In United Kingdom, igA Nephropathy is managed by nephrologists. IgA nephropathy is the most common primary glomerular disease worldwide, caused by deposition of galactose-deficient IgA1 immune complexes in the kidney mesangium. Incidence is roughly 2.5 per 100,000 per year in Western populations and 3-4 times higher in East Asia, where universal urinalysis screening detects asymptomatic cases earlier.
IgA nephropathy (ICD-10: N02.8), also known as Berger disease after Jean Berger who first described the entity in 1968, is a primary glomerular disease defined by mesangial deposition of polymeric, galactose-deficient IgA1 on kidney biopsy with dominant or co-dominant IgA staining on immunofluorescence. The disease is the renal-limited form of a wider IgA-mediated spectrum that includes IgA vasculitis (formerly Henoch-Schonlein purpura). Pathogenesis follows a four-hit model: hit 1, mucosal overproduction of galactose-deficient IgA1; hit 2, generation of anti-glycan IgG autoantibodies; hit 3, formation of circulating immune complexes; hit 4, complex deposition in the mesangium with complement activation and mesangial cell proliferation. The disease is graded histologically by the MEST-C Oxford classification (mesangial hypercellularity, endocapillary proliferation, segmental sclerosis, tubular atrophy/interstitial fibrosis, crescents).
The key symptoms of IgA Nephropathy are: Visible cola-coloured or red urine appearing 24-72 hours after a sore throat, tonsillitis, or gastrointestinal infection, lasting 1-7 days and recurring with successive infections., Persistent microscopic hematuria between gross episodes, detected only on urinalysis with more than 5 red blood cells per high-power field., Foamy urine reflecting proteinuria above 1 g/day, often the first sign noticed by patients., Elevated blood pressure on routine screening, present in 40-60% of patients at diagnosis and worsening as kidney function declines., Flank or loin pain during gross hematuria episodes, attributed to capsular distension or transient tubular obstruction by red blood cell casts., Bilateral lower limb oedema and rising creatinine in nephrotic-range or rapidly progressive disease., Fatigue, reduced exercise tolerance, and pallor as glomerular filtration rate falls toward stage 3-4 chronic kidney disease..
Diagnosis starts with the urinalysis dipstick and microscopic phase-contrast examination of urine sediment — dysmorphic red blood cells and red cell casts confirm a glomerular origin and exclude lower urinary tract bleeding. Quantification of proteinuria with a spot urine protein-to-creatinine ratio (or 24-hour collection in pregnancy) defines risk: levels above 1 g/g correlate with progressive disease. Serum creatinine, electrolytes, and estimated glomerular filtration rate establish baseline kidney function. Serology is largely used to exclude alternatives (anti-nuclear antibody, anti-DNA, ANCA, anti-GBM, complement C3 and C4, hepatitis B and C, HIV); complement levels are normal in classical IgA nephropathy. Serum galactose-deficient IgA1 (Gd-IgA1) and serum/urinary IgG anti-Gd-IgA1 are emerging biomarkers but are not routinely available outside research. Imaging with renal ultrasound confirms normal-sized non-obstructed kidneys before biopsy. The reference standard for diagnosis is percutaneous kidney biopsy with light microscopy (mesangial expansion, hypercellularity), immunofluorescence (dominant or co-dominant mesangial IgA), and electron microscopy (paramesangial electron-dense deposits). Findings are scored by the Oxford MEST-C classification, which feeds the validated International IgAN Prediction Tool used at KDIGO for risk stratification at biopsy.
Long-term outcome correlates with three risk markers at diagnosis: persistent proteinuria above 1 g/day, eGFR under 60 mL/min/1.73 m2, and uncontrolled hypertension. In contemporary cohorts treated with maximised supportive care, the 10-year renal survival is approximately 85% for patients with proteinuria under 0.5 g/day, 75% with 0.5-1 g/day, and below 50% with sustained proteinuria above 3 g/day. Histology adds independent prognostic information through the Oxford MEST-C score: tubular atrophy/interstitial fibrosis (T1, T2) and crescents (C2) signal the highest risk of progression. The International IgAN Prediction Tool at biopsy outperforms clinical assessment alone and is endorsed by KDIGO. Spontaneous clinical remission occurs in 5-15% of patients with minimal proteinuria. Modern combination therapy (RAS blockade plus SGLT2 inhibitor plus sparsentan or budesonide where indicated) is projected to delay end-stage kidney disease by 10-15 years in moderate-risk disease based on slowing eGFR decline by 2-4 mL/min/1.73 m2 per year. Post-transplant recurrence affects 20-50% of grafts but causes graft loss in under 10%.
Persistent hematuria with proteinuria or a rising creatinine warrants nephrology referral. The nephrologist confirms the diagnosis on biopsy, calculates the International IgAN Prediction Tool risk score, and decides between supportive therapy alone or escalation to budesonide, sparsentan, or systemic immunosuppression. Pregnant patients, transplant candidates, and children should be managed in specialist centres with experience of IgA nephropathy.
Find specialists →Proteinuria responses to RAS blockade and SGLT2 inhibitors appear within 4-12 weeks. Budesonide produces a 30-40% proteinuria reduction by 6-9 months, sustained 12-24 months after treatment ends. Crescentic disease treated within 4 weeks of presentation recovers function in 50-70% of patients; established fibrosis (T2 on biopsy) does not regress. Annual eGFR decline falls from 4-5 mL/min/1.73 m2 without treatment to under 1-2 mL/min/1.73 m2 with optimised modern therapy.
Regular moderate aerobic exercise (150 minutes per week of brisk walking, swimming, or cycling) plus two resistance sessions improves blood pressure, glycaemic control, and proteinuria. Avoid extreme dehydration with prolonged endurance events. Patients with eGFR under 30 mL/min/1.73 m2 should taper intensity and discuss exercise plans with their nephrology team.
Choose a nephrologist affiliated with a kidney biopsy programme and access to MEST-C scoring. For high-risk or crescentic disease, ask whether the centre participates in IgA nephropathy clinical trials and has experience with sparsentan, targeted-release budesonide, and rituximab. Renal pathology expertise is essential — biopsy interpretation drives prognosis and treatment selection.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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