🔬 Glomerulonephritis

Comprehensive Guide to Nephritic and Nephrotic Syndromes

Clinical Nephrology Education 2025 Evidence-Based Guidelines

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A leaky filter creates a syndrome

Glomerular barrier injury permits protein loss into urine. Albumin loss and renal sodium retention contribute to edema. Altered coagulation and urinary protein losses increase thrombosis risk; immune protein losses and treatment affect infection risk. Altered hepatic production and lipid clearance cause hyperlipidemia.
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A glomerular problem can explain edema, altered lipid levels, thrombosis, and infection risk in the same patient.

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⚠️ Emergency Recognition

RPGN is a nephrology emergency! Rapidly worsening kidney function with suspected glomerular inflammation needs immediate nephrology assessment. Hemoptysis or hypoxemia raises concern for a pulmonary–renal emergency. Do not wait for a 50% fall in GFR.

📚 Chapter Overview

Glomerular diseases represent a complex group of disorders affecting the kidney's filtering units. This comprehensive chapter covers both nephritic and nephrotic syndromes, their pathophysiology, diagnostic approaches, and evidence-based treatments essential for PA practice.

Learning Objectives

  • Differentiate nephritic from nephrotic syndromes clinically
  • Interpret complement patterns and serological testing
  • Recognize and manage rapidly progressive glomerulonephritis
  • Understand modern treatment approaches and prognosis
  • Identify secondary causes of glomerular disease

🩸 Nephritic vs 💧 Nephrotic Syndrome Differentiation

Nephritic Syndrome

  • Definition: Inflammatory glomerular disease
  • Proteinuria: Variable; may reach nephrotic range
  • Hematuria: +++
  • RBC Casts: Strong diagnostic clue when present; absence does not exclude GN
  • Hypertension: +++
  • Edema: Moderate
  • Serum Albumin: Variable; can fall with heavy protein loss

Nephrotic Syndrome

  • Definition: Proteinuric disease with hypoalbuminemia
  • Proteinuria: >3.5 g/day
  • Hematuria: +/-
  • RBC Casts: Usually absent in a bland nephrotic sediment; casts suggest an overlapping inflammatory process
  • Hypertension: +/-
  • Edema: Severe
  • Serum Albumin: <3.0 g/dL

🩸 Nephritic Syndrome - Detailed Review

🔬 Urine Microscopy Findings

🔴 RBC Casts - Strong Evidence of Glomerular Bleeding

Interpret casts with kidney function, proteinuria, and the full clinical presentation

  • Strongly suggest glomerular bleeding in the appropriate clinical setting
  • Must be differentiated from RBCs alone
  • Best seen in fresh urine (<2 hours)
  • May be missed if urine sits too long
Clinical Pearl: RBC casts strongly support a glomerular source and warrant prompt evaluation, but do not by themselves establish the cause or immune mechanism. Their absence does not exclude GN. Biopsy-correlated urine microscopy study.

🔬 Dysmorphic RBCs

  • Distorted RBC morphology
  • Indicates glomerular origin of bleeding
  • Contrasts with uniform RBCs from lower urinary tract
  • Acanthocytes are particularly useful; assess morphology with experienced microscopy rather than requiring a fixed dysmorphic-RBC percentage

⚪ WBC Casts

  • May be present in proliferative GN
  • Indicates inflammatory response
  • Less specific than RBC casts
  • Can also be seen in interstitial nephritis

🟤 Granular Casts

  • Brown, muddy appearance
  • Indicate tubular damage
  • May be seen with severe GN
  • Non-specific finding

🧬 Serological Evaluation of Glomerular Disease

📊 Complement System Evaluation

Measuring C3 and C4 simultaneously helps narrow the differential diagnosis. These are typical, nonexclusive patterns: normal levels do not exclude active GN, and low levels do not identify its cause.

