Clinical Guides
Glomerulonephritis
A source-grounded syndromic guide to glomerulonephritis, integrating urine and serological patterns, kidney biopsy, rapidly progressive disease, infection exclusion, immunosuppression safety and India-specific referral and treatment access.
MedNext Academy | 15 min read
Glomerulonephritis
A source-grounded syndromic guide to glomerulonephritis, integrating urine and serological patterns, kidney biopsy, rapidly progressive disease, infection exclusion, immunosuppression safety and India-specific referral and treatment access.
Summary
Glomerulonephritis (GN) describes inflammatory injury centred on renal glomeruli. It is a syndrome family, not one diagnosis: immune-complex disease, pauci-immune small-vessel vasculitis, anti-glomerular-basement-membrane disease, infection-related processes and complement-mediated disorders require different treatment. Presentations range from isolated microscopic haematuria and proteinuria to a nephritic syndrome with oedema, hypertension and acute kidney injury, a nephrotic-nephritic overlap, or rapidly progressive glomerulonephritis (RPGN) with loss of function over days to weeks. Systemic features may identify lupus, vasculitis, infection, malignancy or drug exposure.
First identify threats: pulmonary haemorrhage, severe hypertension, pulmonary oedema, dangerous hyperkalaemia, oliguria, uraemic complications and fast creatinine progression. Send urine microscopy and quantified protein, renal and systemic blood tests, complement, infection studies and disease-directed antibodies promptly. Serology changes probability but rarely replaces kidney biopsy. Biopsy with light microscopy, immunofluorescence and electron microscopy is often decisive for pattern, activity, chronic damage and treatment choice; obtain adequate tissue through an experienced pathway.
Supportive care includes salt and fluid decisions matched to congestion, blood-pressure and proteinuria management, avoidance of nephrotoxins, vaccination and cardiovascular risk reduction. Immunosuppression is never a generic response to blood and protein in urine. Exclude active infection and define the pathological syndrome, except when a specialist judges that treatment delay in a compatible life-threatening anti-GBM or ANCA syndrome is more dangerous than starting before biopsy. Screen for tuberculosis, hepatitis and other infections before sustained immunosuppression in India. Dialysis treats complications, while plasma exchange has narrow disease-specific indications. This quarantined draft uses evolving KDIGO chapter updates and requires organisational clinical review.
How Common Is It?
Glomerular diseases are an important cause of chronic kidney disease and kidney failure worldwide, particularly among children and younger adults for whom lifelong consequences are substantial. KDIGO 2021 notes that glomerular diseases account for roughly one fifth to one quarter of prevalent cases in many kidney-failure registries, but registry proportions are not community incidence and are shaped by biopsy practice, access to nephrology and disease classification. The broad term GN combines uncommon but dangerous disorders with more prevalent entities such as IgA nephropathy.
Frequency differs by age, geography, ancestry, infection burden and referral setting. IgA nephropathy is the most common primary glomerular disease globally, yet it is biopsy-defined and can remain undetected when mild haematuria is not investigated. Post-infectious and infection-related GN patterns are more prominent where skin, respiratory and chronic bacterial infections are common. Lupus nephritis disproportionately affects women of reproductive age, while ANCA-associated vasculitis is generally more frequent in older adults but can occur across ages. Anti-GBM disease is rare and clinically urgent.
India has no single current national incidence that can safely populate a patient-facing estimate. Biopsy registries from tertiary centres overrepresent severe, referred and biopsy-eligible disease and underrepresent patients who cannot travel or afford tissue diagnosis. Tuberculosis, hepatitis B and C, HIV, endocarditis, staphylococcal infection and parasitic exposures influence differential diagnosis and the safety of immunosuppression, but their contribution varies by location.
