Conditions · Nephrology and urology
Minimal change disease !
Minimal change disease is the commonest cause of nephrotic syndrome in children: the kidneys leak protein and cause swelling, but steroids usually work.
Updated 2026-11-01
Structures involved
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In the clinical exam
Why it happens
- Edema and effusions: the four mechanisms
- Glomerular filtration: the barrier and its determinants
- Starling forces at the capillary
- Glomerulus and the filtration barrier: podocytes, mesangium, JGA
- Electron microscopy: what it shows that light can't
What it is
A podocyte disease that causes nephrotic syndrome with glomeruli that look normal under the light microscope; the only finding is effacement (fusion) of the podocyte foot processes on electron microscopy. It is the leading cause of nephrotic syndrome in children.
Who gets it
It causes most cases of nephrotic syndrome in children, typically between about 2 and 6 years and more often in boys, and a smaller share (about 10–15%) of adult cases. Episodes often follow a respiratory infection or allergic reaction. The same pattern is seen in Colombian paediatric nephrology services.
Causes
- Primary (idiopathic): most cases, especially in children; circulating factors and anti-nephrin antibodies are being studied
- Drugs: NSAIDs, lithium, interferon, some antibiotics
- Cancers: Hodgkin lymphoma and other lymphoid malignancies
- Allergies and atopy (pollen, insect stings, food), and recent infections
Risk factors
- Age 2–6 years and male sex in childhood
- Atopy and recent upper respiratory infection
- Regular NSAID use
- Hodgkin lymphoma in adults
Pathophysiology
An immune signal, probably from T cells or circulating factors, injures the podocytes. Their foot processes flatten and fuse, and the filtration barrier loses its charge selectivity, so albumin (but not larger proteins) leaks into the urine (selective proteinuria). The result is the nephrotic picture: hypoalbuminaemia, oedema, hyperlipidaemia and a tendency to clotting and infection, usually with normal blood pressure and kidney function.
Classification
- Steroid-sensitive (most children)
- Frequently relapsing or steroid-dependent
- Steroid-resistant (should prompt biopsy and search for FSGS or genetic disease)
Symptoms and signs
- Rapid swelling around the eyes, worse in the morning, then of the legs and abdomen
- Foamy urine
- Weight gain from fluid retention
- Ascites and scrotal or labial swelling in children
- Tiredness and poor appetite
- Usually no visible blood in urine and normal blood pressure
Diagnosis
- Clinical
- A young child with generalised oedema, normal blood pressure and no gross haematuria is treated as minimal change disease without biopsy; response to steroids supports the diagnosis.
- Tests
- Urine dipstick with heavy protein and a high urine protein-to-creatinine ratio; low serum albumin; high cholesterol; usually normal creatinine and complement. Kidney biopsy (adults, atypical children, steroid resistance) shows normal glomeruli on light microscopy, negative immunofluorescence and foot-process effacement on electron microscopy.
- Imaging
- Kidney ultrasound before biopsy; chest X-ray or ultrasound for effusions and ascites when needed.
Differential diagnosis
- Focal segmental glomerulosclerosis
- Membranous nephropathy (adults)
- Nephritic syndromes (post-streptococcal, IgA nephropathy)
- Heart failure, cirrhosis or malnutrition with oedema
- Allergic angioedema
Goal of treatment
Induce remission of proteinuria, control oedema, prevent infection and thrombosis, and limit the cumulative adverse effects of steroids in relapsing patients.
Treatment
- Medical
- Oral glucocorticoids are first-line; most children enter remission within about four weeks.
- Medical
- Steroid-sparing agents for frequent relapses or steroid dependence: calcineurin inhibitors, cyclophosphamide, mycophenolate or rituximab.
- Medical
- Loop diuretics and sometimes albumin for severe oedema; treating or stopping the cause in secondary forms (NSAIDs, lymphoma).
- Lifestyle
- Low-salt diet; pneumococcal and other vaccines according to schedule (live vaccines deferred during high-dose steroids).
- Follow-up
- Nursing care: daily weight, intake and output, home urine dipstick to detect relapse, skin care in oedematous areas, watching for infection, clots and steroid effects (growth, blood pressure, glucose, mood).
Complications
- Relapses (in most children) and steroid toxicity
- Infections, including spontaneous bacterial peritonitis and cellulitis
- Venous thromboembolism
- Acute kidney injury, mainly in adults
- Hypovolaemia with aggressive diuresis
Prognosis
Very good. Most patients respond to steroids and keep normal kidney function long term, and many children outgrow the disease by adolescence despite relapses. Steroid resistance is unusual and suggests another diagnosis such as FSGS.
Test yourself
Think of the answer, then tap the question to see it.
What does electron microscopy show in minimal change disease?
Diffuse effacement (fusion) of podocyte foot processes, with normal light microscopy and negative immunofluorescence.
What is the first-line treatment of minimal change disease?
Glucocorticoids; most children enter remission within weeks.
Which malignancy is classically associated with minimal change disease in adults?
Hodgkin lymphoma.
Why is the proteinuria in minimal change disease called selective?
Mainly albumin is lost because the barrier loses its charge selectivity while keeping its size barrier.
Related conditions
- Nephrotic syndrome
- Focal segmental glomerulosclerosis
- Hodgkin lymphoma
- Acute kidney injury
- Deep vein thrombosis
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Minimal change disease: MedlinePlus Medical Encyclopedia (MedlinePlus (U.S. National Library of Medicine), 2024); Nephrotic Syndrome in Adults (NIDDK (National Institutes of Health), 2024).
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