have recently been described as a possible serologic marker (2022-2024 literature).
References
KDIGO 2021 — KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases (Kidney Int 2021;100:S1-S276)
IPNA — International Pediatric Nephrology Association Clinical Practice Recommendations for Steroid-Sensitive Nephrotic Syndrome (Pediatr Nephrol 2023;38:877-919)
Anti-nephrin Ab — Watts AJB et al. Discovery of autoantibodies targeting nephrin in minimal change disease (JASN 2022;33:238-252)
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