Outcome depends less on the label GN than on cause, starting kidney function, proteinuria, crescents and chronic scarring, speed of treatment and response. A normal complement or negative antibody panel does not make disease harmless. Services should measure time to nephrology, biopsy adequacy, pathology turnaround, dialysis need, infection complications and renal recovery rather than advertise a misleading prevalence number.
Risk Factors
Risk is disease-specific. IgA nephropathy may follow mucosal immune activation and can cluster in families, but an upper respiratory infection preceding visible haematuria is a clinical clue rather than proof. Lupus nephritis risk arises in systemic lupus erythematosus and requires surveillance even when extra-renal symptoms are quiet. ANCA-associated GN may occur with granulomatosis with polyangiitis or microscopic polyangiitis; constitutional symptoms, chronic sinus or ear disease, pulmonary symptoms, neuropathy, skin vasculitis and drug exposures increase suspicion. Anti-GBM disease can involve kidney and lung without a known trigger.
Infection-related GN may accompany recent streptococcal infection, active staphylococcal infection, endocarditis, infected vascular access, abscess, hepatitis B or C, HIV and other infections. Diabetes, older age and immune compromise can modify presentation. In India, ask about fever, heart valve or device risk, skin lesions, dental infection, injecting exposure, tuberculosis symptoms, hepatitis risks and recent antimicrobials. Treating infection-associated immune-complex disease with unexamined corticosteroids can amplify the source and cause death.
Medicines can trigger interstitial or vascular disease that mimics GN, and selected agents are associated with ANCA or lupus-like syndromes. Ask about hydralazine, propylthiouracil, levamisole-adulterated substances and biologic therapies while recognising that association is not causation. NSAIDs can produce haematuria, proteinuria or acute kidney injury through several mechanisms. Malignancy, monoclonal immunoglobulin disorders and complement dysregulation enter the risk framework according to age and laboratory pattern.
Progression risks include delayed recognition, substantial or persistent proteinuria, reduced eGFR, uncontrolled blood pressure, active inflammatory lesions, extensive crescents and chronic fibrosis. Smoking, obesity and recurrent infection add renal and treatment risk. Immunosuppression itself creates susceptibility to tuberculosis, hepatitis reactivation, pneumocystis, herpes viruses, bacterial infection, cytopenia, infertility and malignancy. Social risks—late referral, unaffordable biopsy, fragmented pathology and inability to attend monitoring—must be recorded because they directly affect safe regimen choice.
Diagnosis
Diagnosis proceeds from syndrome to aetiology, with treatment urgency assessed at every step. Haematuria and proteinuria with rising creatinine are a nephrology problem until explained.
History
Define onset and tempo of dark or red urine, frothy urine, reduced output, oedema, weight change, headache, visual symptoms, nausea and breathlessness. Ask about recent sore throat, impetigo, persistent fever, dental or skin infection, endocarditis risk, tuberculosis, hepatitis and HIV exposure. Seek rash, purpura, joint pain, photosensitivity, mouth ulcers, sinus disease, hearing change, haemoptysis, neuropathy and abdominal pain. Record pregnancy, diabetes, autoimmune disease, cancer, family kidney disease, prescribed and traditional medicines, recent antibiotics and prior creatinine, urine protein and serology.
Examination
Measure repeated blood pressure, temperature, pulse, respiratory rate, oxygen saturation, weight and fluid balance. Look for oedema, raised venous pressure, crackles, pleural effusion, pericardial rub and uraemic change. Inspect skin for purpura, infection, lupus features and livedo; examine joints, mouth and upper airway. Cardiac examination must seek a murmur or stigmata of endocarditis. Assess abdomen, bladder, peripheral pulses and nervous system. Haemoptysis or hypoxaemia with anaemia may represent alveolar haemorrhage even when chest signs are limited.
