Glomerulonephritis (GN) Nursing Guide

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What is Glomerulonephritis?

Glomerulonephritis (GN) is a group of conditions characterised by inflammation of the glomeruli — the filtering units of the kidney. The resulting damage impairs filtration, allowing blood and protein to leak into the urine while reducing waste clearance.

Key Features of GN

Haematuria — dysmorphic RBCs (acanthocytes) and RBC casts on urine microscopy (pathognomonic)
Proteinuria — from disrupted glomerular basement membrane
Hypertension — from fluid retention and renin-angiotensin activation
Oedema — from sodium/water retention and/or hypoalbuminaemia
Reduced GFR (glomerular filtration rate) — rising creatinine

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Nephritic vs Nephrotic Syndrome — Key Comparison

NEPHRITIC SYNDROME

NEPHROTIC SYNDROME

Haematuria — dysmorphic RBCs, RBC casts

Heavy proteinuria — >3.5g/24h (frothy urine)

Oliguria — reduced urine output

Hypoalbuminaemia — <30 g/L

Hypertension — significant

Generalised oedema — periorbital, pitting

Mild-moderate proteinuria

Hyperlipidaemia + lipiduria (oval fat bodies)

Examples: PSGN, IgA, anti-GBM, ANCA vasculitis

Examples: minimal change, membranous nephropathy, FSGS, diabetic nephropathy

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Exam Tip: "Nephritic = Haematuria + Hypertension + Oliguria"; Nephrotic = "Heavy Protein + Oedema + Low Albumin"

Some conditions can present with features of both (e.g. MPGN). Renal biopsy is required for definitive diagnosis.

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Common Causes of GN

Most Common Worldwide

IgA Nephropathy (Berger's Disease)

Haematuria concurrent with or immediately after URTI ("synpharyngitic haematuria" — within 24–72 hours)

Normal complement levels (C3/C4 normal); IgA deposits in mesangium on biopsy

Treatment: ACEi/ARB first-line; fish oil for persistent proteinuria; immunosuppression in progressive disease

Post-Infectious

Post-Streptococcal GN (PSGN)

Occurs 2–3 weeks after Group A Strep throat (1–3 weeks after skin infection)

Low C3 (complement consumption); ASOT/anti-DNase B elevated

Usually self-limiting in children; supportive management

Anti-GBM Disease

Goodpasture's Syndrome

Anti-GBM antibodies attack glomerular AND alveolar basement membrane

Lung haemorrhage + renal failure (pulmonary-renal syndrome)

Immunofluorescence: linear IgG deposits on GBM

Emergency: plasmapheresis + cyclophosphamide + high-dose steroids

ANCA Vasculitis

GPA (Wegener's) & MPA

c-ANCA / PR3 = Granulomatosis with Polyangiitis (GPA / Wegener's)

p-ANCA / MPO = Microscopic Polyangiitis (MPA)

Induction: rituximab OR cyclophosphamide + steroids; maintenance: azathioprine/rituximab

Membranoproliferative

MPGN

Both nephritic and nephrotic features; low complement

Associated with hepatitis C, cryoglobulinaemia, complement pathway disorders

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Clinical Assessment

History

Recent URTI or skin infection (PSGN, IgA)
Haematuria: macroscopic vs microscopic; timing relative to infection
Frothy urine (heavy proteinuria = nephrotic)
Joint pains, rash, sinusitis (vasculitis/lupus)
Haemoptysis (anti-GBM / ANCA vasculitis)
Family history of renal disease
Drug history (NSAIDs, contrast agents, aminoglycosides)

Physical Examination

Blood pressure: hypertension common in GN
Oedema: periorbital (worse in morning), pitting ankle oedema, ascites
Skin: purpura (Henoch-Schönlein / IgA vasculitis), butterfly rash (lupus)
Respiratory: crackles / haemoptysis (anti-GBM, ANCA)
Urine output: oliguria indicates significant GFR impairment

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Investigations

Urine

Urine dipstick: blood (+++) and protein (++) or more
Urine microscopy: dysmorphic RBCs and RBC casts = glomerular haematuria (pathognomonic)
24-hour urine protein (or spot protein:creatinine ratio) — >3.5g/24h = nephrotic range
Urine MC&S to exclude infection

Blood

Test	Significance
U&E, Creatinine, eGFR	Degree of renal impairment
Albumin	Low in nephrotic syndrome (<30 g/L)
C3 / C4 complement	Low C3 = PSGN, MPGN; Low C3+C4 = lupus nephritis
ASOT / anti-DNase B	Elevated = recent streptococcal infection (PSGN)
ANCA (c-ANCA / p-ANCA)	Vasculitis screening; PR3 / MPO specificity
Anti-GBM antibodies	Elevated = Goodpasture's syndrome
ANA / anti-dsDNA	Lupus nephritis
HBsAg / HCV antibodies	Hepatitis-associated GN / MPGN

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Definitive Diagnosis = Renal Biopsy

Renal biopsy with light microscopy, immunofluorescence (IF), and electron microscopy (EM) is the gold standard for GN diagnosis and guides treatment decisions.

