Renal: Glomerular Disease

• Approach: How Glomerular Disease Presents | Haematuria and Proteinuria | Tests and Complement | Kidney Biopsy
• Nephrotic diseases: Nephrotic Syndrome — General Care | Minimal Change Disease | Focal Segmental Glomerulosclerosis | Membranous Nephropathy | Diabetic Kidney Disease | Amyloidosis | Myeloma and Paraprotein Kidney Disease
• Nephritic diseases: IgA Nephropathy | IgA Vasculitis | Post-infectious Glomerulonephritis | Anti-GBM Disease | ANCA-associated Vasculitis | Lupus Nephritis | MPGN and C3 Glomerulopathy | Infection-related Kidney Disease
• Revision: Drug Reference Table | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🫘 Glomerular disease is damage to the kidney's filters. Some diseases make the filter leaky to protein (nephrotic); others cause inflammation that lets blood through and reduces filtering (nephritic). Some are slow and benign; others (vasculitis, anti-GBM disease) can destroy the kidneys in days. Most diagnoses need a kidney biopsy, but the blood tests — ANCA, anti-GBM, complement, anti-PLA2R — point you in the right direction.
Your four questions for every patient: Is the picture nephrotic, nephritic, or mixed? How fast is kidney function changing? Is there a systemic disease (vasculitis, lupus, myeloma, infection, cancer)? Does this need urgent treatment before the biopsy?

How Glomerular Disease Presents

• Mainly nephrotic: minimal change disease, FSGS, membranous nephropathy, diabetic kidney disease, amyloidosis.
• Mainly nephritic: IgA nephropathy, post-infectious GN, ANCA vasculitis, anti-GBM disease.
• Either or both: lupus nephritis, MPGN and C3 glomerulopathy.

💡 Clinical Pearl: In nephrotic syndrome the filter's barrier is damaged (podocytes); in nephritic syndrome there is inflammation in the glomerulus. Think "nephrotic = protein" and "nephritic = inflammation".

↑ Back to index

Haematuria and Proteinuria

• Haematuria:
  • Visible (macroscopic) or non-visible (dipstick 1+ or more, confirmed on repeat).
  • Exclude infection, menstruation and exercise; dipstick blood without red cells suggests myoglobin or haemoglobin.
  • Urology (cancer) route — NICE NG12 suspected cancer pathway:
    • Age 45 or over with unexplained visible haematuria (without UTI, or persisting after UTI treatment).
    • Age 60 or over with unexplained non-visible haematuria plus dysuria or a raised white cell count.
  • Nephrology route — think glomerular if there is:
    • Proteinuria (ACR 30 or more).
    • Low or falling eGFR.
    • Hypertension.
    • Dysmorphic red cells or red cell casts.
    • Visible haematuria with a throat infection.
    • Younger age, or systemic symptoms.
  • Isolated non-visible haematuria with normal BP, eGFR and ACR — monitor yearly (BP, eGFR, ACR). Often thin basement membrane disease (now often recognised as a mild form of Alport-type collagen IV disease).
• Proteinuria:
  • Quantify with ACR (or PCR for heavy proteinuria).
  • Transient causes — fever, exercise, UTI, heart failure.
  • Orthostatic proteinuria in young people — present on standing only (normal early-morning sample).
  • Overflow — light chains in myeloma (Bence Jones protein) aren't detected well by dipstick.
  • Tubular proteinuria — low-molecular-weight proteins; PCR much higher than ACR.

↑ Back to index

Tests and Complement

• Urine: Dipstick, microscopy (red cell casts), ACR and PCR.
• Blood:
  • U&E, albumin, lipids, FBC, glucose and HbA1c.
  • ANCA (PR3 and MPO).
  • Anti-GBM antibodies.
  • ANA, dsDNA, ENA.
  • Complement C3 and C4.
  • Anti-PLA2R antibodies (membranous).
  • Serum free light chains, protein electrophoresis, immunoglobulins.
  • Hepatitis B and C, HIV.
  • ASOT and anti-DNase B (streptococcus).
  • Cryoglobulins.
• Ultrasound — kidney size; two kidneys present before biopsy.

