Glomerulonephritis: AU general practice recognition and referral

Glomerulonephritis (GN) is immune-mediated injury to the glomeruli — the kidney’s filtering units — producing haematuria, proteinuria, hypertension, oedema, and reduced kidney function in varying combinations. It encompasses a heterogeneous group of diseases ranging from a benign incidental finding of microscopic haematuria to a renal emergency requiring same-day specialist intervention to prevent permanent kidney failure.

In Australian general practice, the most common form is IgA nephropathy, which accounts for roughly a quarter of all renal biopsies in the ANZDATA registry. The most urgent presentations — grouped as rapidly progressive GN (RPGN) — may destroy kidney function within weeks and require same-day nephrology referral.

The GP’s role is prompt recognition, structured initial investigation, and timely referral. Biopsy — the diagnostic gold standard — is organised by nephrology. Immunosuppressive treatment decisions are specialist-led. The GP coordinates long-term shared care: monitoring kidney function, managing blood pressure and cardiovascular risk, applying sick-day rules, and supporting advance care planning as kidney disease progresses.

A. Core clinical — the AU general-practice framework

The three syndromes to recognise

Nephritic syndrome presents with haematuria (often visible and coloured like cola or tea), dysmorphic red blood cells and red cell casts on urine microscopy, subnephrotic proteinuria (PCR <350 mg/mmol), hypertension, and acute kidney injury. Oedema is variable. Major causes include IgA nephropathy, post-streptococcal GN, ANCA-associated vasculitis, and lupus nephritis.

Nephrotic syndrome is defined by proteinuria ≥3.5 g/day (urine PCR ≥350 mg/mmol), hypoalbuminaemia, oedema, and hyperlipidaemia. Causes include minimal change disease (commonest in children), focal segmental glomerulosclerosis, membranous nephropathy, and secondary causes including diabetes and amyloidosis.

Rapidly progressive GN (RPGN) — creatinine doubling over days to weeks with active urine sediment (dysmorphic red cells, red cell casts, ≥2+ blood and protein on dipstick) — is a renal emergency. Per KHA-CARI and Therapeutic Guidelines (eTG), same-day nephrology referral is mandatory. Causes include ANCA-associated vasculitis, anti-GBM disease, and crescentic lupus nephritis.

History

• Onset and timing — haematuria appearing 24–48 hours after a sore throat or upper respiratory infection suggests IgA nephropathy; haematuria 1–3 weeks after strep throat or a skin infection suggests post-streptococcal GN (complement C3 low)
• Systemic features — haemoptysis (pulmonary–renal syndrome), sinusitis or nasal crusting (granulomatosis with polyangiitis), skin rash, mouth ulcers, joint pain, photosensitivity (lupus nephritis)
• Medication history — NSAIDs, hydralazine, propylthiouracil, levamisole-adulterated cocaine (drug-induced ANCA vasculitis)
• Risk factors — hepatitis B and C exposure, HIV, intravenous drug use (endocarditis), recent streptococcal infection, dental procedures with prosthetic valves
• Family history — Alport syndrome (haematuria from childhood, sensorineural deafness, lenticonus), thin basement membrane disease, polycystic kidney disease

Examination

• Blood pressure — hypertension is almost universal in significant GN; bilateral measurement
• Volume status — pitting oedema of ankles and shins, sacral oedema, raised jugular venous pressure, basal lung crackles
• Skin — malar rash (lupus), palpable purpura on the lower limbs (ANCA vasculitis, IgA vasculitis), livedo reticularis, digital infarcts
• ENT — sinusitis, nasal crusting, saddle nose deformity from nasal septum destruction (granulomatosis with polyangiitis)
• Respiratory — crackles or signs of alveolar haemorrhage (anti-GBM or ANCA vasculitis)
• Neurological — mononeuritis multiplex (wrist drop, foot drop) in ANCA vasculitis; sensorineural hearing loss in Alport syndrome

GP-led initial investigations

Per KHA-CARI and eTG Nephrology:

Urine:

• Dipstick — blood and protein (minimum screen)
• Microscopy — explicitly request dysmorphic red blood cells and casts — this single test distinguishes glomerular from non-glomerular haematuria; must be sent fresh to the laboratory
• Urine ACR and PCR — quantify proteinuria; PCR ≥350 mg/mmol indicates nephrotic-range
• MSU MC&S — exclude UTI as a confounder

Blood:

• UEC and eGFR — serial measurements over days detect RPGN (creatinine doubling)
• FBC, CRP, ESR — inflammatory activity
• LFTs and albumin — hypoalbuminaemia in nephrotic syndrome; hepatitis hint
• Fasting lipids and HbA1c — exclude diabetic nephropathy mimic

Serology (initiate GP panel to accelerate specialist workup):

• Complement C3 and C4 — low in lupus nephritis, post-streptococcal GN, and membranoproliferative GN; normal in IgA nephropathy, ANCA vasculitis, and anti-GBM disease
• ANA and anti-dsDNA — lupus nephritis
• ANCA (PR3 and MPO by ELISA) — ANCA-associated vasculitis
• Anti-GBM antibody — high priority if any suggestion of pulmonary–renal syndrome or rapidly rising creatinine
• Hepatitis B, hepatitis C, and HIV serology — secondary GN screen and mandatory pre-immunosuppression test
• ASOT and anti-DNAse B — post-streptococcal GN

