Acute Glomerulonephritis: A Clinical Guide for Malaysia
Definition
Acute Glomerulonephritis (AGN) is a clinical syndrome, not a single disease, defined by the sudden onset of inflammation targeting the glomeruli—the microscopic filtration units of the kidneys. This inflammatory insult compromises renal function, classically presenting as an "acute nephritic syndrome." This syndrome is a constellation of key findings:
Hematuria: The presence of blood in the urine, which is often macroscopic (visible) and described as "cola-colored" because the red blood cells are altered as they pass through the acidic renal tubules (4).
Edema: Swelling caused by fluid retention, characteristically appearing first in areas of low tissue pressure like the face and eyelids (periorbital edema) before becoming generalized (5).
Hypertension: Elevated blood pressure, driven primarily by sodium and water retention resulting from the kidneys' impaired filtration capacity (5).
Proteinuria: A variable degree of protein leakage into the urine. In a classic nephritic syndrome, this is typically sub-nephrotic (<3.5g/day), but significant overlap with nephrotic-range proteinuria can occur, pointing towards specific underlying causes (4).
Renal Impairment (Azotemia): A rise in nitrogenous waste products in the blood, reflected by an elevated serum creatinine and blood urea nitrogen (BUN), indicating a fall in the glomerular filtration rate (GFR) (4).
Understanding these components is crucial for the house officer, as their severity and combination provide vital clues to the underlying etiology and the urgency of the situation.
Epidemiology
In Malaysia, the epidemiology of AGN reflects a nation in transition, creating a complex "double burden" of disease. This means clinicians must be prepared to manage both diseases of developing nations and the chronic, complex diseases of developed ones.
Historically, Post-Streptococcal Glomerulonephritis (PSGN) was a formidable pediatric health issue. Landmark studies from Kelantan in the late 1980s documented that PSGN accounted for a staggering 97.6% of childhood AGN admissions. Crucially, these cases were predominantly linked to preceding skin infections (pyoderma or impetigo) rather than pharyngitis, a pattern typical of tropical climates and closely associated with lower socioeconomic conditions and household overcrowding (23). While public health improvements have reduced its incidence, PSGN remains an important diagnosis, especially in pediatric patients from rural or underserved communities.
However, contemporary data from adult renal biopsy registries paint a starkly different picture, highlighting a significant epidemiological shift. Among patients undergoing biopsy for primary glomerular disease, IgA Nephropathy (IgAN) is now the most frequently diagnosed condition (24). This is clinically significant as IgAN often follows a chronic, progressive course and is a leading global cause of end-stage renal disease (ESRD).
Even more striking is the pattern among secondary causes. Lupus Nephritis (LN) is overwhelmingly predominant in the Malaysian adult population requiring biopsy, accounting for a remarkable 44.2% of all secondary GN cases in a 2023 multi-center review (24). This finding, consistent with older data from the 1980s, firmly establishes autoimmune diseases, particularly Systemic Lupus Erythematosus (SLE), as a major driver of severe, potentially life-threatening glomerular disease in Malaysia (25). This epidemiological reality means a young woman presenting with an acute nephritic syndrome has a high pre-test probability of having lupus nephritis, a diagnosis that requires urgent confirmation and specialized management.
Etiology
A systematic approach to the causes of AGN is essential for guiding the diagnostic workup. The etiologies are broadly classified as post-infectious, primary (idiopathic), or secondary to a systemic disease.
Post-Infectious Glomerulonephritis (PIGN): The glomerular injury is not a direct infection of the kidney but an immunological reaction to a remote infection.
Post-Streptococcal GN (PSGN): The archetypal PIGN, caused by specific "nephritogenic" strains of Group A β-hemolytic streptococci. A key diagnostic clue is the latency period: nephritis appears 1-2 weeks after pharyngitis or 3-6 weeks after impetigo. This delay represents the time needed to mount an adaptive immune response (5).
Staphylococcus-Associated GN: An increasingly important cause, particularly in elderly, diabetic, or hospitalized patients. Unlike PSGN, the nephritis often occurs concurrently with an active staphylococcal infection (e.g., a skin abscess, infected ulcer, or endocarditis). It is often IgA-dominant on biopsy, creating a diagnostic challenge (4).