Complement levels narrow the list:

↑ Back to index

Kidney Biopsy

• When:
  • Nephrotic syndrome in adults (in children, minimal change is assumed and steroids given first).
  • Unexplained AKI or rapidly progressive GN.
  • Haematuria with significant proteinuria or falling eGFR.
  • Kidney involvement in systemic disease (lupus, vasculitis).
  • Transplant dysfunction.
• What it shows:
  • Light microscopy — structure, crescents, scarring.
  • Immunofluorescence — deposits (IgA, IgG, C3, light chains; linear IgG in anti-GBM disease).
  • Electron microscopy — podocyte foot process effacement (minimal change), deposit location.
  • Chronic damage (scarring, tubular atrophy) predicts how much recovery is possible.
• Before biopsy:
  • Check platelets, clotting, and Hb; group and save.
  • BP controlled (e.g. under 160/90).
  • Stop anticoagulants and antiplatelets (according to local protocol).
  • Consent — bleeding is the main risk (visible haematuria, perinephric haematoma; transfusion or embolisation about 1 in 100; nephrectomy and death very rare).
• After: Bed rest, observations, check urine for blood and Hb.
• Relative contraindications: Single kidney, small scarred kidneys, uncontrolled BP, bleeding disorder, active infection.

↑ Back to index

Nephrotic Syndrome — General Care

Complications:

• Venous thromboembolism — loss of anticoagulant proteins (antithrombin) in the urine and high liver production of clotting factors:
  • DVT, PE, renal vein thrombosis (loin pain, haematuria, worsening kidney function).
  • Highest risk in membranous nephropathy and when albumin is very low.
• Infection — loss of immunoglobulins; cellulitis, spontaneous bacterial peritonitis (pneumococcus), especially in children.
• High cholesterol.
• AKI — volume depletion from over-diuresis, renal vein thrombosis, drugs.
• Loss of binding proteins — low total thyroxine and vitamin D.

Supportive treatment (alongside treatment of the cause):

• Oedema:
  • Salt restriction.
  • Loop diuretic — often high doses (e.g. furosemide 80–250 mg), sometimes IV because gut oedema reduces absorption. Add a thiazide or amiloride if needed.
  • Aim for weight loss of 0.5–1 kg/day; daily weights.
  • Mild fluid restriction.
  • IV albumin with diuretics only in selected severe cases.
• Proteinuria and BP — ACE inhibitor or ARB (may wait in minimal change disease, which usually responds quickly to steroids).
• Anticoagulation:
  • Consider prophylactic anticoagulation when albumin is very low (e.g. under 20–25 g/L, or higher in membranous nephropathy) and bleeding risk is low — LMWH or warfarin; DOACs used in some units.
  • Treat established clots as usual.
• Statin if nephrotic syndrome persists.
• Vaccines — pneumococcal and influenza.
• Bone protection during long steroid courses; PJP prophylaxis with intensive immunosuppression.

↑ Back to index

Minimal Change Disease

• Who: The cause of about 90% of nephrotic syndrome in young children, and 10–15% in adults.
• Causes (usually none found):
  • NSAIDs.
  • Hodgkin lymphoma (and other lymphomas).
  • Allergies, bee stings.
  • Lithium.
  • Recent infection.
• Features:
  • Sudden severe nephrotic syndrome — over days, with heavy oedema.
  • Normal BP and kidney function (AKI can occur in adults).
  • Little or no blood in the urine.
• Biopsy: Normal on light microscopy; podocyte foot process effacement on electron microscopy. Anti-nephrin antibodies are found in many patients.
• Treatment:
  • Children — prednisolone (60 mg/m² daily for 4 weeks, then on alternate days and tapered) without biopsy; about 90% respond.
  • Adults — prednisolone 1 mg/kg daily (maximum 80 mg) until remission (can take up to 16 weeks in adults), then tapered over months.
  • Frequent relapses or steroid dependence — rituximab, calcineurin inhibitors (tacrolimus, ciclosporin), cyclophosphamide or mycophenolate.
• Prognosis: Good — kidney failure is rare, but relapses are common.