Imaging:

• Renal ultrasound — kidney size, echogenicity, symmetry, obstruction; biopsy planning

B. IgA nephropathy — the Australian general practice picture

IgA nephropathy is the commonest primary GN in Australia, accounting for 25–30% of native renal biopsies in ANZDATA registry data. Peak incidence is in adults aged 20–40, with a 2:1 male predominance. The characteristic presentation is visible haematuria within 24–48 hours of an upper respiratory infection — synpharyngitic haematuria — which is the key distinguishing feature from post-streptococcal GN, where haematuria lags the precipitating infection by 1–3 weeks and complement C3 is transiently low.

Most patients with IgA nephropathy have a benign course, but approximately one-third progress to end-stage kidney disease over 20 years. Predictors of progression include persistent proteinuria >1 g/day, hypertension, and declining eGFR.

Management is specialist-led and guided by the KDIGO 2024 Glomerular Diseases Guideline. The current standard is a 90-day optimisation phase with maximum-tolerated ACE inhibitor or ARB, plus SGLT2 inhibitor, plus dietary salt restriction, before any escalation. Both DAPA-CKD and EMPA-KIDNEY demonstrated renoprotective benefit of SGLT2 inhibitors across GN subtypes, including IgA nephropathy, supporting their place as a universal supportive therapy pillar.

If proteinuria remains ≥1 g/day on optimised supportive care, targeted-release budesonide (Nefecon) is now the PBS Authority-Required first escalation step for eligible adults with primary IgA nephropathy, following the NefIgArd trial, which showed sustained proteinuria reduction and slower eGFR decline over 2 years compared with placebo.

C. Investigation strategy and the pitfall to avoid

The most clinically important bedside distinction is dysmorphic red blood cells on urine microscopy. When red cells originate from glomerular bleeding, they are distorted as they traverse the damaged glomerular membrane — these dysmorphic cells are recognisable on phase-contrast microscopy. Uniform, round red cells suggest lower urinary tract bleeding (stone, malignancy, UTI). Red cell casts are pathognomonic for glomerular bleeding. Explicitly requesting microscopy for dysmorphic red cells is essential — a routine dipstick positive for blood does not make this distinction.

The pitfall to avoid: treating dipstick haematuria with proteinuria as a simple UTI without urine microscopy. This is the most common reason for delayed RPGN diagnosis — a delay that translates directly to lost kidney function.

Key diagnostic discriminators:

Presentation	Most likely cause	Priority next step
Haematuria 24–48 h after URTI	IgA nephropathy	C3/C4 (normal), urine microscopy
Haematuria 1–3 weeks after strep throat	Post-streptococcal GN	ASOT, C3 (low, transient)
Haemoptysis + AKI	Anti-GBM or ANCA vasculitis	Same-day: anti-GBM + ANCA, renal consult
Nephrotic proteinuria + oedema in adult	Membranous or FSGS	Anti-PLA2R, hepatitis B and C, ANA, ANCA
Sinusitis + neuropathy + haematuria	Granulomatosis with polyangiitis	ANCA PR3/MPO
Young woman + multisystem + low C3/C4	Lupus nephritis	ANA, anti-dsDNA, nephrology referral
Family history + deafness + haematuria from childhood	Alport syndrome	Genetics referral, audiology

All adults with confirmed dysmorphic haematuria plus proteinuria — or any nephrotic syndrome — warrant nephrology referral. The GP workup panel sent before the appointment accelerates the diagnostic pathway significantly.

D. Australian operations

MBS items: Standard GP consultations item 23, 36, 44 — use Level C or D for new GN workup with full systems review. GP Chronic Condition Management Plan (item 965 preparation, item 967 review) for chronic GN. Aboriginal and Torres Strait Islander Health Assessment item 715 — annual screening with urinalysis in high-risk communities. Pathology items: UEC/eGFR (item 66500); urine ACR/PCR (item 66536 range); urine MC&S (item 69300); FBC (item 65070); renal ultrasound (item 55036 range). Telehealth equivalents: video items 91890–91892; phone item 92029.

PBS: ACE inhibitors and ARBs — general schedule. Dapagliflozin 10 mg daily (eGFR ≥25) and empagliflozin 10 mg daily (eGFR ≥20) — PBS Authority Streamlined for proteinuric CKD with UACR >22.6 mg/mmol. Targeted-release budesonide (Nefecon) — PBS Authority Required for adults with primary IgA nephropathy and proteinuria ≥1 g/day on optimised RAS blockade (verify current PBS criteria and schedule listing). Specialist-initiated agents — rituximab, mycophenolate, cyclophosphamide, avacopan, voclosporin, belimumab — PBS Authority Required via nephrologist or rheumatologist.

Sick-day rules per NPS MedicineWise: temporarily withhold ACE inhibitor, ARB, SGLT2 inhibitor, and diuretics during vomiting, diarrhoea, fever, or significant dehydration; resume once eating and drinking normally. This prevents acute-on-chronic kidney injury during intercurrent illness.