Other Infections: Can be associated with infective endocarditis (look for fever, new murmur, and embolic phenomena), viral infections like Hepatitis B, Hepatitis C (often with cryoglobulinemia), and HIV (1).
Primary (Idiopathic) Glomerulonephritis: The disease process is confined to the kidneys.
IgA Nephropathy (Berger's Disease): The most common primary GN worldwide and in Malaysia (24). The classic presentation is episodic macroscopic hematuria that occurs concurrently with an upper respiratory tract infection (hence, synpharyngitic hematuria). This lack of a latency period is a key feature distinguishing it from PSGN (6).
Membranoproliferative GN (MPGN): A histological pattern of injury rather than a single disease. It often presents with a mixed nephritic-nephrotic picture and is frequently associated with persistent low C3 levels, suggesting alternative complement pathway dysregulation (4).
Secondary (Systemic) Glomerulonephritis: The kidney is a target of a multi-system disease.
Lupus Nephritis (LN): A frequent and severe complication of SLE and a leading cause of secondary GN in Malaysia (1, 24). The clinical presentation is highly variable, and a biopsy is crucial for classification (from Class I to VI), which dictates treatment and prognosis.
ANCA-Associated Vasculitis (AAV): Includes Granulomatosis with Polyangiitis (GPA) and Microscopic Polyangiitis (MPA). This is a leading cause of Rapidly Progressive Glomerulonephritis (RPGN) in older adults and is a medical emergency. Suspect AAV in a patient with AKI plus constitutional symptoms (fever, weight loss) and respiratory tract involvement (sinusitis, hemoptysis) (11).
Anti-GBM Disease (Goodpasture's Syndrome): A rare but aggressive autoimmune cause of RPGN. The combination of RPGN and pulmonary hemorrhage (hemoptysis) is the classic presentation of Goodpasture's syndrome and requires immediate, aggressive treatment (1).
IgA Vasculitis (Henoch-Schönlein Purpura): A systemic vasculitis, primarily of childhood, presenting with a classic tetrad: palpable purpuric rash (buttocks, lower limbs), arthritis, colicky abdominal pain, and nephritis. The renal histology is identical to IgA Nephropathy (4).
Pathophysiology
The clinical signs of AGN are the macroscopic expression of microscopic immunological warfare within the glomeruli. The predominant mechanism is immune-complex mediated injury (Type III Hypersensitivity). In this process, antigen-antibody complexes form, either in circulation (like in PSGN or LN) or in-situ within the glomerulus, and deposit in the glomerular structures (5).
These deposited complexes are foreign bodies that trigger the complement cascade, a powerful arm of the innate immune system. This activation, either via the classical pathway (triggered by IgG/IgM complexes, as in lupus) or the alternative pathway (as in PSGN), is the central engine of damage. It generates two key destructive forces:
Chemoattraction: Potent anaphylatoxins like C3a and C5a are generated, acting as chemical sirens that recruit a flood of inflammatory cells (neutrophils, macrophages) into the delicate glomerulus.
Direct Cell Damage: The cascade culminates in the formation of the Membrane Attack Complex (MAC, C5b-9), a molecular drill that punches holes in glomerular cells, causing direct lysis and injury (5).
This inflammatory influx and the proliferation of resident glomerular cells lead to a swollen, hypercellular glomerulus. This "traffic jam" physically obstructs the capillaries, causing the GFR to plummet. The damaged capillary walls, now riddled with inflammatory pores, lose their integrity, allowing large elements like red blood cells and proteins to leak into the urine, causing hematuria and proteinuria (5).
Less common but more aggressive mechanisms include pauci-immune injury (Type II Cell-Mediated Hypersensitivity), where ANCAs activate neutrophils to attack the vessel walls, and anti-GBM disease (Type II Antibody-Mediated Hypersensitivity), where autoantibodies directly bind to the structure of the glomerular basement membrane, inciting a relentless inflammatory response (7, 11).
Clinical Presentation
The clinical spectrum of AGN is broad, but a house officer must be adept at recognizing the classic features and, more importantly, the red flags.