↑ Back to index

Focal Segmental Glomerulosclerosis

• What it is: Scarring of some glomeruli (focal), affecting part of each glomerulus (segmental). It is a pattern of injury with different causes.
• Types:
  • Primary — a circulating factor (anti-nephrin antibodies in some); full nephrotic syndrome, sudden onset.
  • Secondary (adaptive) — obesity, reduced kidney mass (reflux nephropathy, single kidney), hypertension, sickle cell disease. Usually sub-nephrotic proteinuria with normal albumin.
  • Viral and drug-related — HIV (collapsing type), parvovirus, COVID-19, heroin, pamidronate, lithium, interferon, anabolic steroids.
  • Genetic — podocyte gene mutations; APOL1 risk variants in people of West African ancestry.
• Treatment:
  • All — ACE inhibitor or ARB, SGLT2 inhibitor, BP control.
  • Primary FSGS — high-dose steroids (prednisolone 1 mg/kg for up to 16 weeks); calcineurin inhibitors if steroid-resistant or steroids aren't suitable; rituximab in some.
  • Secondary FSGS — treat the cause (weight loss); no immunosuppression.
  • Genetic — doesn't respond to immunosuppression; genetic testing helps avoid unnecessary treatment.
• Prognosis: A common cause of kidney failure; primary FSGS can recur in a kidney transplant (sometimes within days).

↑ Back to index

Membranous Nephropathy

• Who: The commonest cause of nephrotic syndrome in white adults; peak age 40–60, more often men.
• Causes:
  • Primary (about 75%) — autoantibodies against a podocyte protein: anti-PLA2R (about 70–80%), anti-THSD7A.
  • Secondary:
    • Cancer — lung, bowel, breast, prostate (especially over 60; screen as age-appropriate).
    • Infection — hepatitis B, hepatitis C, syphilis, malaria.
    • Lupus (class V).
    • Drugs — NSAIDs, gold, penicillamine.
    • Other autoimmune disease (thyroid, Sjögren's).
• Biopsy: Thickened basement membrane; IgG deposits under the podocytes ("spikes" on silver stain); PLA2R staining.
• Anti-PLA2R antibodies:
  • A positive test with typical features can avoid the need for biopsy in some patients.
  • Levels track disease activity — falling titres predict remission.
• Course — "rule of thirds" (roughly): one-third remit spontaneously, one-third have persistent proteinuria, one-third progress to kidney failure.
• Treatment:
  • Supportive for all — ACE inhibitor or ARB, diuretics, statin, anticoagulation (highest VTE risk of all causes; consider when albumin is under about 25 g/L).
  • Low risk (normal eGFR, proteinuria under 3.5 g/day) — supportive care and watch (often 6 months).
  • Moderate to high risk — rituximab (MENTOR trial — better than ciclosporin).
  • High risk or failing kidney function — cyclophosphamide with steroids (modified Ponticelli regimen, alternating months); calcineurin inhibitors as an alternative.
  • Secondary — treat the cause (remove the tumour, antivirals for hepatitis B, stop the drug).

⚠️ Safety Pearl: Sudden loin pain, visible haematuria and a fall in kidney function in a patient with membranous nephropathy suggest renal vein thrombosis — request CT venography and anticoagulate.

