GLOMERULONEPHRITIS

✓ Medically ReviewedDISEASEID: MDBT0077🚨 TRIAGE: URGENTICD-10: N05.9

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Definition

CLINICAL DEFINITION

Glomerulonephritis is inflammation of glomeruli (tiny kidney filtering units). It impairs filtration (cleaning of blood by kidneys). It often causes haematuria (blood in urine) and proteinuria (excess protein in urine). It often causes hypertension (high blood pressure) and oedema (swelling from fluid retention). It can be acute (sudden onset) or chronic (long term) and may cause kidney failure (loss of kidney function).

IN PLAIN ENGLISH

Glomerulonephritis means kidney filters are inflamed and irritated. Urine may look bloody or brown or foamy from protein. Face and legs may swell with fluid. Blood pressure may rise. It can harm kidneys over time without care.

COMMON MISCONCEPTION / WHAT IT DOES NOT MEAN

Glomerulonephritis is not pyelonephritis (bacterial infection of kidney pelvis). It is not acute tubular necrosis (injury of tubules from low flow or toxins). It is not simple dehydration (fluid loss) or uncomplicated cystitis (bladder infection). Diagnosis needs urine and blood findings plus often biopsy (tiny kidney sample).

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Word Breakdown

glomerulo-

=glomerulus (ball of capillaries)

nephr-

=kidney

-itis

=inflammation

Literal Meaning: inflammation of kidney glomeruli (filtering units)

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Abbreviations

GN=Glomerulonephritis - inflammation of glomeruli (kidney filtering units)

RPGN=Rapidly progressive glomerulonephritis - rapid loss of kidney function over days to weeks

PIGN=Postinfectious glomerulonephritis - glomerulonephritis after infection (often streptococcal germ)

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Synonyms & Variants

Glomerular nephritis›Glomerulonephritic syndrome›

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Category-Specific Context

Glomerulonephritis is a Disease with distinct pathology (tissue injury), causes and course. It is not a single symptom (patient complaint) or sign (examination finding). It groups many glomerular disorders by immune injury (immune attack). It leads to syndromes such as nephritic (inflammatory urine) or nephrotic (heavy protein loss).

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Clinical Context & Usage

CLINICAL SETTINGS

Primary Care ClinicEmergency DepartmentNephrology ClinicInpatient Medical WardIntensive Care Unit

USAGE & DOCUMENTATION NOTES

Use glomerulonephritis when inflammation of glomeruli (filters) is suspected or proven by biopsy. Specify cause and acuity (speed of onset) when known. Avoid using it for all kidney failure or all proteinuria alone. Document haematuria (blood in urine), proteinuria (protein in urine), creatinine (kidney function marker) and blood pressure.

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Primary Causes & Pathophysiology

PATHOPHYSIOLOGY

Most forms involve immune injury to glomeruli (filters). Immune complexes (antibody clumps) deposit in glomeruli and activate complement (inflammation proteins). Autoantibodies (self-attacking antibodies) may target basement membrane (filter wall) or neutrophil enzymes (white cell proteins). This recruits leukocytes (white blood cells) and injures endothelium (vessel lining) and podocytes (filter cells). Injury causes haematuria (blood in urine), proteinuria (protein in urine) and reduced filtration. Severe crescentic disease (aggressive scarring) can destroy nephrons (kidney units) within weeks.

PRIMARY CAUSES

IgA nephropathy (Berger disease)

Galactose-deficient IgA1 forms immune complexes that lodge in mesangium (central filter stalk) and trigger inflammation

Poststreptococcal glomerulonephritis

Streptococcal antigens trigger antibodies that settle in glomeruli (filters) and activate complement, causing injury

Lupus nephritis

Autoantibodies and immune complexes settle in glomerular zones and drive inflammation in systemic lupus (body-wide autoimmune disease)

ANCA-associated vasculitis

ANCA autoantibodies activate neutrophils (white cells) that injure small vessels and glomeruli (filters) without immune deposits

Anti-glomerular basement membrane disease

Autoantibodies bind basement membrane (filter wall) collagen and cause linear injury with crescents (aggressive scars) and lung bleeding

Primary membranous nephropathy

Antibodies, often anti-PLA2R (filter cell protein antibodies), target podocyte antigens and form outer wall deposits that thicken wall and cause protein loss

C3 glomerulopathy including dense deposit disease

Dysregulated complement via alternative pathway (innate immune route) injures glomeruli (filters) with dominant C3 deposits