Complement Patterns and Associated Diseases

Complement Pattern Pathway Renal-Limited Diseases Systemic Diseases % of Cases
Low C3 & C4 Classical Pathway Activation • Idiopathic MPGN Type I
• Dense deposit disease (rare) 		• SLE nephritis
• Cryoglobulinemia
• Subacute bacterial endocarditis
• Shunt nephritis
• Hepatitis C-associated GN 		~30%
Low C3, Normal C4 Alternative Pathway Activation • Post-infectious GN
• C3 glomerulopathy
• Dense deposit disease 		• Atypical HUS
• Partial lipodystrophy 		~25%
Normal C3 & C4 No detectable serum depletion; complement activation may still occur • IgA nephropathy
• Thin basement membrane
• Renal-limited vasculitis
• Anti-GBM nephritis 		• ANCA-associated vasculitis
• Goodpasture syndrome
• Henoch-Schönlein purpura
• Alport syndrome
• Polyarteritis nodosa 		~45%

🎯 ANCA Testing Clinical Correlation

High Positive Predictive Value

C-ANCA with sinusitis + pulmonary infiltrates + active urinary sediment = 98% PPV for GPA

However, C-ANCA with sinusitis alone has only 7-16% PPV

Combined Testing Approach

Use both immunofluorescence pattern AND antigen-specific ELISA (MPO/PR3) for optimal sensitivity and specificity

Clinical Context is Key

ANCA results must always be interpreted in the clinical context. PPV >95% in patients with classic RPGN features

ANCA Patterns and Associated Diseases

P-ANCA/MPO

Microscopic Polyangiitis (MPA)

  • Perinuclear staining pattern
  • Directed against myeloperoxidase (MPO)
  • More likely renal involvement (80%)
  • Pulmonary-renal syndrome common
  • Diffuse capillaritis

C-ANCA/PR3

Granulomatosis with Polyangiitis (GPA)

  • Cytoplasmic staining pattern
  • Directed against proteinase 3 (PR3)
  • Upper respiratory tract involvement
  • Pulmonary nodules
  • Necrotizing granulomatous inflammation

💧 Nephrotic Syndrome - Detailed Review

Pathophysiology Flow

1 Glomerular Basement Membrane Damage - Loss of charge selectivity and size selectivity
2 Massive Proteinuria - Primarily albumin loss (>3.5 g/day)
3 Hypoalbuminemia - Decreased plasma oncotic pressure
4 Fluid Retention - Edema formation and volume expansion
5 Compensatory Liver Synthesis - Increased protein and lipid production

🔬 Urine Microscopy in Nephrotic Syndrome

Oval Fat Bodies

  • Tubular epithelial cells containing lipid droplets
  • Highly characteristic of nephrotic syndrome
  • Result from reabsorption of filtered lipoproteins
  • Appear refractile under polarized light

Fatty Casts

  • Casts containing lipid droplets
  • Show "Maltese cross" appearance under polarized light
  • Pathognomonic for significant proteinuria
  • May persist even after treatment

Waxy Casts

  • Broad, homogeneous casts
  • May indicate chronic kidney disease
  • Non-specific finding
  • Can be seen with prolonged proteinuria

Minimal Hematuria

  • Usually <5 RBCs per high-power field
  • RBC casts are typically absent
  • Contrasts with nephritic syndrome
  • If significant hematuria present, consider mixed picture

Primary Causes of Nephrotic Syndrome

Minimal Change Disease (MCD)

Epidemiology
  • Most common cause in children (90%)
  • 20-25% of adult nephrotic syndrome
  • Male predominance in children
  • Peak incidence: 2-6 years old
Clinical Features
  • Sudden onset of edema and proteinuria
  • Normal blood pressure typically
  • Normal renal function
  • Minimal hematuria
Treatment
1 Initial Treatment: Prednisone 1 mg/kg/day (max 80 mg) for 4-16 weeks
2 Frequently Relapsing/Steroid-Dependent: Cyclophosphamide, Calcineurin inhibitors, Mycophenolate mofetil, or Rituximab

Focal Segmental Glomerulosclerosis (FSGS)

Epidemiology
  • Most common primary cause in adults
  • Higher prevalence in African Americans
  • 40% of adult nephrotic syndrome
  • Increasing incidence over past decades
Clinical Features
  • Often presents with hypertension
  • Microscopic hematuria common
  • May have reduced GFR at presentation
  • More resistant to treatment than MCD
Treatment
1 Initial Treatment: Prednisone 1 mg/kg/day for at least 8-16 weeks
2 Steroid-Resistant FSGS: Calcineurin inhibitors (first-line), Mycophenolate mofetil, or Sirolimus

Note: African Americans and patients with collapsing FSGS are generally unresponsive to treatment and progress to kidney failure.