Investigations
Repeat creatinine, urea, electrolytes, bicarbonate, albumin, CBC and inflammatory markers; quantify urine protein with protein-creatinine or albumin-creatinine ratio. Urine microscopy should seek dysmorphic erythrocytes and red-cell casts, while culture excludes infection. Order C3 and C4, ANA and anti-dsDNA, ANCA with PR3/MPO specificity, anti-GBM antibody, hepatitis B/C and HIV according to consent and risk; add blood cultures before antibiotics for possible endocarditis. ASO or anti-DNase B supports preceding streptococcal exposure but does not prove current cause. Consider immunoglobulins, electrophoresis, free light chains, cryoglobulins and complement-pathway tests selectively. Ultrasound checks size and biopsy safety. Kidney biopsy should include light microscopy, immunofluorescence and electron microscopy wherever possible; tissue must be divided correctly before fixation.
Differential Diagnosis
Not all haematuria is glomerular. Urinary infection, stone, tumour, trauma, menstruation, catheter injury, sickle disease and prostatic or gynaecological bleeding require clinical distinction. Glomerular haematuria is supported by dysmorphic red cells, acanthocytes, red-cell casts, proteinuria and impaired function, but microscopy is operator-dependent. Visible blood with clots or colic points away from a glomerular source. Myoglobin and haemoglobin can make dipstick blood positive without urine erythrocytes.
Acute tubular injury, acute interstitial nephritis, obstruction, thrombotic microangiopathy, malignant hypertension, renal infarction, cholesterol emboli and cortical necrosis can cause AKI with urinary abnormalities. Interstitial nephritis may have pyuria, white-cell casts, rash or eosinophilia, but classic features are often absent. Thrombotic microangiopathy is suggested by thrombocytopenia, haemolysis and organ injury; severe hypertension can be cause or consequence. Diabetic kidney disease can coexist with GN, particularly when the decline is rapid or sediment active.
The GN differential is structured by immunopathology. Granular immune-complex deposition occurs in IgA nephropathy, lupus nephritis, infection-related GN, membranoproliferative patterns and cryoglobulinaemia. Linear IgG supports anti-GBM disease. Pauci-immune crescentic GN usually accompanies ANCA-associated vasculitis but may be ANCA-negative. Low C3 with normal or low C4 narrows mechanisms but is not diagnostic. Serum ANCA can be positive in infection, inflammatory disease, medicines and without active vasculitis; a negative result does not exclude pauci-immune GN.
Rapidly progressive GN is a clinical trajectory with crescentic pathology, not one aetiology. Pulmonary-renal syndrome includes ANCA vasculitis, anti-GBM disease and lupus but also mimics such as severe infection, pulmonary oedema, embolism and coagulopathy. Before immunosuppression, actively reconsider endocarditis, tuberculosis and hepatitis. The final formulation should name the nephritic phenotype, progression rate, serological pattern, infection probability, biopsy status, complications and leading competing diagnoses.
Management
Triage physiology first. Severe hypertension, pulmonary oedema, hyperkalaemia, acidosis, uraemic manifestations and rapidly declining urine output require monitored hospital care. Treat an active infection promptly with cultures and source control. Manage fluid and sodium according to congestion, not by reflex: oedematous hypertensive patients generally need restriction and diuretic-based decongestion, whereas true intravascular depletion needs cautious correction. Track weight, intake, output, blood pressure, creatinine, potassium, albumin and proteinuria. Avoid NSAIDs and unnecessary contrast; adjust all renally cleared medicines.
Supportive renal protection is foundational once haemodynamics permit. Control blood pressure, reduce proteinuria, address smoking and cardiovascular risk, vaccinate and manage lipids according to overall risk. Renin-angiotensin system blockade and newer kidney-protective agents have disease-, eGFR-, potassium-, pregnancy- and approval-specific roles; they are not started indiscriminately during unstable AKI. Prevent thrombosis selectively in severe nephrotic states after balancing bleeding. Provide nutrition without routine high-protein loading or unsupported extreme restriction.