↑ Back to index

Diabetic Kidney Disease

• The commonest cause of kidney failure in the UK.
• Natural history:
  • Early hyperfiltration (high GFR).
  • Moderately increased albuminuria (ACR 3–30).
  • Severely increased albuminuria (ACR over 30), then nephrotic-range proteinuria.
  • Falling eGFR, then kidney failure.
  • In type 2 diabetes, some patients lose GFR without much albuminuria.
• Biopsy (not usually needed) — thickened basement membrane, mesangial expansion, Kimmelstiel–Wilson nodules.
• Consider another cause (and refer for biopsy) if:
  • No diabetic retinopathy (especially in type 1 diabetes).
  • Rapid decline in eGFR or sudden nephrotic syndrome.
  • Haematuria or red cell casts.
  • Short duration of diabetes (under 5 years in type 1).
  • Signs of another systemic disease.
• Treatment:
  • Glucose control (HbA1c target individualised).
  • BP control.
  • ACE inhibitor or ARB (ACR over 3).
  • SGLT2 inhibitor.
  • Finerenone (persistent albuminuria).
  • GLP-1 receptor agonist (semaglutide — kidney and cardiovascular benefits).
  • Statin.
  • See the CKD chapter.

↑ Back to index

Amyloidosis

• What it is: Misfolded proteins deposit as fibrils in organs. The kidneys are often affected, usually with nephrotic syndrome.
• AL amyloidosis (light chain):
  • From a plasma cell clone — MGUS or myeloma.
  • Features:
    • Nephrotic syndrome; normal-sized or large kidneys.
    • Heart — restrictive cardiomyopathy, heart failure, low-voltage ECG (the main cause of death).
    • Peripheral and autonomic neuropathy, carpal tunnel syndrome.
    • Macroglossia; periorbital purpura ("raccoon eyes").
    • Large liver.
  • Treatment: Chemotherapy against the plasma cell clone — daratumumab with bortezomib, cyclophosphamide and dexamethasone; stem cell transplant for some.
• AA amyloidosis (serum amyloid A):
  • From chronic inflammation — rheumatoid arthritis, IBD, familial Mediterranean fever, bronchiectasis, TB, injecting drug use (chronic skin infections).
  • Treatment: Control the inflammation (biologics; colchicine for FMF).
• Diagnosis:
  • Biopsy (kidney, fat pad, or rectum) — Congo red stain with apple-green birefringence under polarised light.
  • Typing (which protein) — essential for treatment.
  • Serum free light chains; SAP scan (National Amyloidosis Centre, London).

↑ Back to index

Myeloma and Paraprotein Kidney Disease

• Myeloma cast nephropathy ("myeloma kidney"):
  • Free light chains block the tubules — AKI, often with high calcium and dehydration.
  • Little albuminuria (light chains are poorly detected by dipstick); PCR much higher than ACR.
  • Treatment: IV fluids, correct calcium, stop nephrotoxic drugs, and urgent anti-myeloma treatment (bortezomib-based regimens with dexamethasone) to cut light chain levels fast.
• Light chain deposition disease — nodular glomerular deposits, proteinuria.
• AL amyloidosis — see above.
• Monoclonal gammopathy of renal significance (MGRS) — a small plasma cell or B cell clone (not enough to be myeloma) that damages the kidney. It is treated with chemotherapy to protect the kidney.
• Other myeloma-related kidney problems — high calcium, Fanconi syndrome (proximal tubule damage), NSAIDs, contrast, bisphosphonates.
• See the Lymphoma and Myeloma chapter.