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General Management Principles

Blood pressure control: Target <130/80 mmHg; ACEi or ARB first-line (also reduce proteinuria)
Oedema management: Fluid restriction + loop diuretics (furosemide)
Dietitian review: Low sodium, adequate protein; low potassium if hyperkalaemic
Renal function monitoring: U&E, eGFR, urine PCR at regular intervals
VTE prophylaxis: High risk in nephrotic syndrome (low ATIII, loss of protein C/S) — anticoagulate if albumin <20 g/L with risk factors
Infection risk: Immunosuppressed patients — vaccinations (avoid live vaccines), vigilance for opportunistic infections
Bone protection: Long-term steroids → bisphosphonates + calcium/vitamin D

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Disease-Specific Management

IgA Nephropathy

ACEi/ARB: first-line for proteinuria >0.5g/24h
Fish oil (omega-3): for persistent proteinuria
Targeted-release budesonide (Nefecon): new; reduces proteinuria
Systemic immunosuppression if progressive decline in eGFR
Oxford MEST-C score guides prognosis on biopsy

Post-Streptococcal GN

Usually self-limiting; supportive care
Eradicate streptococcal infection: penicillin/amoxicillin
Manage hypertension and fluid overload
Monitor renal function; most children recover fully

Anti-GBM (Goodpasture's)

Plasmapheresis — removes circulating anti-GBM antibodies
High-dose cyclophosphamide — suppress antibody production
High-dose corticosteroids
Lung-protective ventilation if pulmonary haemorrhage
Monitoring: serial anti-GBM titres

ANCA Vasculitis (GPA / MPA)

Induction: Rituximab OR cyclophosphamide + high-dose steroids
Maintenance: Rituximab every 6 months OR azathioprine
Plasma exchange if severe renal involvement or pulmonary haemorrhage
PCP prophylaxis: co-trimoxazole while on immunosuppression
Monitor: ANCA titres, renal function, BP

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Complications of Glomerulonephritis

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RPGN (Rapidly Progressive GN) — Medical Emergency

Crescent formation on biopsy → loss of >50% renal function within weeks. Requires urgent renal biopsy and immediate immunosuppression. If untreated → ESRD within weeks.

Renal Complications

Acute Kidney Injury (AKI)
Rapidly Progressive GN (RPGN) — crescentic GN
End-Stage Renal Disease (ESRD) → dialysis/transplant
Chronic Kidney Disease (CKD)

Systemic Complications

Hypertension → cardiovascular disease, stroke
Pulmonary oedema (fluid overload)
Hyperkalaemia → cardiac arrhythmias
VTE risk (nephrotic syndrome) — DVT/PE
Infection risk (nephrotic syndrome / immunosuppression)
Pulmonary haemorrhage (anti-GBM, ANCA)

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GCC-Specific Context

Post-Streptococcal GN — GCC Relevance ▼

PSGN following untreated pharyngitis remains common in GCC paediatric populations, particularly among lower-income expatriate communities with limited access to primary healthcare. Nurses should maintain high suspicion in children presenting with haematuria and oedema 2–3 weeks after throat or skin infection.

High density expatriate accommodation = streptococcal transmission risk
Late presentation = increased AKI risk
Nursing role: health education on completing antibiotic courses for throat infections

High ESRD Rate in GCC — Diabetes + GN ▼

The GCC has one of the highest rates of ESRD globally, driven by the high prevalence of type 2 diabetes (25–35% in some GCC populations) and uncontrolled hypertension. GN contributes significantly alongside diabetic nephropathy.