Diagnostic Clues: The presence of red cell casts in a fresh urine microscopy sample is pathognomonic for glomerulonephritis, as it proves the blood originated from within the renal tubules (5). The clinical dyad of RPGN and hemoptysis is highly suggestive of a pulmonary-renal syndrome like Anti-GBM disease or ANCA vasculitis and warrants immediate senior input (1).
Common Symptoms (>50%):
Edema: The most frequent presenting sign (98.4% in a Malaysian pediatric series) (23). It is a soft, pitting edema, typically starting as periorbital puffiness upon waking and progressing to dependent edema in the ankles and sacrum as the day progresses (4).
Macroscopic Hematuria: The urine is often described by patients as "cola-colored," "tea-colored," or "smoky." This brownish discoloration is a strong clue for a glomerular source of bleeding, as the hemoglobin is converted to methemoglobin in the acidic tubular environment (1, 23).
Hypertension: Driven by volume expansion, this can range from mild to severe. It is a critical sign to manage, as it can lead to acute complications like posterior reversible encephalopathy syndrome (PRES) or heart failure (5, 23).
Oliguria: A urine output of <400-500 mL per day. This is a clear and ominous sign of a significant fall in GFR and more severe kidney injury (5).
Less Common Symptoms (10-50%):
Non-specific constitutional symptoms like malaise, anorexia, and nausea are common, especially in severe disease or in older adults, where they can mask the underlying renal diagnosis.
Uremic symptoms such as lethargy, pruritus, or a metallic taste can develop if renal failure is severe and prolonged.
⚠️ Red Flag Signs & Symptoms: These signs indicate clinical urgency and require immediate action and escalation.
Rapidly rising creatinine or severe oliguria: Suggests Rapidly Progressive Glomerulonephritis (RPGN), a nephrological emergency where renal function can be irreversibly lost in days to weeks.
Hemoptysis (coughing up blood): Indicates life-threatening pulmonary hemorrhage (a pulmonary-renal syndrome) and requires immediate, aggressive immunosuppression and potential plasma exchange.
Confusion, seizures, or severe headache: May indicate hypertensive encephalopathy or uremia, requiring urgent blood pressure control and potential dialysis.
Fever, new heart murmur, or signs of sepsis: Suggests an underlying systemic infection like endocarditis, which requires urgent antibiotic therapy and investigation.
Complications
The complications of AGN are direct consequences of failed kidney function and uncontrolled inflammation.
Renal: The primary complication is acute kidney injury (AKI). If the inflammation is severe and uncontrolled, this can evolve into RPGN, leading to irreversible scarring, chronic kidney disease (CKD), and ultimately, end-stage renal disease (ESRD) requiring dialysis or transplantation.
Cardiovascular: Severe hypertension can lead to hypertensive encephalopathy or heart failure. Fluid overload from sodium and water retention is the primary driver of this and can also lead to acute pulmonary edema, a medical emergency.
Metabolic: Impaired GFR leads to the retention of potassium, causing potentially fatal hyperkalemia. The kidneys' inability to excrete acid leads to metabolic acidosis. Impaired phosphate excretion causes hyperphosphatemia.
Prognosis
The prognosis of AGN is entirely dependent on the underlying etiology, the severity at presentation, and the timeliness of treatment. Classic post-streptococcal GN in children has an excellent prognosis, with over 95% achieving a complete recovery with supportive care alone (10). In contrast, conditions like ANCA vasculitis and anti-GBM disease are medical emergencies; without aggressive treatment, they carry a high risk of progression to ESRD and significant mortality (11). The prognosis in lupus nephritis is variable and is closely tied to the histological class on biopsy and the patient's response to immunosuppressive therapy. For IgA nephropathy, key predictors of progression to ESRD include the degree of proteinuria at diagnosis, persistent hypertension, and the GFR at the time of presentation.
Differential Diagnosis
Acute Interstitial Nephritis (AIN): This is a key differential, especially in a patient with AKI and a history of new medication (e.g., antibiotics, PPIs). While it causes AKI, the classic presentation involves fever, rash, and arthralgia. The urine sediment is characterized by white blood cell casts and eosinophils, with less prominent edema and hypertension compared to AGN.