What to send with the nephrology referral: trended eGFR and UACR/PCR (at least two timepoints), urine microscopy report, immunology panel results (complement, ANCA, ANA, anti-GBM), hepatitis B, C, and HIV serology, renal ultrasound, and complete medication list including NSAIDs and supplements.

ATSI considerations: Post-streptococcal GN remains a significant cause of acute GN in remote Aboriginal and Torres Strait Islander communities, driven by scabies and group A streptococcal skin infections. RHDAustralia and the APSGN surveillance programs (One Disease, CARPA) support recognition and management. Lupus nephritis has higher incidence and worse outcomes in Aboriginal and Torres Strait Islander women — early referral and cultural safety in specialist care are essential. The AIHW documents significantly elevated CKD and end-stage kidney disease rates in Aboriginal and Torres Strait Islander populations.

E. Special populations

Pregnancy: Lupus nephritis frequently flares during pregnancy and the postpartum period. Pre-eclampsia closely mimics GN — new hypertension plus proteinuria after 20 weeks — and distinguishing the two is clinically critical, as they have entirely different management pathways. ACE inhibitors, ARBs, mycophenolate, and cyclophosphamide are contraindicated in pregnancy. Specialist obstetric–nephrology co-management is mandatory for pregnant patients with known GN. Pre-conception counselling about medication safety should be part of ongoing GN care for women of reproductive age.

Children and adolescents: Minimal change disease is the commonest cause of nephrotic syndrome in children and typically responds well to corticosteroids. IgA vasculitis (Henoch–Schönlein purpura) presents with palpable purpura, arthralgia, abdominal pain, and GN — usually self-limiting but warrants urine monitoring for proteinuria over 6–12 months. Post-streptococcal GN is more common in children than adults. Paediatric nephrology input is recommended for all significant paediatric GN.

Older adults: Drug-induced GN — particularly NSAID-associated minimal change nephropathy or interstitial nephritis — is underrecognised in older patients taking regular over-the-counter ibuprofen or naproxen. ANCA-associated vasculitis is more prevalent with advancing age and may present atypically without the classical ENT or pulmonary features. Shared decision-making about the burden of immunosuppression relative to comorbidity, frailty, and life expectancy is particularly important in this group.

Migrants and refugee populations: HBV-associated membranous nephropathy remains prevalent in communities from HBV-endemic regions. HIV-associated nephropathy (collapsing FSGS) occurs with untreated or advanced HIV. Refugee Health Assessment item 707 supports targeted screening, including hepatitis B and C and HIV serology.

When to escalate

Same-day nephrology referral (call before sending to emergency department) when any of the following are present:

• Creatinine doubling over days to weeks with active urine sediment — suspected RPGN
• Haemoptysis with AKI — pulmonary–renal syndrome; anti-GBM or ANCA vasculitis is a simultaneous renal and respiratory emergency
• Oliguria or anuria
• Hyperkalaemia >6.5 mmol/L not correctable in the rooms
• Suspected anti-GBM disease — treatment window is measured in days; outcomes worsen directly with delay
• Uraemic features — confusion, pericardial rub, severe nausea

Within 1–2 weeks when:

• New nephrotic-range proteinuria (PCR ≥350 mg/mmol)
• Dysmorphic haematuria confirmed on microscopy with proteinuria, even if creatinine is currently normal
• Positive ANCA or anti-GBM antibody on GP-initiated serology
• Suspected lupus nephritis (multisystem features with active urine sediment)
• Stable IgA nephropathy with increasing proteinuria or declining eGFR over serial measurements

What this article is and is not

This is general health information for Australian patients drawn from current guidelines — KHA-CARI, Therapeutic Guidelines (eTG), KDIGO 2024 Glomerular Diseases Guideline, Kidney Health Australia, and NPS MedicineWise. It is not personal medical advice and does not create a doctor–patient relationship. Treatment decisions — including immunosuppression, biopsy, and PBS Authority medications — are made collaboratively with your nephrologist, rheumatologist, and GP.

If you notice blood in your urine, persistent frothy urine, or unexplained leg swelling, see your GP promptly. If you develop breathlessness, cough up blood, or notice a marked reduction in urine output, call 000 or go to the nearest emergency department immediately.

Australian patient resources: Kidney Health Australia; HealthDirect — Glomerulonephritis; Better Health Channel; Lupus Australia.

---

Sources cited

1. KHA-CARI Glomerulonephritis Guidelines
2. Therapeutic Guidelines (eTG) — Nephrology
3. KDIGO 2024 Glomerular Diseases Clinical Practice Guideline
4. Kidney Health Australia
5. RACGP
6. Australian Medicines Handbook
7. NPS MedicineWise
8. ANZDATA Registry
9. RHDAustralia
10. AIHW
11. Heerspink et al. — DAPA-CKD (NEJM 2020)
12. EMPA-KIDNEY Collaborative Group (NEJM 2023)
13. Lafayette et al. — NefIgArd (Lancet 2023)
14. HealthDirect — Glomerulonephritis
15. Better Health Channel