Saudi Arabia, UAE, Kuwait: dialysis prevalence among highest globally
IgA nephropathy may be underdiagnosed due to limited biopsy access in some areas
Nurses in dialysis units require strong understanding of GN progression
Renal transplant programs: King Fahad Medical City (Riyadh), Hamad Medical Corporation (Qatar), Cleveland Clinic Abu Dhabi

IgA Nephropathy in GCC ▼

IgA nephropathy is the most common GN worldwide and is increasingly recognised in GCC countries. However, underdiagnosis remains a concern due to low rates of renal biopsy in some centres and asymptomatic microscopic haematuria being missed on routine checks.

Nurses should ensure follow-up of patients with persistent microscopic haematuria + proteinuria
Work visa medical screening in GCC may detect haematuria — nurses should know referral pathway

GCC Exam Relevance ▼

DHA: Nephritic vs nephrotic differentiation frequently tested
HAAD/DOH: Anti-GBM (Goodpasture's) — pulmonary-renal syndrome recognition
SCFHS: ANCA types and treatment principles
QCHP: Renal biopsy indications and post-procedure nursing care

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High-Yield Exam Facts

RBC casts in urine = glomerulonephritis (pathognomonic)
Most common GN worldwide = IgA nephropathy
IgA: haematuria with URTI, normal complement
PSGN: 2–3 weeks post-throat infection, low C3
Goodpasture's: lung haemorrhage + GN, linear IgG on IF, anti-GBM antibodies
c-ANCA / PR3 = GPA (Wegener's); p-ANCA / MPO = MPA
Nephrotic: proteinuria >3.5g/24h + hypoalbuminaemia + oedema + hyperlipidaemia
Definitive GN diagnosis = renal biopsy
RPGN = crescentic GN = renal emergency → urgent biopsy + immunosuppression
First-line treatment for proteinuric GN = ACEi or ARB
Goodpasture's treatment = plasmapheresis + cyclophosphamide + steroids
Complement normal = IgA nephropathy; Low C3 only = PSGN/MPGN; Low C3+C4 = lupus

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Practice MCQs

Question 1 of 4

A 10-year-old child develops periorbital oedema, haematuria, and hypertension 2 weeks after a sore throat. Urine microscopy shows RBC casts. C3 is low. What is the most likely diagnosis?

A. IgA nephropathy

B. Nephrotic syndrome

C. Post-streptococcal glomerulonephritis

D. Anti-GBM disease

Correct answer: C — Post-streptococcal GN (PSGN) presents 2–3 weeks after streptococcal throat infection with haematuria, oliguria, hypertension, and oedema. Low C3 with normal C4 is characteristic. RBC casts confirm glomerular involvement. IgA nephropathy would show haematuria during (not after) the infection.

Question 2 of 4

A 28-year-old male presents with haemoptysis and haematuria. Anti-GBM antibody titre is markedly elevated. Renal biopsy shows linear IgG deposits on immunofluorescence. What is the first-line treatment?

A. ACE inhibitor + dietary protein restriction

B. Plasmapheresis + cyclophosphamide + high-dose steroids

C. Rituximab monotherapy

D. Supportive care and watchful waiting

Correct answer: B — Anti-GBM disease (Goodpasture's syndrome) requires emergency plasmapheresis to remove circulating anti-GBM antibodies, plus cyclophosphamide to suppress antibody production, and high-dose corticosteroids. This is a medical emergency with risk of rapid ESRD and fatal pulmonary haemorrhage if untreated.

Question 3 of 4

A patient has heavy proteinuria (>4g/24h), serum albumin of 22 g/L, pitting oedema, and hyperlipidaemia. Urine microscopy shows oval fat bodies but no RBC casts. Which syndrome does this describe?

A. Nephritic syndrome

B. Rapidly progressive GN

C. Nephrotic syndrome

D. Urinary tract infection

Correct answer: C — This is nephrotic syndrome: heavy proteinuria (>3.5g/24h), hypoalbuminaemia (<30g/L), oedema, and hyperlipidaemia. Oval fat bodies (lipid-laden tubular cells) are characteristic. Nephritic syndrome features haematuria, RBC casts, oliguria, and hypertension.

Question 4 of 4

A nurse reviews results for a patient with suspected GN. Which finding on urine microscopy is most specific for glomerulonephritis?

A. White cell casts

B. Granular casts

C. Waxy casts

C. Dysmorphic RBCs and RBC casts

Correct answer: C (last option) — Dysmorphic red blood cells (acanthocytes) and RBC casts are pathognomonic of glomerular haematuria and strongly indicate GN. White cell casts = pyelonephritis; granular casts = non-specific tubular injury; waxy casts = advanced CKD.