IgA nephropathy !

IgA nephropathy is a kidney disease in which IgA antibody deposits inflame the kidney filters, typically causing blood in the urine after a sore throat.

Updated 2026-11-01

Structures involved

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In the clinical exam

Nephrotic vs nephritic syndrome

Why it happens

What it is

A chronic immune glomerulonephritis defined by deposits of immunoglobulin A in the mesangium of the glomeruli, seen on kidney biopsy. It is the most common primary glomerulonephritis worldwide. When the same IgA deposits also affect the skin, joints and gut it is called IgA vasculitis (Henoch-Schönlein purpura), which is more common in children.

Who gets it

It usually starts between the second and fourth decades and is more frequent in men. It is most common in East Asia, less in people of African ancestry. In Latin America it is a leading biopsy diagnosis among primary glomerular diseases in young adults, and a cause of chronic kidney disease in that age group.

Causes

Abnormal IgA1 with poor glycosylation (galactose-deficient IgA1), partly genetic
Autoantibodies (IgG) that bind this abnormal IgA and form immune complexes
Triggers of mucosal immunity: upper respiratory or gastrointestinal infections
Secondary forms: liver cirrhosis, coeliac disease, inflammatory bowel disease, HIV infection

Risk factors

Young adult male
East Asian or Indigenous American ancestry
Family history of IgA nephropathy
Chronic liver disease, coeliac disease or inflammatory bowel disease

Pathophysiology

Galactose-deficient IgA1 is recognised by autoantibodies, and the resulting circulating immune complexes deposit in the mesangium. They activate mesangial cells and complement (mainly the alternative and lectin pathways), causing mesangial proliferation, inflammation and, over years, glomerular scarring and interstitial fibrosis. Haematuria often follows mucosal infections within one to two days (synpharyngitic), which distinguishes it from post-streptococcal glomerulonephritis, where the delay is one to three weeks.

Classification

Primary versus secondary (liver, gut, infection)
Oxford MEST-C histological score: mesangial and endocapillary hypercellularity, segmental sclerosis, tubular atrophy or interstitial fibrosis, crescents
Clinical patterns: isolated haematuria, persistent proteinuria, nephrotic, rapidly progressive (crescentic)

Symptoms and signs

Episodes of visible (cola- or tea-coloured) urine one to two days after a sore throat or gastroenteritis
Persistent microscopic haematuria found on a routine urine test
Foamy urine from proteinuria
High blood pressure
Swelling of the legs when proteinuria is heavy
Mild flank ache during episodes

Diagnosis

Clinical: Timing of haematuria relative to infections, blood pressure, oedema, skin rash, and features of liver or gut disease.
Tests: Urinalysis with dysmorphic red cells and red cell casts; urine protein-to-creatinine ratio; creatinine and eGFR; complement C3 and C4 are normal (low in post-streptococcal and lupus nephritis); serum IgA may be high but is not diagnostic. Kidney biopsy with immunofluorescence showing dominant mesangial IgA confirms the diagnosis.
Imaging: Kidney ultrasound to check size and exclude stones, tumours or structural causes of haematuria before biopsy.

Differential diagnosis

Post-streptococcal glomerulonephritis (low complement, longer delay after infection)
Thin basement membrane disease and Alport syndrome
Lupus nephritis
Urological causes of haematuria: stones, tumours, infection
ANCA-associated glomerulonephritis

Goal of treatment

Lower proteinuria and blood pressure to slow loss of kidney function, reserve immunosuppression for high-risk disease, and manage cardiovascular risk.

Treatment

Medical: Supportive care is the base: ACE inhibitors or ARBs to the highest tolerated level to reduce proteinuria and blood pressure.
Medical: SGLT2 inhibitors and, in selected patients, endothelin receptor antagonists further reduce proteinuria and slow progression.
Medical: Systemic or targeted-release glucocorticoids, or other immunosuppressants, are considered for persistent proteinuria despite supportive care or for crescentic disease.
Lifestyle: Low-salt diet, no smoking, healthy weight and avoidance of NSAIDs.
Follow-up: Follow-up of blood pressure, proteinuria and eGFR; preparation for dialysis or transplantation if kidney failure develops (the disease can recur in the graft).

Complications

Chronic kidney disease and kidney failure
Hypertension and cardiovascular disease
Nephrotic syndrome
Acute kidney injury during episodes of visible haematuria
Recurrence after kidney transplantation

Prognosis

Highly variable. Many patients with isolated haematuria and little proteinuria keep stable function, but about a quarter to a third progress to kidney failure over 20 to 30 years. Persistent proteinuria, hypertension, low eGFR at diagnosis and scarring on biopsy predict a worse outcome.

Test yourself

Think of the answer, then tap the question to see it.

What is the most common primary glomerulonephritis worldwide?

IgA nephropathy.

How does the timing of haematuria distinguish IgA nephropathy from post-streptococcal glomerulonephritis?

IgA nephropathy: one to two days after infection; post-streptococcal: one to three weeks later.

What are serum complement levels in IgA nephropathy?

Normal, unlike post-streptococcal and lupus nephritis, where C3 is low.

Which biopsy finding confirms IgA nephropathy?

Dominant IgA deposits in the mesangium on immunofluorescence.

Which drug class is the base of treatment to slow progression?

ACE inhibitors or ARBs to lower proteinuria and blood pressure.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: IgA nephropathy: MedlinePlus Medical Encyclopedia (MedlinePlus (U.S. National Library of Medicine), 2025); IgA Nephropathy - NIDDK (NIDDK (National Institutes of Health), 2022).

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Representative model, for educational purposes only.

Kidneys highlighted on the Durgical 3D model