Why this topic matters: Glomerulonephritis (GN) is inflammation or immune injury of the kidney’s glomeruli. It can present with haematuria, proteinuria, oedema, hypertension and acute kidney injury, and may be part of a life-threatening systemic disease such as vasculitis, lupus, anti-GBM disease or infection. Emergency providers must recognise nephritic features, identify pulmonary–renal and hypertensive emergencies, avoid nephrotoxins and arrange urgent nephrology referral.
Learning objectives
- Explain the nephritic syndrome and common causes of glomerular inflammation.
- Recognise haematuria, proteinuria, oedema, hypertension, AKI and systemic red flags.
- Perform focused history, examination, urine assessment and emergency investigations.
- Outline acute care for fluid overload, hyperkalaemia, severe hypertension, pulmonary haemorrhage and infection.
- Plan nursing care, referral, patient education and follow-up.
Definition and clinical patterns
Glomerulonephritis is a group of disorders that damage the glomerular filtration barrier. Inflammation allows blood and protein to enter urine and reduces filtration. The term may describe a primary kidney disease or renal involvement in systemic illness.
- Nephritic syndrome: haematuria, dysmorphic red cells or casts, variable proteinuria, reduced GFR, oliguria and hypertension.
- Nephrotic features: heavy protein loss, low albumin, generalised oedema and hyperlipidaemia; some diseases have mixed nephritic-nephrotic features.
- Rapidly progressive GN: rapidly declining kidney function over days to weeks, often with crescentic injury and urgent need for immunosuppressive specialist care.
- Pulmonary–renal syndrome: GN with haemoptysis, pulmonary haemorrhage or hypoxaemia, commonly from ANCA vasculitis or anti-GBM disease.
Causes and triggers
| Cause | Examples | Clues |
|---|---|---|
| Post-infectious | After streptococcal throat/skin infection or other bacterial infection. | Dark urine, oedema and hypertension after a latent period; low complement may occur. |
| IgA nephropathy | Immune deposits in glomeruli. | Haematuria during or soon after respiratory infection. |
| Autoimmune/immune-complex | Lupus nephritis, vasculitis, cryoglobulinaemia. | Rash, arthralgia, ulcers, fever, neuropathy or low complement. |
| Anti-GBM disease | Antibodies attack glomerular and alveolar basement membranes. | Haematuria plus haemoptysis, anaemia or rapidly progressive AKI. |
| Infection-associated | HIV, hepatitis, endocarditis, malaria and chronic infections. | Fever, weight loss, murmurs, rash or relevant exposure. |
| Drugs/malignancy | Selected medicines, cancer-associated immune disease. | New exposure, systemic symptoms or unexplained renal decline. |
Emergency red flags
- Breathlessness, crackles, hypoxia or frothy sputum suggesting pulmonary oedema or pulmonary haemorrhage.
- Severe headache, visual changes, seizures, confusion or very high BP suggesting hypertensive encephalopathy.
- Rapidly falling urine output, anuria, rising creatinine, hyperkalaemia or severe metabolic acidosis.
- Haemoptysis, falling haemoglobin and hypoxia suggesting pulmonary–renal syndrome.
- Fever, rigors, purpura, murmur or sepsis in an immunosuppressed patient.
- Generalised oedema, painful skin, abdominal distension or sudden weight gain.
Triage and first contact
- Move unstable patients to resuscitation, apply ECG/SpO₂/BP monitoring and call senior medical, renal and critical-care support.
- Ask about urine colour/output, recent sore throat or skin infection, systemic symptoms, medicines, pregnancy, autoimmune disease and baseline kidney function.
- Check ABCDE, glucose, fluid status, BP in both arms when appropriate, lungs, oedema, rash and neurological status.
- Keep a strict fluid-balance record and avoid NSAIDs, contrast and other nephrotoxins unless specifically justified.
- Arrange urgent referral for suspected rapidly progressive GN, pulmonary–renal syndrome, severe AKI or resistant hypertension.
Focused history and examination
- Haematuria: visible or microscopic, cola/tea colour, clots, timing and recurrence.