Lower Urinary Tract Bleeding: Conditions like bladder tumors, stones, or UTIs can cause hematuria. However, the blood is typically bright red, clots may be present, and there are no red cell casts on microscopy. Crucially, the other signs of nephritic syndrome (edema, hypertension, significant proteinuria) are absent.
Congestive Heart Failure: This can present with severe edema, shortness of breath, and renal impairment (cardiorenal syndrome). However, the jugular venous pressure (JVP) is typically elevated, and lung auscultation reveals crackles. Significant glomerular hematuria and red cell casts are not features of heart failure.
Investigations
Immediate & Bedside Tests
Urine Dipstick: An essential first step to immediately screen for the hallmark abnormalities of hematuria and proteinuria (28).
Bedside ECG: Mandatory in any patient with significant AKI to screen for the cardiotoxic effects of hyperkalemia (e.g., peaked T waves, widened QRS, sine wave pattern), which is a life-threatening emergency requiring immediate intervention (4).
Diagnostic Workup
First-Line Investigations:
Urine Microscopy: The most critical initial diagnostic test, often called a "liquid biopsy." It is essential to identify dysmorphic red cells (cells with distorted, blebbed shapes from being squeezed through the damaged GFB) and, most importantly, red blood cell casts (cylindrical molds of the renal tubules formed by compacted red cells). The presence of casts is highly specific for glomerular bleeding and virtually confirms a diagnosis of glomerulonephritis (the action) (5).
Renal Profile (Urea, Electrolytes, Creatinine): Crucial to quantify the severity of AKI, stage it, and detect urgent metabolic derangements like hyperkalemia or acidosis (the action), which directly guide immediate life-saving management (the rationale) (4).
Full Blood Count (FBC): Performed to assess for anemia (which can be dilutional from fluid overload or from chronic inflammation) and leukocytosis that may point towards an underlying infectious trigger (the action) (4).
Gold Standard:
Percutaneous Renal Biopsy: The definitive gold standard for diagnosis in most adult cases and any atypical presentation. It is essential for providing a precise histological diagnosis by combining light microscopy, immunofluorescence, and electron microscopy (the rationale). This detailed diagnosis (e.g., identifying crescentic GN, determining the class of lupus nephritis) is absolutely critical for guiding the use of specific, high-risk immunosuppressive therapies and determining prognosis (the action) (15).
Monitoring & Staging
Complement Levels (C3, C4): A vital blood test to immunologically categorize the GN and narrow the differential diagnosis (the action). Low C3 with normal C4 suggests alternative pathway activation (e.g., PSGN). Low levels of both C3 and C4 indicate classical pathway consumption and are characteristic of lupus nephritis (the rationale) (4).
Autoantibody Screen (ANA, anti-dsDNA, ANCA, anti-GBM): These targeted blood tests are ordered based on clinical suspicion to specifically diagnose systemic autoimmune causes like lupus or vasculitis (the rationale). A positive result allows for targeted, definitive therapy (the action) (4).
Renal Ultrasound: An important early imaging study primarily performed to assess kidney size (small, scarred kidneys suggest underlying chronic disease) and, most importantly, to definitively rule out a post-renal cause of AKI, such as bilateral ureteric obstruction, which is a key reversible cause requiring urgent urological intervention (the action) (15).
Management
Management Principles
The management of AGN is a two-pronged strategy: (1) urgent supportive care to manage life-threatening complications of AKI, which is the responsibility of all front-line clinicians, and (2) definitive therapy targeted at the underlying immunological disease, which is directed by a nephrologist.
Acute Stabilisation (The First Hour)
Airway/Breathing: Administer high-flow oxygen via a non-rebreather mask to maintain SpO2 >94% (the action), which is crucial to prevent tissue hypoxia in a critically ill patient (the rationale). Auscultate the lungs for crackles indicating pulmonary edema.
Circulation:
Secure two large-bore IV cannulas. If the patient is hypotensive (a rare finding in AGN), a cautious fluid bolus may be given with careful reassessment.
For severe hypertension with encephalopathy: This is a neurological emergency. Administer IV Labetalol or a Nicardipine infusion (the action) to carefully lower the mean arterial pressure by no more than 25% in the first hour. Overly rapid correction risks cerebral ischemia (the rationale) (5).