Membranous Nephropathy

Epidemiology
  • Most common cause in older adults
  • Male predominance (2:1)
  • Peak incidence: 40-60 years
  • 30-40% of adult nephrotic syndrome
Non-Invasive Diagnosis
Anti-PLA2R Antibodies
  • Sensitivity: 78%
  • Specificity: 99%
  • Positive in 70-80% of primary MN cases
  • Kidney biopsy not required if positive with appropriate clinical context
  • Antibody levels correlate with disease activity
Risk Stratification (KDIGO 2021)
Risk Category Criteria Management
Low Risk Normal eGFR, Proteinuria <3.5 g/day, Serum albumin >3.0 g/dL Supportive care only
Moderate Risk Proteinuria 3.5-8 g/day, Stable eGFR, Albumin 2.5-3.0 g/dL Rituximab or calcineurin inhibitors
High/Very High Risk Proteinuria >8 g/day, Declining eGFR, High anti-PLA2R levels (>150 RU/mL) Immunosuppressive treatment required
Treatment Options
1 Rituximab (First-Line, KDIGO 2021): 375 mg/m² weekly × 4 doses or 1g × 2 doses
2 Modified Ponticelli Regimen: Alternating months of steroids and cyclophosphamide
3 Calcineurin Inhibitors: Cyclosporine 3-5 mg/kg/day (trough 125-175 ng/mL)

Complications of Nephrotic Syndrome

Thromboembolism (Critical)

Pathophysiology: Loss of antithrombin III and protein S, increased fibrinogen and platelets, hemoconcentration from diuretic use

  • Deep vein thrombosis
  • Pulmonary embolism
  • Renal vein thrombosis

Management: Consider prophylactic anticoagulation if albumin <2.0 g/dL

Infections

Pathophysiology: Loss of immunoglobulins in urine, complement factor losses, immunosuppressive medications

  • Pneumococcal pneumonia
  • Peritonitis (especially with ascites)
  • Cellulitis

Protein Malnutrition

  • Loss of binding proteins
  • Muscle wasting
  • Poor wound healing
  • Growth retardation in children

Cardiovascular Disease

  • Accelerated atherosclerosis
  • Hypertension
  • Coronary artery disease
  • Increased mortality risk

🚨 MEDICAL EMERGENCY

Rapidly Progressive Glomerulonephritis

Risk of irreversible kidney injury without prompt treatment Time is kidney function Immediate nephrology consultation required

Emergency Definition & Recognition

RPGN is a clinical syndrome of rapidly worsening kidney function with suspected glomerular inflammation, often over days to weeks. Evaluate urgently while excluding other causes of AKI; do not wait for a specified percentage GFR loss or biopsy crescent burden.

Recognition Criteria

Rapid GFR Decline

Rapid creatinine rise or falling filtration with a compatible clinical presentation; a 50% decline is not a referral threshold

Nephritic Urine

Hematuria, dysmorphic RBCs, RBC casts, proteinuria

Biopsy Activity and Chronicity

Crescents and necrosis support active injury; assess viable glomeruli and chronic scarring. A fixed crescent percentage is not required before urgent evaluation

Systemic Features

Constitutional symptoms, fever, malaise, arthralgias

RPGN Classification by Immunofluorescence Pattern

Type I: Linear Pattern (Anti-GBM Disease) - 10% of RPGN

Pathophysiology: Autoantibodies against NC1 domain of α3 chain of type IV collagen in glomerular and alveolar basement membranes

Clinical Presentations
  • Anti-GBM nephritis: Kidney involvement only
  • Goodpasture syndrome: Kidney plus lung involvement (pulmonary hemorrhage)
Emergency Treatment
1 Plasmapheresis: Daily exchanges for 14 days or until anti-GBM antibodies undetectable. Start immediately, do not wait for biopsy results
2 IV Methylprednisolone: 1g daily for 3 days, then oral prednisone 1 mg/kg/day
3 Cyclophosphamide: 2 mg/kg/day oral or IV monthly pulses

Type II: Granular Pattern (Immune Complex Disease) - 40% of RPGN

Associated Conditions
Systemic Lupus Erythematosus
  • Most common cause in this category
  • Class IV lupus nephritis
  • Requires aggressive immunosuppression
IgA Nephropathy
  • Crescents alone do not define rapidly progressive IgAN
  • Rapid functional decline requires urgent biopsy and specialist selection of treatment
  • Monitor for progression
Post-Infectious GN
  • Usually self-limiting
  • Prioritize infection treatment and kidney supportive care; routine immunosuppression is generally inadvisable
  • Supportive care in most cases
Other
  • Cryoglobulinemia
  • Endocarditis
  • MPGN

