IgA Nephropathy in Saudi Arabia: Symptoms, Causes & Treatment | aihealz
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IgA Nephropathy.Care & specialists in Saudi Arabia
In Saudi Arabia, 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.
aliases · IgA Nephropathy (Berger disease)· Berger disease· IgA腎症· IgA肾病· reviewed May 14, 2026
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Reviewed by AIHealz Medical Editorial Board · NephrologyLast reviewed May 13, 2026
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).
key facts
Prevalence
Approximately 2.5 per 100,000 per year in Western Europe and North America; 9-45 per 100,000 in East Asia
Demographics
Male:female ratio 2:1 in Caucasians; near 1:1 in East Asians; rare in people of African ancestry
Avg. age
Peak presentation age 16-35 years; can occur at any age including childhood and over 65
Global cases
Estimated 25-50 cases per 100,000 prevalence; the single most common primary glomerulonephritis on biopsy registries worldwide
Specialist
Nephrology
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How you might notice it
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..
01Visible 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.
02Persistent microscopic hematuria between gross episodes, detected only on urinalysis with more than 5 red blood cells per high-power field.
03Foamy urine reflecting proteinuria above 1 g/day, often the first sign noticed by patients.
04Elevated blood pressure on routine screening, present in 40-60% of patients at diagnosis and worsening as kidney function declines.
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How it’s diagnosed
diagnosis
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.
Key tests
01
Urinalysis with phase-contrast microscopy of urine sedimentConfirms glomerular hematuria by visualizing dysmorphic red blood cells, acanthocytes, and red cell casts
02
Urine protein-to-creatinine ratio and 24-hour urine collectionQuantifies proteinuria, the strongest modifiable prognostic factor
03
Serum creatinine and estimated GFR (eGFR)Establishes baseline kidney function and stages chronic kidney disease
✓Targeted-release budesonide (Tarpeyo/Kinpeygo, 16 mg daily for 9 months, then 8 mg for 1 month)
surgical options
TonsillectomyReduces gross hematuria episodes by 60-80% in observational Japanese cohorts; long-term renal benefit remains contested outside Japan
Kidney transplantation5-year graft survival 85-90% for living-donor and 75-80% for deceased-donor grafts in modern IgAN cohorts
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Causes & risk factors
known causes
Galactose-deficient IgA1 overproduction
Plasma cells in mucosal lymphoid tissue (tonsils, gut Peyer patches) produce IgA1 with abnormal O-linked glycosylation in genetically susceptible individuals. Galactose-deficient IgA1 levels are heritable and elevated in 75% of patients and many first-degree relatives.
Autoantibodies against galactose-deficient IgA1
Patients generate IgG and IgA1 autoantibodies that recognize the abnormally glycosylated hinge region. These antibodies form circulating immune complexes that lodge in the kidney mesangium.
Streptococcal pharyngitis, viral upper respiratory infection, and gastrointestinal infection drive surges in mucosal IgA1 production. These surges underlie the synpharyngitic gross hematuria episodes characteristic of the disease.
Genetic susceptibility loci
Genome-wide association studies have identified more than 25 risk loci including HLA-DQ/DR, the complement factor H cluster, and CARD9. Risk alleles cluster in East Asian populations and are rare in people of African ancestry.
Secondary IgA nephropathy from chronic liver disease
Cirrhosis from any cause reduces hepatic clearance of polymeric IgA and produces mesangial IgA deposition with or without clinical nephritis. Alcohol-associated cirrhosis is the most common setting.
Associated immune diseases
IgA nephropathy occurs in coeliac disease, inflammatory bowel disease, ankylosing spondylitis, dermatitis herpetiformis, and HIV. These associations support a mucosa-driven model of disease.
risk factors
East Asian or European ancestry
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Living with it
01Treat upper respiratory and gastrointestinal infections promptly to reduce mucosal IgA1 surges.
02Maintain blood pressure under 120/80 mmHg with regular home monitoring.
03Restrict sodium intake to under 2 g/day to improve responsiveness to renin-angiotensin blockade.
04Stop smoking; smoking accelerates eGFR decline in glomerular diseases by 1-2 mL/min per year.
05Avoid nephrotoxins including NSAIDs, IV iodinated contrast where possible, and high-dose proton pump inhibitors.
06Vaccinate against influenza, pneumococcus, and SARS-CoV-2 to reduce infection-triggered flares.