For severe fluid overload/pulmonary edema: Administer a stat bolus of IV Furosemide 40-80mg (or higher, e.g., 1mg/kg) (the action) to induce a rapid and potent diuresis, offload the circulation, and relieve respiratory distress (the rationale) (3).
Disability: Check capillary blood glucose and assess GCS. Control seizures with IV benzodiazepines if present.
Exposure: Check for fever. Perform a thorough skin examination for rashes (purpura, malar rash) or signs of infection.
Definitive Therapy
This is guided by the specific biopsy diagnosis and should always be directed by a nephrologist.
First-Line Treatment:
Post-Infectious GN: Primarily supportive care. Antibiotics (e.g., Penicillin for PSGN) are given to eradicate the organism and prevent transmission, but it is crucial to understand they do not alter the established course of the nephritis itself (3, 10).
Lupus Nephritis (Class III/IV): Induction therapy involves high-dose corticosteroids plus a second agent, either Mycophenolate Mofetil (MMF) or IV Cyclophosphamide. Malaysian guidelines recommend MMF as a preferred induction agent due to its favorable side-effect profile (19, 39).
ANCA Vasculitis/Anti-GBM Disease: Treatment is a medical emergency. The regimen involves high-dose corticosteroids plus either Cyclophosphamide or Rituximab. Plasma exchange (plasmapheresis) is a key, urgent intervention to physically remove the pathogenic autoantibodies, especially in anti-GBM disease and severe AAV with pulmonary hemorrhage (11, 19).
Second-Line/Escalation: For refractory or relapsing disease, treatment may be switched to alternative agents like Rituximab, Calcineurin inhibitors (e.g., tacrolimus), or other biologics, guided by specialist opinion (11).
Supportive & Symptomatic Care
Hypertension & Proteinuria: ACE inhibitors (e.g., Perindopril) or ARBs (e.g., Losartan) are the cornerstone of long-term management. They provide a dual benefit: controlling systemic blood pressure and reducing intraglomerular pressure, which decreases proteinuria and provides a direct reno-protective effect (18).
Fluid & Salt Restriction: Strict limitation of dietary sodium (<2g/day) and tailored fluid restriction are essential non-pharmacological measures to control edema and hypertension (3).
Diuretics: Oral loop diuretics (e.g., Furosemide) are used chronically to manage fluid balance and prevent volume overload (3).
Dietary Management: In severe AKI, protein, potassium, and phosphate intake must be restricted to manage uremia and prevent metabolic complications. A referral to a clinical dietitian is highly recommended (31).
Key Nursing & Monitoring Instructions
Strict hourly input/output chart monitoring is mandatory in the acute phase.
Daily weight measurement, ideally at the same time each day, is the most sensitive indicator of fluid balance changes.
4-hourly blood pressure monitoring, titrated to more frequently if the patient is on IV anti-hypertensives or is unstable.
Inform medical staff immediately if systolic BP >160 mmHg, urine output is <0.5mL/kg/hr for more than 2 hours, or if the patient develops confusion, new shortness of breath, or chest pain.
When to Escalate
Call Your Senior (MO/Specialist) if:
The patient has any Red Flag Signs & Symptoms (e.g., hemoptysis, new neurological signs, seizures).
Serum potassium is >6.0 mmol/L or there are any ECG changes of hyperkalemia.
The patient has severe, refractory hypertension or signs of acute pulmonary edema.
Creatinine is rising rapidly (e.g., >50% increase in 48 hours), suggesting RPGN.
Referral Criteria:
Urgent referral to a Nephrologist is required for any patient with suspected RPGN, severe AKI (Stage 2 or 3), nephrotic-range proteinuria (>3.5g/day), or any clinical/serological evidence of a systemic vasculitis or autoimmune disease (34).
All cases where a renal biopsy or initiation of immunosuppressive therapy is being considered must be managed by or in close consultation with the nephrology team.
Indications for urgent Renal Replacement Therapy (Dialysis) - AEIOU: Refractory Acidosis, Electrolyte abnormalities (especially hyperkalemia), Intoxications, fluid Overload (refractory pulmonary edema), or symptomatic Uremia (encephalopathy, pericarditis) (1).
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