Type III: Pauci-Immune (ANCA-Associated) - 50% of RPGN

ANCA Patterns and Associated Vasculitides
P-ANCA/MPO - Microscopic Polyangiitis (MPA)
  • More likely renal involvement (80%)
  • Pulmonary-renal syndrome
  • Diffuse capillaritis
C-ANCA/PR3 - Granulomatosis with Polyangiitis (GPA)
  • Upper respiratory tract involvement
  • Pulmonary nodules
  • Necrotizing granulomatous inflammation
Emergency Treatment Protocol
1 Corticosteroids: IV methylprednisolone 0.5-1 g/day for 3 days, followed by oral prednisone 1 mg/kg for 1 month
2 Induction Immunosuppression: Cyclophosphamide (IV 15 mg/kg or oral 1.5-2 mg/kg daily) OR Rituximab (375 mg/m² weekly for 4 doses)
3 Plasmapheresis Indications: Serum creatinine >4 mg/dL, dialysis dependence, pulmonary hemorrhage, concomitant anti-GBM antibodies
4 Avacopan — historical evidence update: The pivotal ADVOCATE report (PMID 33596356; RETRACTED) was retracted in 2026 (retraction notice). Its efficacy claims should not guide treatment. FDA proposed withdrawal on April 27, 2026; this proposal is not a completed withdrawal. Review current status and alternatives with the treating specialist (FDA notice).
Maintenance Therapy
  • Azathioprine: 2 mg/kg/day
  • Mycophenolate mofetil: 1g twice daily
  • Rituximab: 500mg every 6 months
  • Duration: Minimum 18-24 months

Emergency Action Plan for PA Students

1 Recognition: Rapidly worsening kidney function with active sediment or systemic features needs immediate evaluation; do not wait for a 50% GFR loss
2 Immediate Actions: STAT nephrology consultation, fresh urine microscopy for RBC casts, STAT labs (creatinine, CBC, ANCA, anti-GBM), assess for systemic features
3 Stabilization: Manage fluid balance and electrolytes, control blood pressure, prepare for possible dialysis, consider empiric treatment if high suspicion
4 Definitive Care: Follow nephrology recommendations, monitor for treatment complications, coordinate multidisciplinary care, long-term follow-up planning

📊 RPGN Classification Summary

Type Pattern Main Causes % of RPGN Treatment Priority
Type I Linear (Anti-GBM) Goodpasture's, Anti-GBM nephritis 10% Plasmapheresis + Immunosuppression
Type II Granular (IC) Lupus, Post-infectious, IgA 40% Treat underlying cause
Type III Pauci-immune ANCA-associated vasculitis 50% Steroids + Cyclophosphamide/Rituximab

🆕 New and Emerging Treatments

Biologics and Monoclonal Antibodies

Rituximab

  • Anti-CD20 monoclonal antibody
  • Effective steroid-sparing agent
  • First-line for membranous nephropathy
  • Pediatric and adult efficacy

Daratumumab

  • Anti-CD38 monoclonal antibody
  • Targets long-lived plasma cells
  • Being studied in combination with rituximab
  • Novel approach to B-cell targeting

Gene Therapy

Podocyte-Targeted Gene Therapy

  • Experimental AAV gene delivery studied in human cell and mouse models of NPHS2-related nephrotic syndrome
  • Restored podocin expression and improved disease measures in those experimental models
  • Preclinical findings do not establish clinical benefit or safety in people
  • The 2023 study does not demonstrate a human cure or an available routine treatment (primary study)

Epigenetic Therapies

HDAC Inhibitors

  • Anti-fibrotic and anti-inflammatory effects
  • May attenuate renal sclerosis and proteinuria
  • Multiple agents under investigation

Network Pharmacology

  • Valproic acid and all-trans retinoic acid
  • Target epigenetic mechanisms
  • May promote disease regression

🔄 Secondary Causes of Glomerular Disease

Systemic Diseases

  • Diabetic nephropathy (most common overall)
  • Amyloidosis (AL, AA, or hereditary)
  • Lupus nephritis
  • Multiple myeloma