•Plant-based protein sources (lentils, soy, beans) which produce less acid load than animal protein
•Moderate protein intake of 0.8-1.0 g/kg/day in patients not on dialysis
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When to seek help
why see a nephrology
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.
01Progressive chronic kidney disease leading to end-stage kidney disease in 25-30% of patients within 20 years; monitor eGFR every 3-6 months.
02Resistant hypertension and accelerated cardiovascular disease — left ventricular hypertrophy, coronary disease, stroke; screen with ambulatory blood pressure and echocardiography.
03Nephrotic syndrome with hypoalbuminemia, edema, hyperlipidemia, and venous thromboembolism when proteinuria exceeds 3.5 g/day.
04Acute kidney injury during gross hematuria episodes, sometimes requiring temporary dialysis; usually recovers fully within 1-3 months.
05Crescentic transformation with rapidly progressive glomerulonephritis — rising creatinine, oliguria, and red cell casts; needs urgent biopsy and immunosuppression.
Asymptomatic urinary abnormalityMicroscopic hematuria with or without low-grade proteinuria, typically detected on routine urinalysis or screening in East Asia. Accounts for 30-50% of incident cases in screened populations.
Synpharyngitic gross hematuriaRecurrent episodes of visible (cola-coloured) hematuria within 24-72 hours of upper respiratory or gastrointestinal infection. The most recognizable phenotype, classically in adolescents and young adults.
Persistent proteinuria with hypertensionThe dominant chronic phenotype after age 30; proteinuria above 1 g/day plus hypertension drives long-term kidney function loss and warrants treatment intensification.
Nephrotic-range diseaseProteinuria above 3.5 g/day with hypoalbuminemia; may overlap with minimal change disease (so-called MCD/IgAN dual diagnosis) and sometimes responds to corticosteroids.
Crescentic IgA nephropathyRapidly progressive glomerulonephritis with cellular crescents in more than 25-50% of glomeruli, rising creatinine over weeks, often requiring immunosuppression including pulse methylprednisolone and cyclophosphamide or rituximab.
Living with IgA Nephropathy
Timeline
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.
Lifestyle
01Adhere to the prescribed RAS blocker, SGLT2 inhibitor, sparsentan, or budesonide every day at the same time.
02Measure home blood pressure twice weekly and share readings with the nephrology team.
03Limit dietary sodium to under 2 g/day; read food labels and avoid processed foods.
04Maintain a healthy body mass index of 18.5-24.9 kg/m2; obesity worsens proteinuria.
05Limit alcohol intake to under 14 units per week and avoid heavy episodic drinking.
06Use paracetamol rather than ibuprofen or naproxen for analgesia; long-term NSAIDs accelerate kidney decline.
Daily management
01Take RAS blocker, SGLT2 inhibitor, sparsentan, or targeted-release budesonide at the scheduled time each day.
Complementary approaches
Omega-3 fatty acids (fish oil 3-4 g/day)Older trials (Donadio 1994) suggested benefit in slowing eGFR decline; subsequent meta-analyses are mixed. KDIGO 2024 gives a conditional weak recommendation against routine use.
Tonsillectomy plus methylprednisolone pulse (Japanese 'Pozzi-Hotta' protocol)Combined surgical and immunological approach used widely in Japan. Reduces proteinuria and hematuria in observational cohorts but lacks high-quality randomized evidence for long-term renal protection.
Choosing a doctor
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.
IgA nephropathy is a kidney disease in which an abnormal form of the antibody IgA1 deposits in the kidney filters. The deposits cause inflammation, leaking of blood and protein into the urine, and slow scarring of the kidneys. It is the most common primary glomerular disease worldwide.
Is IgA nephropathy the same as Berger disease?▾▴
Yes. Berger disease is the eponym for IgA nephropathy after the French nephrologist Jean Berger, who first described the entity in 1968. Both names refer to the same condition with IgA-dominant deposits in the kidney mesangium on biopsy.
What are the first symptoms of IgA nephropathy?▾▴
The first symptom is often visible cola-coloured urine 24-72 hours after a sore throat or gastrointestinal infection in a young adult. Many patients have only microscopic blood and small amounts of protein in the urine detected on routine urinalysis without symptoms.
How is IgA nephropathy diagnosed?▾▴
Diagnosis requires a kidney biopsy showing IgA-dominant immune deposits in the mesangium on immunofluorescence. Urinalysis, urine protein quantification, blood pressure, serum creatinine, and serology for lupus, vasculitis, and other glomerular diseases support the diagnosis before biopsy.