Disease-modifying treatment follows the exact diagnosis and activity. Infection-related GN is managed primarily by eradicating infection and controlling complications; routine immunosuppression can be dangerous. Lupus nephritis regimens depend on biopsy class, activity, chronicity, kidney function, pregnancy and prior therapy. ANCA-associated GN generally requires specialist induction with glucocorticoid-sparing strategy plus rituximab- or cyclophosphamide-based therapy, followed by maintenance; current KDIGO guidance contains patient-specific selection. Anti-GBM disease may require immediate glucocorticoids, cyclophosphamide and plasma exchange under a specialist protocol. IgA nephropathy management integrates optimized supportive care and, for selected risk groups, disease-targeted therapy under the 2025 update.
Do not wait for biopsy when a nephrologist judges that compatible pulmonary haemorrhage or rapidly progressive anti-GBM/ANCA disease threatens irreversible harm, but obtain blood and tissue as soon as safely possible. Conversely, do not give empirical steroids to every patient with crescents or active sediment. Dialysis indications are physiological. Follow response using creatinine trajectory, urine output, proteinuria, haematuria, serology where disease-valid, adverse effects and patient goals; persistent abnormalities may reflect activity, chronic damage, toxicity or wrong diagnosis.
Prescribing Information
Immunosuppression should be prescribed only after diagnosis, severity, infection risk, fertility, pregnancy, comorbidity and monitoring capacity are defined. Before substantial glucocorticoid, rituximab, cyclophosphamide, mycophenolate or calcineurin-inhibitor exposure, screen for active infection and assess tuberculosis, hepatitis B and C, HIV, vaccination status, CBC, liver function, kidney function, immunoglobulins where relevant and pregnancy. In India, tuberculosis assessment must combine symptoms, imaging, epidemiology and programme pathways; a screening assay alone neither proves nor excludes active disease. Hepatitis B reactivation prevention requires serology interpretation and specialist coordination.
Glucocorticoids can cause severe infection, hyperglycaemia, hypertension, psychiatric effects, bone loss, gastrointestinal complications, cataract and adrenal suppression. Use the disease-specific lowest effective regimen and define taper and prophylaxis. Cyclophosphamide risks cytopenia, infection, haemorrhagic cystitis, infertility and malignancy; cumulative exposure and fertility preservation require discussion. Rituximab entails infusion reactions, hepatitis reactivation, hypogammaglobulinaemia and late infection. Mycophenolate, methotrexate and cyclophosphamide have major reproductive risks. Calcineurin inhibitors require trough, creatinine, potassium, blood-pressure and interaction monitoring.
Pneumocystis prophylaxis, gastric and bone protection, vaccination and antimicrobial prevention depend on regimen and patient factors. Live vaccines are generally avoided during significant immunosuppression. Trimethoprim-sulfamethoxazole can raise creatinine and potassium and needs renal adjustment; alternatives also have toxicities. Never prescribe prophylaxis without a stop date and monitoring owner. Screen for strong enzyme or transporter interactions and avoid duplicated immunosuppression from fragmented specialists.
Supportive drugs also require precision. Renin-angiotensin blockers can reduce proteinuria but may raise creatinine and potassium and are contraindicated in pregnancy. Diuretics treat oedema and need daily-weight, pressure, sodium and potassium review. Anticoagulation is individualized, not automatic. New IgA, lupus and vasculitis agents have rapidly changing Indian licensing, cost and access; an international guideline mention is not regulatory approval. Plasma exchange is a procedure with line, bleeding, infection and replacement-fluid risks, not a medicine-like default for all crescentic GN.
When to Refer
Urgent nephrology referral is required for rising creatinine with haematuria and proteinuria, red-cell casts, substantial proteinuria, nephrotic-nephritic overlap, unexplained low complement, positive anti-GBM or disease-consistent ANCA, suspected lupus nephritis, or systemic features suggesting vasculitis. The referral should include previous and current creatinine, urine protein quantification, microscopy, blood pressure, urine output, potassium, bicarbonate, albumin, CBC, complement, infection tests and medication timeline. Send actual laboratory and imaging records rather than a label alone.