Infections

  • Hepatitis B (membranous pattern)
  • Hepatitis C (MPGN pattern)
  • HIV (collapsing FSGS)
  • Syphilis, malaria

Medications

  • NSAIDs (MCD pattern)
  • Gold, penicillamine
  • Immune checkpoint inhibitors
  • Interferon

Malignancies

  • Solid tumors (lung, breast, GI)
  • Hodgkin lymphoma (MCD pattern)
  • Non-Hodgkin lymphoma

🎯 Clinical Pearls for PA Practice

Emergency Recognition

RPGN Emergency: Suspected RPGN with rapid kidney-function decline needs immediate nephrology consultation. Do not wait for a percentage GFR threshold, urine microscopy results, or a completed biopsy before escalating care.

RBC Casts Require Clinical Correlation

RBC casts strongly support glomerular bleeding and prompt a glomerular workup, but do not identify its cause. Examine fresh urine when possible; absence of casts does not exclude GN.

Complement Testing Strategy

Often-normal C3/C4 suggests ANCA-associated, IgA, or anti-GBM disease; low C3 with relatively preserved C4 suggests infection-related GN or C3 glomerulopathy; low C3/C4 suggests lupus or other immune-complex disease. Exceptions occur; use clinical features, serology, and biopsy.

ANCA Clinical Correlation

C-ANCA with sinusitis + lung nodules + active urine sediment = 98% PPV for GPA. Always correlate ANCA results with clinical presentation.

Nephrotic Syndrome Complications

Watch for thromboembolism (hypercoagulable state), infections (immunoglobulin loss), and protein malnutrition. Consider prophylactic anticoagulation.

Anti-PLA2R Testing

Positive anti-PLA2R with nephrotic syndrome can diagnose membranous nephropathy without biopsy (78% sensitivity, 99% specificity).

Serial Complement Testing

Follow C3/C4 trends when relevant to the suspected disease, alongside creatinine, quantified proteinuria, urine sediment, and clinical findings. Complement trends alone cannot establish activity or treatment response.

Fresh Urine is Critical

RBC casts may dissolve in older urine specimens. Examine fresh urine (<2 hours) when possible for accurate diagnosis.

Anticoagulation Decision

Assess thrombosis risk against bleeding risk individually, including the underlying disease, severity of hypoalbuminemia, prior thrombosis, and contraindications. A low albumin value alone is not an automatic anticoagulation order.

Treatment Response Monitoring

In PLA2R-positive membranous nephropathy, the goal should be complete disappearance of anti-PLA2R antibodies.

Secondary Cause Screening

Always screen adults with new nephrotic syndrome for secondary causes, especially malignancy and systemic disease.

Pulmonary-Renal Syndrome

Hemoptysis plus rapidly declining kidney function = medical emergency. Consider anti-GBM disease, ANCA vasculitis, or SLE.

🔄 Diagnostic Algorithm for Glomerular Disease

1 Suspect and Evaluate Glomerular Disease: Hematuria + proteinuria ± hypertension ± reduced GFR; quantify protein and assess the clinical trajectory
2 Urine Microscopy: Look for RBC casts and acanthocytes as clues to glomerular bleeding, plus oval fat bodies and fatty casts for lipiduria; sediment alone does not identify the immune mechanism
3 Classify Syndrome: Nephritic (inflammatory) vs Nephrotic (proteinuric) vs Mixed
4 Complement Testing: Measure C3 and C4 simultaneously to determine pathway activation
5 Targeted Serological Testing: Based on complement pattern and clinical presentation (ANCA, anti-GBM, ANA, anti-PLA2R)
6 Assess Urgency: Rapid kidney-function decline with suspected GN or pulmonary–renal features requires immediate nephrology assessment; do not wait for 50% GFR loss
7 Arrange Renal Biopsy: Promptly when suspected RPGN or when histology will change management; review activity and chronicity, and investigate infection before immunosuppression

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Evidence-based immunosuppressive regimens for glomerulonephritis - induction, maintenance, and monitoring strategies.

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🔬 Additional Glomerular Disease Topics

  • IgA Nephropathy - Most common primary GN worldwide
  • Anti-GBM Disease - Goodpasture syndrome
  • Membranous Nephropathy - Anti-PLA2R testing
  • FSGS and Minimal Change - Nephrotic syndrome causes

Additional modules coming soon...