What causes IgA nephropathy?▾▴
The disease is driven by overproduction of galactose-deficient IgA1 by mucosal plasma cells, followed by autoantibodies against this abnormal IgA1 and deposition of the resulting immune complexes in the kidney mesangium. Genetic susceptibility, infections, and gut-mucosal triggers contribute.
Is IgA nephropathy curable?▾▴
There is no cure, but modern treatment can put the disease into prolonged remission and substantially slow kidney function loss. Spontaneous clinical remission occurs in 5-15% of patients. Combination therapy with RAS blockers, SGLT2 inhibitors, and budesonide or sparsentan delays kidney failure by years in many patients.
What is the life expectancy with IgA nephropathy?▾▴
Most patients live a normal lifespan. Approximately 25-30% develop end-stage kidney disease within 20 years without intensive treatment. Modern combination therapy is expected to delay or prevent this in many patients. Cardiovascular disease becomes the main competing risk in advanced chronic kidney disease.
Is IgA nephropathy hereditary?▾▴
Most cases are sporadic, but 5-10% show familial clustering. First-degree relatives of patients have a higher prevalence of microscopic hematuria (around 16% versus 4% in controls). Genome-wide association studies have identified more than 25 susceptibility loci including HLA-DQ and the complement factor H cluster.
Does IgA nephropathy go away on its own?▾▴
Around 5-15% of patients enter sustained clinical remission with persistently normal urinalysis. Most patients have at least low-grade hematuria and proteinuria for years, and treatment is aimed at preventing kidney function loss rather than abolishing all urinary abnormalities.
What is the role of sparsentan in IgA nephropathy?▾▴
Sparsentan is a dual endothelin and angiotensin receptor antagonist FDA-approved in 2023 for adults with primary IgA nephropathy at risk of progression. In the PROTECT trial it reduced proteinuria 50% more than irbesartan and slowed eGFR decline by 1.1 mL/min/1.73 m2 per year at 2 years.
What is Tarpeyo (targeted-release budesonide)?▾▴
Tarpeyo (Kinpeygo in Europe) is an oral budesonide formulation that releases in the distal ileum to suppress Peyer-patch B cells producing galactose-deficient IgA1. The NefIgArd trial showed a 7 mL/min/1.73 m2 eGFR benefit at 2 years over placebo when added to optimised supportive care.
Can children get IgA nephropathy?▾▴
Yes. Pediatric IgA nephropathy peaks at ages 9-10 years and presents more often with gross hematuria after upper respiratory infection. Long-term renal survival is generally better than in adults, with under 10% reaching end-stage kidney disease in childhood.
Does IgA nephropathy affect pregnancy?▾▴
Pregnancy outcomes are usually good when blood pressure, eGFR, and proteinuria are well controlled before conception. Women with proteinuria above 1 g/day or eGFR under 60 mL/min/1.73 m2 face higher risk of pre-eclampsia, preterm birth, and accelerated decline. Care should be co-led by nephrology and maternal-fetal medicine.
Should I have a tonsillectomy for IgA nephropathy?▾▴
Tonsillectomy is offered in Japan and a few European centres for patients with recurrent synpharyngitic hematuria and chronic tonsillitis. It reduces hematuria episodes in observational studies but long-term renal protection outside Japan is uncertain. Discuss the trade-offs with your nephrologist.
Can diet cure IgA nephropathy?▾▴
No diet cures IgA nephropathy. A low-sodium DASH-style diet with adequate plant protein supports blood pressure control and reduces proteinuria. Coeliac disease should be screened for and treated with a gluten-free diet, which may reduce mesangial IgA in coeliac-associated cases.
Does IgA nephropathy come back after kidney transplant?▾▴
Mesangial IgA deposits recur in 20-50% of kidney grafts, but clinically significant recurrence with proteinuria affects 10-30% and graft loss from recurrence is under 10% at 10 years. Living-donor and pre-emptive transplants give the best long-term outcomes.
Is IgA nephropathy a form of lupus?▾▴
No. IgA nephropathy and lupus nephritis are distinct diseases. Lupus has positive ANA and anti-DNA antibodies, low complement, and a full-house immunofluorescence pattern. IgA nephropathy has dominant IgA, normal complement, and lacks systemic lupus features.