↑ Back to index

IgA Nephropathy

• Who: The commonest glomerulonephritis worldwide; young men; more common in East Asia.
• What it is: Abnormal IgA1 molecules form immune complexes that deposit in the mesangium.
• Features:
  • Visible haematuria within 1–2 days of a sore throat or other infection ("synpharyngitic") — compare post-streptococcal GN, which follows 1–3 weeks after.
  • Persistent invisible haematuria and proteinuria found at a check-up.
  • Hypertension; slow CKD.
  • Occasionally nephrotic, or rapidly progressive (crescentic).
• Tests: Complement normal; serum IgA raised in about half (not diagnostic).
• Biopsy: Mesangial IgA deposits on immunofluorescence; MEST-C score predicts outcome.
• Treatment:
  • Supportive care — the main treatment for all:
    • ACE inhibitor or ARB at maximum dose.
    • SGLT2 inhibitor.
    • BP control (under 130/80 if proteinuria).
    • Statin; lifestyle; stop smoking.
  • Persistent proteinuria (e.g. over 0.5–1 g/day) despite supportive care — newer options:
    • Targeted-release budesonide (Kinpeygo; NICE TA937) — acts on gut lymphoid tissue where abnormal IgA is made; a 9-month course.
    • Sparsentan (NICE TA1074) — a dual endothelin and angiotensin receptor antagonist, used in place of an ACE inhibitor or ARB.
    • Systemic steroids — selected high-risk patients (TESTING trial showed benefit, but with serious infections at higher doses).
  • Crescentic IgA — treated like ANCA vasculitis (steroids and cyclophosphamide).
  • Tonsillectomy — used in Japan; not routine in the UK.
• Prognosis: About 20–40% reach kidney failure within 20 years. Worse with heavy proteinuria, high BP, and low eGFR at diagnosis.

↑ Back to index

IgA Vasculitis

• What it is: Small-vessel vasculitis with IgA deposits (formerly Henoch–Schönlein purpura). The kidney lesion looks like IgA nephropathy.
• Who: Mainly children aged 3–15, often after an upper respiratory infection; less common but more severe in adults.
• Features:
  • Palpable purpura on the buttocks and legs (with a normal platelet count).
  • Joint pain (knees, ankles).
  • Abdominal pain, GI bleeding, intussusception (children).
  • Nephritis — haematuria and proteinuria in up to half.
  • Scrotal swelling.
• Management:
  • Usually self-limiting — supportive care (simple analgesia; avoid NSAIDs if the kidneys are involved).
  • Monitor BP and urine for at least 6 months (kidney involvement can appear later).
  • Refer if there is significant proteinuria, nephrotic or nephritic syndrome, high BP, or reduced kidney function.
  • Steroids and immunosuppression for severe kidney disease.

↑ Back to index

Post-infectious Glomerulonephritis

• Post-streptococcal GN (mainly children):
  • 1–3 weeks after a sore throat, or 3–6 weeks after a skin infection (impetigo), with group A streptococcus.
  • Features: Nephritic syndrome — cola-coloured urine, oedema (periorbital), hypertension, oliguria, AKI.
  • Tests:
    • Low C3 with normal C4 (C3 recovers within 6–8 weeks — if not, think C3 glomerulopathy).
    • Raised ASOT (throat) or anti-DNase B (skin).
  • Biopsy (if done): Inflamed glomeruli with "humps" (deposits under the epithelium).
  • Treatment: Supportive — salt and fluid restriction, loop diuretics, BP control; penicillin to clear the infection; dialysis rarely.
  • Prognosis: Excellent in children; less good in older adults.
• Infection-related GN in adults:
  • Often during the infection (not after) — staphylococcal infection (skin, bone, endocarditis), especially in diabetes, alcohol excess and older people.
  • May show IgA-dominant deposits.
  • Treat the infection; avoid immunosuppression.
• Endocarditis and shunt nephritis — immune complex GN with low C3 and C4.