- Protein loss: frothy urine, oedema, weight gain, reduced urine and fatigue.
- Systemic clues: rash, photosensitivity, joint pain, nasal ulcers, sinus disease, neuropathy, fever and weight loss.
- Infection: recent sore throat/skin infection, HIV/hepatitis risk, endocarditis symptoms, malaria or TB exposure.
- Pulmonary–renal symptoms: cough, haemoptysis, pleuritic pain, breathlessness and reduced exercise tolerance.
- Examine BP, lungs, JVP, heart murmur, oedema, skin, joints, abdomen, urine, neurological status and fundi if trained.
Investigations
| Investigation | Purpose | Key interpretation |
|---|---|---|
| Urinalysis/microscopy | Detect blood, protein, casts and infection. | Red-cell casts/dysmorphic cells support glomerular bleeding; quantify protein. |
| Creatinine, urea, electrolytes and bicarbonate | Assess filtration, AKI and complications. | Trend urgently; ECG and immediate treatment for hyperkalaemia. |
| FBC and haemolysis profile | Detect anaemia, inflammation and pulmonary haemorrhage. | Falling haemoglobin with haemoptysis is a critical red flag. |
| Complement, ANA, ANCA, anti-GBM and immunoglobulins | Identify immune-mediated cause. | Results guide specialist treatment but do not delay emergency stabilisation. |
| ASO/anti-DNase B, cultures, HIV/hepatitis/malaria tests | Assess post-infectious or infection-associated GN. | Interpret with timing and clinical context. |
| Ultrasound and renal biopsy | Assess size/obstruction and establish histology. | Biopsy is specialist-led; control BP/coagulation first. |
| Chest imaging and blood gas | Evaluate pulmonary oedema, haemorrhage and respiratory failure. | Urgent imaging for haemoptysis, hypoxia or severe breathlessness. |
Initial supportive management
- Position upright for pulmonary oedema, give oxygen for hypoxaemia and prepare non-invasive/invasive ventilation if respiratory failure develops.
- Restrict sodium and fluid according to volume status and prescription; avoid indiscriminate fluid boluses in oedema.
- Use prescribed diuretics for clinically significant overload while arranging renal review; monitor response and electrolytes.
- Treat sepsis promptly, choosing renal-adjusted antimicrobials and avoiding nephrotoxins.
- Control severe hypertension gradually according to the emergency pathway; prevent encephalopathy, heart failure and further kidney injury.
- Manage hyperkalaemia, acidosis, uraemia and other AKI complications immediately.
Pulmonary–renal syndrome
GN with pulmonary haemorrhage may deteriorate rapidly. Haemoptysis can be absent, especially when bleeding is diffuse. Suspect it when a patient has falling haemoglobin, hypoxia, diffuse infiltrates and active urinary sediment.
- ABCDE, oxygenation/ventilation and urgent critical-care review.
- Check FBC trend, coagulation, renal profile, urinalysis, blood gas and chest imaging.
- Call nephrology, respiratory and rheumatology teams; arrange anti-GBM/ANCA testing without delaying life-saving treatment.
- Prepare for immunosuppression and plasma exchange only under specialist direction after infection and bleeding risks are assessed.
- Monitor for airway flooding, shock, anaemia and rapid renal deterioration.
Rapidly progressive GN and severe AKI
- Urgent renal referral is required for a rapid creatinine rise, oliguria, active sediment, systemic vasculitis signs or pulmonary involvement.
- Record baseline and serial creatinine, urine output, potassium, bicarbonate, BP and weight.
- Prepare for renal biopsy and specialist immunosuppressive therapy; do not self-start steroids without senior direction.
- Discuss dialysis early when hyperkalaemia, acidosis, pulmonary oedema, uraemia or anuria is not responding to medical care.
Nursing interventions and monitoring
- Monitor BP, pulse, RR, SpO₂, temperature, neurological state, lung sounds, oedema and daily weight.
- Measure urine output accurately and document colour, sediment and fluid balance.
- Administer antihypertensives, diuretics, antibiotics and immunosuppressive medicines exactly as prescribed; monitor adverse effects.