Membranoproliferative glomerulonephritis

Chronic immune complexes or complement dysregulation cause mesangial proliferation (cell growth) and wall duplication with filtration loss

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Drug-Induced Causes

💊 Hydralazine ↗

Mechanism: Induces ANCA and lupus-like autoimmunity with glomerular injury and necrotising inflammation

→ Stop hydralazine promptly and refer to nephrology and rheumatology for immunosuppression if severe

💊 Propylthiouracil ↗

Mechanism: Triggers ANCA vasculitis with necrotising glomerulonephritis via neutrophil activation

→ Stop propylthiouracil and switch thyroid therapy plus urgent nephrology review for immunosuppression

💊 Penicillamine and gold salts ↗

Mechanism: Induce membranous pattern with immune deposits and proteinuria from podocyte injury

→ Withdraw offending drug and monitor proteinuria and kidney function with nephrology follow-up

💊 Nonsteroidal anti-inflammatory drugs (NSAIDs) ↗

Mechanism: Rarely linked with minimal change or membranous injury plus interstitial nephritis (tube inflammation)

→ Stop NSAID and avoid rechallenge and treat proteinuria and kidney injury supportively

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Epidemiology

Prevalence:Glomerulonephritis is common worldwide as a cause of chronic kidney disease. IgA nephropathy is the most frequent primary form in many regions. Postinfectious disease remains important where streptococcal infection is widespread. Secondary forms follow lupus and vasculitis patterns.

Age Group:It affects all ages from children to older adults. Postinfectious glomerulonephritis is classic in children after streptococcal throat infection or impetigo (skin infection). IgA nephropathy often presents in teens and young adults. Membranous nephropathy and ANCA vasculitis are more common in middle-aged and older adults.

Geographic Distribution:Glomerulonephritis occurs worldwide with cause-specific patterns. IgA nephropathy is reported more in East Asia and Southern Europe. Poststreptococcal disease clusters where streptococcal throat or skin infection spreads easily. Lupus nephritis follows lupus prevalence and is important worldwide.

Red Flags & Triage ★

TRIAGE LEVEL

🚨 URGENT

DO NOT MISS — LIFE-THREATENING PRESENTATIONS

Rapidly progressive glomerulonephritis with crescents
Anti-glomerular basement membrane disease with lung haemorrhage
ANCA vasculitis with active urinary sediment
Lupus nephritis with active serology
Poststreptococcal disease with hypertension and oedema in children

URGENT EVALUATION TRIGGERS

Rising creatinine over days
Oliguria or anuria with oedema
Haemoptysis with haematuria
Severe hypertension with headache or visual change
Hyperkalaemia or acidosis with ECG change

Contraindications & Precautions

CONTRAINDICATIONS

Avoid nephrotoxins such as NSAIDs without supervision
Avoid iodinated contrast without kidney protection when active inflammation is present
Do not delay biopsy when rapidly progressive disease is suspected
Avoid live vaccines during intense immunosuppression

SPECIAL PRECAUTIONS

Monitor blood pressure and fluid balance closely
Monitor creatinine, potassium and urine protein serially
Screen for infection before and during immunosuppression
Adjust drug doses for kidney function
Counsel on pregnancy risks with certain immunosuppressants and ACE inhibitors

Complications

DOWNSTREAM CLINICAL COMPLICATIONS

Acute kidney injury with sudden loss of filtering
Chronic kidney disease with long term loss
End-stage kidney failure needing dialysis
Hypertensive emergency with severe pressure crisis
Nephrotic-range proteinuria with oedema
Pulmonary haemorrhage in anti-GBM disease
Hyperkalaemia and metabolic acidosis

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Confused With (LASA & DDx) ★

LEXICAL (LASA) — SIMILAR NAMES

Glomerulosclerosis

Shares glomerulo prefix and causes proteinuria but is scarring of glomeruli (filters) without active inflammation, often from diabetes

Pyelonephritis

Shares nephritis suffix and causes flank pain and fever but is bacterial infection of pelvis and tubules, not filter inflammation

Tubulointerstitial nephritis

Confused because both cause kidney injury and carry nephritis label but it affects tubules and interstitium (support tissue), often drug-related

CLINICAL DIFFERENTIAL DIAGNOSES (DDx)

Acute tubular necrosis

Key Distinguishing Feature: Muddy brown casts after low flow or toxins with bland urine rather than red cell casts