↑ Back to index

Anti-GBM Disease

• What it is: Autoantibodies against type IV collagen (alpha-3 chain) in the glomerular and alveolar basement membranes. "Goodpasture's disease" is the name used when the lungs are involved.
• Who: Two peaks — young men (20s–30s, more lung haemorrhage) and older women (60s–70s, more kidney-only disease). Smoking and inhaled hydrocarbons increase lung bleeding.
• Features:
  • Rapidly progressive GN — kidney failure over days.
  • Lung haemorrhage (in about half) — haemoptysis, breathlessness, anaemia, infiltrates on chest X-ray, raised transfer factor (KCO).
  • Few systemic symptoms.
• Tests:
  • Anti-GBM antibodies in the blood (urgent).
  • Biopsy — linear IgG along the basement membrane; crescents.
  • ANCA — about 30–40% are also ANCA-positive ("double positive"), with a risk of relapse like vasculitis.
• Treatment (urgent, before biopsy if suspected):
  • Plasma exchange — daily, to remove antibodies (usually for about 14 days or until antibodies are gone).
  • High-dose steroids — IV methylprednisolone then oral prednisolone.
  • Cyclophosphamide (rituximab as an alternative).
  • Stop smoking.
• Prognosis:
  • Kidney recovery is unlikely if the patient needs dialysis at presentation and nearly all glomeruli have crescents — though treatment is still given for lung haemorrhage.
  • Relapse is rare (unlike ANCA vasculitis), except in double-positive patients.
  • Transplant only after antibodies have been undetectable for at least 6 months.

↑ Back to index

ANCA-associated Vasculitis

• What it is: Small-vessel vasculitis with antibodies against neutrophil enzymes. The kidney lesion is a pauci-immune (few deposits) necrotising crescentic GN.
• Types:
  • Granulomatosis with polyangiitis (GPA) — usually PR3-ANCA (c-ANCA):
    • Ear, nose and throat — crusting, nosebleeds, sinusitis, deafness, saddle-nose.
    • Lungs — nodules, cavities, haemorrhage.
    • Kidneys — GN.
    • Eyes (scleritis, orbital mass), subglottic stenosis.
  • Microscopic polyangiitis (MPA) — usually MPO-ANCA (p-ANCA): kidney and lung (haemorrhage, fibrosis); no granulomas; older people.
  • Eosinophilic GPA (EGPA) — asthma, nasal polyps, eosinophilia, neuropathy (mononeuritis multiplex), heart involvement; MPO-ANCA in about 40%; kidney disease less common.
• General features: Fever, weight loss, joint pains, purpuric rash, mononeuritis multiplex, raised CRP, anaemia.
• Drug-induced — hydralazine, propylthiouracil, levamisole-contaminated cocaine, minocycline.
• Treatment (KDIGO 2024, BSR):
  • Induction:
    • Steroids — IV methylprednisolone then oral prednisolone, using a reduced-dose taper (PEXIVAS — as effective, with fewer infections).
    • Plus rituximab or cyclophosphamide (rituximab preferred for relapsing disease, PR3-ANCA, younger people wanting fertility).
    • Avacopan (NICE TA825) — a C5a receptor blocker, with rituximab or cyclophosphamide, for severe active GPA or MPA; allows much less steroid.
    • Plasma exchange — consider with creatinine over about 300 µmol/L, rapidly falling function or dialysis, or lung haemorrhage with hypoxia.
  • Maintenance (for 2–4 years):
    • Rituximab every 6 months (better than azathioprine — MAINRITSAN).
    • Azathioprine or methotrexate as alternatives.
  • EGPA — steroids; mepolizumab (anti-IL-5) for relapsing or refractory disease.
  • Prophylaxis:
    • Co-trimoxazole (PJP prophylaxis).
    • Bone protection.
    • Vaccines (before rituximab).
    • Check immunoglobulins (rituximab can cause low IgG).
• Prognosis: Mostly good with treatment, but relapse is common (especially PR3); infection is a major cause of death in the first year.

💡 Clinical Pearl: An older person with "pneumonia that doesn't respond to antibiotics", a rising creatinine, and blood and protein on dipstick has ANCA vasculitis until proven otherwise.