- Maintain infection precautions for immunosuppressed patients and report fever promptly.
- Use pressure-area care, nutrition support and psychosocial support during prolonged admission.
- Communicate new haematuria, oliguria, rising BP, dyspnoea, haemoptysis, confusion or ECG changes immediately.
Complications
| Complication | Signs | Response |
|---|---|---|
| AKI/hyperkalaemia | Oliguria, weakness, ECG changes, acidosis or rising creatinine. | Emergency renal/electrolyte pathway and dialysis assessment. |
| Pulmonary oedema | Crackles, orthopnoea, hypoxia, frothy sputum and hypertension. | Upright, oxygen/ventilation, diuresis and renal/critical-care review. |
| Pulmonary haemorrhage | Haemoptysis, falling haemoglobin, infiltrates and severe hypoxia. | Airway/critical care, blood products and specialist immune therapy. |
| Hypertensive encephalopathy | Headache, visual symptoms, seizure, confusion or very high BP. | Controlled IV BP management and neurocritical-care assessment. |
| Thromboembolism/infection | Oedema, chest pain, fever or immunosuppression. | Risk assessment, cultures/imaging and prophylaxis/treatment as prescribed. |
Discharge, prevention and follow-up
- Teach patients to monitor BP when possible, report dark urine, reduced urine, swelling, breathlessness or severe headache.
- Complete antibiotics for infection-associated GN and attend renal follow-up and repeat urine/creatinine testing.
- Avoid NSAIDs, unregulated remedies and dehydration; check all new medicines with a clinician.
- Discuss salt restriction, prescribed fluid limit, smoking cessation, pregnancy planning and vaccination before immunosuppression.
- Provide a written emergency plan and confirm access to renal, laboratory and specialist services.
Clinical scenarios
Scenario 1 – Post-infectious nephritis: A child develops cola-coloured urine, periorbital oedema and headache two weeks after a sore throat. Check BP, urine, renal function and fluid status; assess for pulmonary oedema and refer for paediatric/renal review.
Scenario 2 – Pulmonary–renal syndrome: An adult with haemoptysis, anaemia, hypertension, haematuria and rising creatinine becomes hypoxic. Treat ABCDE, oxygenate, arrange urgent imaging and renal/respiratory review; do not delay specialist therapy while awaiting every antibody result.
Scenario 3 – Severe hypertension: A patient with GN has headache, visual changes and a seizure. Treat as hypertensive encephalopathy, protect airway, control BP under protocol and arrange neuro-renal critical care.
Common errors to avoid
- Assuming visible haematuria is a urinary infection without urine microscopy and renal assessment.
- Giving large fluid volumes to an oedematous patient.
- Delaying renal referral in rapidly progressive disease or pulmonary–renal syndrome.
- Starting immunosuppression without infection assessment and specialist direction.
- Missing severe hypertension, hyperkalaemia or pulmonary oedema.
- Failing to ask about recent infections, NSAIDs, herbal medicines and systemic symptoms.
GN RAPID: G – Glomerular blood/protein; N – Note BP and nephritic signs; R – Renal function/urine trend; A – Assess lungs and oedema; P – Pulmonary–renal red flags; I – Immunology/infection tests; D – Discuss urgently with nephrology.
Revision questions
- What findings make a urine abnormality glomerular rather than lower urinary tract?
- Differentiate nephritic and nephrotic patterns.
- List emergency complications of glomerulonephritis.
- What is pulmonary–renal syndrome and how would you recognise it?
- Which investigations help identify immune-mediated GN?
- Why must severe hypertension and fluid overload be treated urgently?
- Write a nursing care plan for a patient with acute GN and oliguria.
Key takeaways
- Haematuria, proteinuria, oedema and hypertension should prompt renal assessment.
- Rapidly progressive GN and pulmonary–renal syndrome are emergencies.
- Monitor BP, urine output, creatinine, potassium, fluid status and respiratory function closely.
- Supportive treatment and specialist immune therapy must be coordinated with nephrology.
- Early referral prevents avoidable kidney failure and pulmonary complications.