Pyelonephritis

Key Distinguishing Feature: High fever with flank tenderness and bacteriuria without glomerular haematuria

Diabetic kidney disease

Key Distinguishing Feature: Gradual proteinuria with retinopathy (eye disease) and bland sediment without active haematuria or red cell casts

Minimal change disease

Key Distinguishing Feature: Heavy selective proteinuria with oedema but without active sediment or hypertension

Obstructive uropathy

Key Distinguishing Feature: Hydronephrosis (swollen kidney) on imaging with no urine or colic rather than red cell casts and proteinuria

Hypertensive nephrosclerosis

Key Distinguishing Feature: Long hypertension with mild proteinuria and bland urine without nephritic sediment

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Clinical Pearls

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Use red cell casts to point to glomerular bleeding. Misshapen red cells favour kidney origin over bladder source and change workup.

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Pair lung bleeding with glomerulonephritis as pulmonary-renal emergency. Check anti-GBM and ANCA at once and involve nephrology same day.

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Use complement to split causes. Low complement suggests lupus or postinfectious disease, while normal complement favours IgA or ANCA disease.

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Biopsy early when cause is unclear or disease is severe. Do not wait for full serology when rapidly progressive disease is suspected because crescents destroy nephrons within weeks.

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Track proteinuria and pressure to predict course. Persistent protein and high pressure need ACE inhibitor or ARB (pressure drugs) plus cause therapy with long follow-up.

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Example Usage & SOAP

CLINICAL SENTENCE

""19-year-old with dark urine, swelling and high pressure has suspected acute glomerulonephritis.""

IN A SOAP NOTE

S: 28-year-old man with dark urine and eye swelling for 5 days, reduced urine and headache. O: BP 168/102, HR 94, RR 18, Temp 37.1C, SpO2 97 percent on air, facial and leg oedema, urine shows blood and protein. A: Acute glomerulonephritis with nephritic features. P: Check creatinine and salts and urine protein, control pressure and restrict salt, refer nephrology urgently for biopsy workup.

DIFFERENTIAL DIAGNOSIS CONTEXT

Haematuria with proteinuria plus oedema suggests nephritic syndrome from glomerulonephritis. Recent throat infection with low complement favours postinfectious disease. Blood with throat infection and normal complement favours IgA nephropathy. Systemic features need ANCA testing plus biopsy.

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Classifications & Scoring

GRADING SYSTEM

ISN/RPS Lupus Nephritis Classification

Defines classes I to VI from mesangial to diffuse proliferative to sclerosing injury to guide therapy

GRADING SYSTEM

Oxford MEST-C Classification for IgA Nephropathy

Scores mesangial and endocapillary cells plus sclerosis, tubular atrophy and crescents to predict outcome

STAGING SCALE

KDIGO Chronic Kidney Disease G and A Stages

Stages filtration from G1 normal to G5 failure and albuminuria from A1 normal to A3 severe to stratify risk and follow-up

SCORING TOOL

Birmingham Vasculitis Activity Score

Measures vasculitis activity across organ systems including renal items to track response

SCORING TOOL

ANCA Renal Risk Score

Combines filtration, tubular atrophy and glomerular loss to predict end-stage disease in ANCA glomerulonephritis

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Prognosis

SHORT-TERM OUTCOME

Short term course depends on acuity (speed) and cause. Postinfectious disease often improves with supportive care. Rapidly progressive disease can cause kidney failure within days without treatment. Early immunosuppression and plasma exchange (blood filtering) can rescue kidney function in selected types.

LONG-TERM PROGNOSIS

Long term risk is chronic kidney disease and end-stage failure. Persistent proteinuria (ongoing protein loss) and hypertension (high pressure) predict worse outcomes. Relapsing diseases like IgA nephropathy and ANCA vasculitis need long surveillance. Timely biopsy and cause-directed therapy improve kidney and patient survival.

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References & Coding

ICD-10 DIAGNOSTIC CODE

N05.9

LITERATURE CITATIONS & GUIDELINES

[1]KDIGO Glomerular Diseases Guideline

[2]Harrisons Principles of Internal Medicine

[3]Davidsons Principles and Practice of Medicine

MEDICAL DISCLAIMER — This content is intended for educational purposes and qualified healthcare professionals only. Always refer to current clinical diagnostic criteria, institutional protocols, and official guidelines. Medobo is not responsible for clinical decisions made based on this content.