Same-day transfer to a centre with nephrology, kidney biopsy, dialysis and critical care is needed for RPGN, pulmonary haemorrhage, severe or refractory hypertension, pulmonary oedema, dangerous hyperkalaemia, severe acidosis, oliguria or uraemic complications. KDIGO 2024 advises that ANCA vasculitis be treated in experienced centres with serology, histology, immunosuppressive therapies, plasma exchange, intensive care and acute haemodialysis access. Do not wait locally for every antibody result or a scheduled outpatient appointment while kidney function falls.
Add rheumatology for systemic lupus or vasculitis, infectious diseases and microbiology when infection is possible, haematology for monoclonal or thrombotic processes, respiratory or critical care for pulmonary haemorrhage and obstetrics for pregnancy. A native-kidney biopsy should be planned with pathology before the procedure so tissue reaches light microscopy, immunofluorescence and electron microscopy; a single formalin container can make the biopsy nondiagnostic.
In India, referral must be operational. Confirm which medical college or renal centre can perform urgent biopsy, immunofluorescence, dialysis and immunosuppression monitoring; state whether plasma exchange is available; arrange transport and financial navigation; and send samples before steroids when safe. Lower the threshold when travel is long or tests cannot be repeated. After treatment, nephrology follow-up remains necessary for remission, relapse, infection, fertility, vaccination, drug toxicity, CKD and transplantation planning.
Red Flags
Pulmonary-renal syndrome is an emergency. Haemoptysis may be absent despite diffuse alveolar haemorrhage; falling haemoglobin, new bilateral infiltrates, hypoxaemia and a rapidly rising creatinine require urgent respiratory, renal and critical-care coordination. Send ANCA and anti-GBM antibodies and arrange biopsy, but a specialist may begin treatment before histology when the clinical probability and threat are high. Anticoagulation and bronchoscopy decisions require individualized risk assessment.
Severe hypertension with headache, visual change, seizure, confusion, retinal injury, heart failure or microangiopathic haemolysis is an emergency. Pulmonary oedema, refractory hyperkalaemia, severe acidosis, pericarditis, encephalopathy, bleeding and anuria are kidney-failure complications needing dialysis assessment. Rapid doubling of creatinine, crescents on biopsy or steep urine-output decline indicates RPGN even if oedema is modest.
Fever, murmur, embolic lesions, persistent positive blood cultures, an infected line, abscess, hepatitis or tuberculosis symptoms are warnings against uncritical immunosuppression. Endocarditis can produce low complement, ANCA positivity and GN. A steroid-responsive fever does not prove autoimmunity. In an immunosuppressed patient, new cough, hypoxaemia, shingles, severe diarrhoea, urinary symptoms, cytopenia or liver-test change requires urgent infection and toxicity review.
Biopsy red flags include uncontrolled pressure, coagulopathy, thrombocytopenia, a solitary high-risk anatomy and unavailable post-procedure observation; the response is risk mitigation or an alternative approach, not abandoning diagnosis without specialist discussion. After biopsy, flank pain, hypotension, visible haematuria or falling haemoglobin requires immediate imaging and haemorrhage management. Patients discharged on immunosuppression need written instructions for fever, breathlessness, bleeding, reduced urine and missed monitoring. Inability to obtain medicines or attend tests is itself a safety signal because abrupt interruption or unmonitored continuation can both be dangerous.
Indian Clinical Context
The Indian pathway must hold autoimmune inflammation and infection in view simultaneously. Tuberculosis, hepatitis B and C, HIV, endocarditis, staphylococcal infection, post-infectious disease and tropical febrile illnesses can cause GN, mimic vasculitis or become catastrophic during immunosuppression. Ask about fever pattern, weight loss, cough, contacts, devices, wounds, dental disease, injected substances and prior antibiotics. Use current NTEP, NACO, ICMR, NCDC, state and hospital protocols for infection testing and treatment; KDIGO does not replace Indian antimicrobial or tuberculosis policy.