How does SGLT2 inhibition help IgA nephropathy?▾▴
SGLT2 inhibitors such as dapagliflozin reduce intraglomerular pressure, lower proteinuria by 30-40%, and slow eGFR decline. In the DAPA-CKD IgAN subgroup, dapagliflozin reduced the renal composite endpoint by 44% on top of RAS blockade and is now recommended by KDIGO 2024.
What blood pressure target is recommended?▾▴
KDIGO 2024 recommends a systolic blood pressure target under 120 mmHg in most adults with IgA nephropathy, measured with standardised office or ambulatory technique. Home blood pressure under 120/80 mmHg supports the same goal and improves proteinuria control.
Do steroids help in IgA nephropathy?▾▴
Systemic high-dose corticosteroids are no longer first-line because of infection and metabolic toxicity demonstrated in STOP-IgAN and TESTING trials. Reduced-dose methylprednisolone with antibiotic prophylaxis may benefit selected high-risk patients. Targeted-release oral budesonide is preferred when steroid action is needed.
When should I see a nephrologist?▾▴
Seek nephrology referral for persistent microscopic hematuria with any proteinuria, visible hematuria episodes after infection, new hypertension before age 35 with bland urinalysis, or a serum creatinine above the local reference range. Early referral improves long-term outcomes.
International IgAN Prediction ToolCalculates 5-year risk of a 50% drop in eGFR or end-stage kidney disease using clinical and histological data
Outlook
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%.
genetic
Prevalence on biopsy registries is 3-4 times higher in East Asia and intermediate in Europe; the disease is rare in people of African ancestry, mirroring frequencies of risk alleles at HLA and complement factor H.
Family history of IgA nephropathy or unexplained kidney failuregenetic
Familial clustering is described in 5-10% of cases. First-degree relatives have 16% prevalence of microscopic hematuria versus 4% in controls.
Age 16-35 years at presentationnon-modifiable
Peak incidence is in adolescents and young adults, although diagnosis is increasingly made in patients over 50 with persistent proteinuria.
Male sex (Caucasian populations)non-modifiable
Men account for roughly two-thirds of biopsied Caucasian cases and have worse renal survival, with hazard ratios for kidney failure of 1.4-1.7 in pooled cohorts.
Recurrent mucosal infectionsmodifiable
Frequent tonsillitis, pharyngitis, or chronic sinusitis drives synpharyngitic flares. Tonsillectomy reduces hematuria episodes in selected patients, though survival benefit remains debated outside Japan.
Coeliac disease and inflammatory bowel diseasemodifiable
Both conditions occur 2-4 times more often in IgA nephropathy cohorts. Gluten exposure may worsen mesangial IgA deposition in coeliac patients.
Persistent proteinuria above 1 g/daymodifiable
The single strongest modifiable predictor of progression. Each gram of daily proteinuria roughly doubles the risk of doubling serum creatinine or reaching end-stage kidney disease.
Hypertensionmodifiable
Untreated blood pressure above 140/90 mmHg accelerates fibrosis and amplifies the harm of proteinuria. Treat-to-target strategies aim for under 120/80 mmHg in most adults.
•Adequate hydration with 2-2.5 L/day of water unless fluid restriction is advised
foods to avoid
•Processed and packaged foods high in sodium
•Sugary drinks and excess fruit juice; obesity worsens proteinuria
Treatment-related infections, hyperglycemia, weight gain, and avascular necrosis from corticosteroid use; mitigated by targeted-release budesonide.
choosing the right hospital
01On-site percutaneous kidney biopsy programme with renal pathology
02Access to MEST-C Oxford scoring
03Availability of sparsentan and targeted-release budesonide
04Multidisciplinary kidney clinic with dietitian and clinical pharmacist
05Kidney transplantation and pre-dialysis education service
Essential facilities
Tertiary nephrology centres with biopsy and transplant programmesRenal pathology services with electron microscopyMultidisciplinary glomerulonephritis clinicsPediatric nephrology units for childrenKidney transplant and dialysis units for end-stage disease
02
Check home blood pressure twice weekly using a validated upper-arm device.
03Test urine with home dipsticks monthly for new visible blood or heavy proteinuria.
04Keep a record of any new infections, antibiotics, or NSAID use to share at nephrology visits.
05Attend scheduled blood tests every 3-6 months for creatinine, potassium, urine protein, and HbA1c if diabetic.
06Maintain influenza, pneumococcal, and COVID-19 vaccinations as advised by the renal team.
Exercise
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.