📖 Evidence-Based Resources

🏆 Priority Resources

  • KDIGO GN Guidelines 2024 - Latest evidence-based recommendations for glomerulonephritis management
  • NKF Clinical Guidelines - National Kidney Foundation practice guidelines
  • RPGN Emergency Protocol - Rapid reference for nephrology emergencies

📚 Additional Reading

  • American Journal of Kidney Diseases - Latest research updates
  • Kidney International - Peer-reviewed nephrology research
  • Clinical Journal of the American Society of Nephrology
  • UpToDate - Current clinical recommendations

📚 Sources

  1. Rovin BH, Adler SG, Barratt J, et al; KDIGO Glomerular Diseases Work Group. KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int. 2021;100(4S):S1-S276. PMID: 34556256. — Foundational KDIGO 2021 GD guideline covering IgAN, lupus nephritis, MCD, FSGS, MN, ANCA vasculitis, anti-GBM disease.
  2. Barratt J, Lafayette R, Kristensen J, et al; NefIgArd Trial Investigators. Results from part A of the multi-center, double-blind, randomized, placebo-controlled NefIgArd trial (TARPEYO). Kidney Int. 2023;103(2):391-402. PMID: 36270561. — Targeted-release budesonide (Tarpeyo) in IgAN.
  3. Heerspink HJL, Radhakrishnan J, Alpers CE, et al; PROTECT Investigators. Sparsentan in patients with IgA nephropathy: a prespecified interim analysis from a randomised, double-blind, active-controlled clinical trial. Lancet. 2023;401(10388):1584-1594. PMID: 37015244. — PROTECT trial; sparsentan dual ET-A/AT1 antagonist in IgAN.
  4. Trimarchi H, Barratt J, Cattran DC, et al. Oxford Classification of IgA nephropathy 2016: an update from the IgA Nephropathy Classification Working Group. Kidney Int. 2017;91(5):1014-1021. PMID: 28341274. — Oxford 2016 update — MEST-C scoring including C lesions.
  5. Furie RA, Aroca G, Cascino MD, et al. B-cell depletion with obinutuzumab for the treatment of proliferative lupus nephritis: a randomised, double-blind, placebo-controlled trial. Ann Rheum Dis. 2022;81(1):100-107. DOI | PubMed . — Phase 2 obinutuzumab + standard-of-care vs SOC in proliferative lupus nephritis. CRR at week 76 approximately 35-38%.
  6. Rovin BH, Teng YKO, Ginzler EM, et al; AURORA 1 Investigators. Efficacy and safety of voclosporin versus placebo for lupus nephritis (AURORA 1): a double-blind, randomised, multicentre, placebo-controlled, phase 3 trial. Lancet. 2021;397(10289):2070-2080. PMID: 33971155. — AURORA 1 voclosporin in active lupus nephritis.
  7. Houssiau FA, Vasconcelos C, D'Cruz D, et al. Immunosuppressive therapy in lupus nephritis: the Euro-Lupus Nephritis Trial. Arthritis Rheum. 2002;46(8):2121-2131. PMID: 12209517. — Euro-Lupus low-dose IV cyclophosphamide regimen.
  8. Stone JH, Merkel PA, Spiera R, et al; RAVE-ITN Research Group. Rituximab versus cyclophosphamide for ANCA-associated vasculitis (RAVE). N Engl J Med. 2010;363(3):221-232. PMID: 20647199. — Rituximab non-inferior to cyclophosphamide in ANCA-associated vasculitis induction.
  9. Glomerular Hematuria for the Diagnosis of Glomerulonephritis. Biopsy-correlated diagnostic study. PMID: 40406196. Urine sediment supports diagnosis; its sensitivity and specificity are not absolute.
  10. KDIGO 2024 ANCA-Associated Vasculitis Guideline. Official guideline. Practice Point 9.1.1: in a compatible rapidly deteriorating presentation with MPO/PR3-ANCA, awaiting biopsy must not delay specialist-directed treatment.
  11. KDIGO 2025 IgAN/IgAV Guideline. Official guideline. Crescents without functional deterioration do not alone establish rapidly progressive IgAN.
  12. KDIGO infection-related GN guidance. Official clinical takeaways. Treat infection and provide kidney supportive care; immunosuppression is generally inadvisable.
Andrew Bland MD - Clinical Nephrology Education
For Educational Use Only
Glomerulonephritis - Comprehensive Review 2025