Diagnostic capacity varies. Urine microscopy quality, complement, ANCA specificity, anti-GBM testing, cryoglobulin handling, electrophoresis, immunofluorescence and electron microscopy may not coexist at one facility. Before biopsy, telephone the renal pathologist and divide tissue correctly. If advanced pathology is unavailable, transfer tissue or patient through a documented pathway; do not report nonspecific proliferative GN as a complete aetiological diagnosis. A negative test from delayed, mishandled or method-limited sampling needs cautious interpretation.
High-cost biologics, complement-pathway drugs, targeted IgA therapies and plasma exchange may be inaccessible or licensed differently. Cost matters, but substitution must remain evidence-based and openly discussed. Compare expected benefit, infection risk, fertility, monitoring, travel and public-scheme availability. Established lower-cost regimens still require dosing, prophylaxis and toxicity surveillance; affordability does not make unmonitored cyclophosphamide or prolonged high-dose steroid safe. Biosimilars require regulated procurement and traceability.
Acute haemodialysis, intensive care and biopsy beds may require inter-district transfer. Refer before hyperkalaemia, hypoxaemia or uraemia makes transport unsafe. Provide the patient with a portable record of creatinine, urine protein, serology, biopsy blocks and slides, immunosuppression exposure and infection screening. No Indian national incidence, uniform biopsy threshold or universal regimen is claimed here. The correct plan is the current diagnosis-specific protocol agreed by nephrology and relevant specialists, adapted transparently to real local capacity.
NMC Competency Mapping
NMC CBME 2024 Pathology competency PA28.5 requires learners to define and classify glomerular diseases and describe the aetiology, pathogenesis, mechanisms of glomerular injury, pathology, distinguishing features and clinical manifestations of glomerulonephritis. PA28.6 separately addresses IgA nephropathy. This guide maps those pathological objectives to bedside syndrome recognition, urine interpretation, serology, biopsy and safe referral without suggesting that an undergraduate should independently select immunosuppression.
Learners should distinguish nephritic syndrome from nephrotic syndrome and recognise overlap. They should link glomerular capillary inflammation to dysmorphic haematuria, red-cell casts, proteinuria, reduced filtration, sodium retention, oedema and hypertension. Classification should integrate immune-complex, pauci-immune and anti-GBM patterns with light microscopy, immunofluorescence and electron microscopy. A useful pathology answer includes activity and chronicity because crescents, necrosis and cellular inflammation carry different implications from global sclerosis and fibrosis.
Clinical competence includes eliciting infection, autoimmune, pulmonary, skin, joint, neurological, medicine and family clues; measuring blood pressure and volume status; quantifying proteinuria; and ordering complement and targeted antibodies. Students must state that IgA nephropathy is biopsy-diagnosed and that ANCA positivity alone does not prove vasculitis. They should identify pulmonary haemorrhage, RPGN and kidney-failure complications for emergency escalation.
Integration spans medicine, paediatrics, rheumatology, microbiology, pharmacology, pathology, radiology, obstetrics and emergency care. Pharmacology learning covers glucocorticoid, cyclophosphamide, rituximab, mycophenolate and calcineurin-inhibitor toxicities, infection screening and reproductive safety rather than memorising one regimen. Communication competence includes an operational biopsy and referral handover. Reading this draft does not certify biopsy interpretation, immunosuppressive prescribing, plasma exchange or dialysis competence.
Key Exam Pearls for NEET PG
Nephritic syndrome classically combines glomerular haematuria, variable proteinuria, hypertension, oedema and reduced GFR. Dysmorphic red cells and red-cell casts support glomerular bleeding. Nephrotic-range proteinuria can coexist with nephritic inflammation. RPGN describes rapid loss of function and usually correlates with extensive crescent formation; classify causes as immune-complex, pauci-immune or anti-GBM rather than treating RPGN as one disease.