↑ Back to index

Lupus Nephritis

• Who: About 40–50% of people with SLE develop kidney involvement, usually in the first 5 years; more common and severe in people of African, Caribbean and Asian descent.
• Screen all SLE patients regularly — BP, urine dipstick, ACR or PCR, eGFR.
• Signs of activity:
  • Proteinuria (PCR over 50 mg/mmol is an indication for biopsy), haematuria, casts.
  • Rising creatinine.
  • Low C3 and C4.
  • Rising anti-dsDNA.
• Classes (ISN/RPS, on biopsy):
  • I–II — mesangial (mild); no specific immunosuppression for the kidney.
  • III (focal) and IV (diffuse) proliferative — the most serious; nephritic picture; needs immunosuppression.
  • V — membranous — nephrotic syndrome; immunosuppression if heavy proteinuria.
  • VI — advanced scarring (over 90% sclerosed); prepare for kidney failure.
• Treatment (class III, IV, and V with heavy proteinuria):
  • Induction:
    • Steroids — IV methylprednisolone then oral prednisolone, tapered.
    • Plus mycophenolate (MMF) or low-dose IV cyclophosphamide (Euro-Lupus regimen).
    • Add-on options — voclosporin (with MMF; NICE TA882) or belimumab.
    • Rituximab for refractory disease.
  • Maintenance — MMF (or azathioprine, especially in pregnancy) for at least 3 years.
  • Hydroxychloroquine for all (reduces flares).
  • ACE inhibitor or ARB, BP control, statin.
  • Pregnancy — plan when disease is quiet for 6 months or more; switch MMF to azathioprine; aspirin; watch for flares and pre-eclampsia.
• Antiphospholipid syndrome can cause kidney thrombotic microangiopathy in SLE — anticoagulation.

↑ Back to index

MPGN and C3 Glomerulopathy

• Membranoproliferative GN (MPGN) — a pattern of injury with thickened capillary walls ("tram-track" appearance) and increased cells. Mixed nephrotic and nephritic picture, often with low complement.
• Immune-complex MPGN (low C3 and C4) — look for a cause:
  • Hepatitis C with cryoglobulinaemia — purpura, joint pain, neuropathy, low C4; treat with direct-acting antivirals.
  • Hepatitis B; endocarditis; other chronic infections.
  • Monoclonal gammopathy (MGRS).
  • Autoimmune disease (lupus, Sjögren's).
• C3 glomerulopathy (low C3, normal C4):
  • Over-activity of the alternative complement pathway — often C3 nephritic factor (an autoantibody) or genetic defects.
  • Includes dense deposit disease (linked to partial lipodystrophy and retinal drusen).
  • Often presents after an infection, like post-streptococcal GN — but C3 stays low beyond 8–12 weeks.
  • Treatment: Supportive care; mycophenolate with steroids; complement inhibitors (e.g. iptacopan is licensed; NICE was unable to make a recommendation — TA1102).
  • Recurs often after transplant.

↑ Back to index

Infection-related Kidney Disease

• Hepatitis B — membranous nephropathy (children), MPGN, polyarteritis nodosa. Treat with antivirals.
• Hepatitis C — cryoglobulinaemic MPGN. Treat with direct-acting antivirals; rituximab for severe vasculitis.
• HIV:
  • HIV-associated nephropathy (HIVAN) — collapsing FSGS, heavy proteinuria, large echogenic kidneys, rapid kidney failure; mainly people of African ancestry (APOL1).
  • Immune complex disease; drug toxicity (tenofovir disoproxil — Fanconi syndrome, AKI).
  • Antiretroviral therapy improves HIVAN.
• Endocarditis — immune complex GN, emboli, drug-induced AIN and antibiotic toxicity (gentamicin, vancomycin).
• Syphilis, malaria, schistosomiasis — membranous or other glomerular disease (travel history).
• Hantavirus and leptospirosis — interstitial disease and AKI.

↑ Back to index

Drug Reference Table

↑ Back to index

Spot the Diagnosis