Complement patterns narrow the differential. Low complement suggests lupus, infection-related disease, membranoproliferative patterns, cryoglobulinaemia or complement dysregulation, while normal complement is common in IgA nephropathy, ANCA disease and anti-GBM disease; exceptions occur. Granular immunofluorescence indicates immune complexes, linear IgG suggests anti-GBM disease, and little or no staining supports pauci-immune GN. ANCA-negative pauci-immune disease exists.
IgA nephropathy requires kidney biopsy; no serum biomarker establishes it. Synpharyngitic visible haematuria is a clue, whereas classic post-streptococcal GN usually follows infection after a latent interval. Lupus nephritis therapy depends on biopsy class and activity. ANCA-associated GN can proceed rapidly; current guidance says biopsy should be considered, but compatible positive PR3/MPO serology and urgent disease may justify specialist-led treatment without waiting. Anti-GBM pulmonary-renal disease traditionally requires urgent combined immunosuppression and plasma exchange under protocol.
Always exclude active infection before routine immunosuppression. Endocarditis can mimic vasculitis with low complement, ANCA and GN. Treat oedema and hypertension supportively, monitor potassium and renal function, and use dialysis for physiological complications rather than a fixed creatinine. Kidney biopsy needs light microscopy, immunofluorescence and electron microscopy. For NMC remember PA28.5 for GN classification and injury mechanisms and PA28.6 for IgA nephropathy.
Frequently Asked Questions
Can glomerulonephritis be diagnosed from blood and urine tests alone?
Tests can establish a glomerular syndrome and make particular causes more or less likely, but they often cannot define the exact disease or distinguish active inflammation from chronic scarring. ANCA, anti-GBM antibody, complement and lupus serology need clinical interpretation. Kidney biopsy with light microscopy, immunofluorescence and electron microscopy is commonly decisive for diagnosis and treatment. In an immediately threatening pulmonary-renal or rapidly progressive syndrome, a nephrologist may start treatment before biopsy while arranging tissue urgently.
Why must infection be excluded before starting immunosuppression?
Endocarditis, hepatitis, tuberculosis and other infections can cause immune-complex GN or mimic systemic vasculitis. Corticosteroids or cytotoxic therapy may suppress fever temporarily while worsening the source, dissemination and mortality. Obtain cultures and targeted infection testing early, review devices and examine for a focus. In India, tuberculosis and hepatitis screening is especially important before sustained therapy. Genuine life-threatening autoimmune disease may still require immediate specialist treatment, but that decision includes concurrent infection investigation and antimicrobial or prophylactic planning.
What makes a glomerulonephritis rapidly progressive clinically?
RPGN is a clinical pattern of substantial kidney-function loss over days to weeks, usually associated with extensive crescentic injury on biopsy. Falling urine output, a steep creatinine rise, active sediment and pulmonary haemorrhage increase urgency. It can result from ANCA-associated vasculitis, anti-GBM disease, lupus, infection-related and other immune-complex processes. Send disease-directed serology and arrange biopsy and nephrology transfer immediately. The phrase does not identify the cause, and treatment must be diagnosis-specific rather than a generic steroid course.
Does every patient with crescents need plasma exchange or dialysis?
No. Crescents indicate severe glomerular injury but their proportion, cellular or fibrous character, underlying disease, kidney function and systemic features determine meaning. Plasma exchange has narrow indications that differ among anti-GBM disease, ANCA vasculitis and other conditions, and current guidance must be used. Dialysis treats refractory potassium, acidosis, fluid overload, uraemic complications and selected other physiological needs; it is not triggered by histology alone. Both treatments require specialist facilities and should not delay cause-directed diagnosis.
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