Acute Glomerulonephritis: Hypertension and Edema are Common Clinical Findings
The correct answer is C: Hypertension and edema are common clinical findings in acute glomerulonephritis. These manifestations result from the hallmark pathophysiology of acute GN—glomerular inflammation leading to sodium and water retention, which directly causes volume overload 1.
Why This is True
Acute glomerulonephritis characteristically presents with the nephritic syndrome, which includes:
- Hematuria (often with dysmorphic red blood cells and red cell casts)
- Proteinuria (typically sub-nephrotic range, though can be nephrotic)
- Hypertension (due to volume expansion)
- Edema (periorbital and peripheral, from salt and water retention)
- Oliguria (reduced urine output)
- Acute kidney injury (variable degree of renal dysfunction)
The Asian Pediatric Nephrology Association guidelines specifically recommend diagnosing acute GN when hematuria and proteinuria are accompanied by edema, oliguria, or hypertension 2. This triad of findings reflects the underlying glomerular inflammation and resultant hemodynamic changes.
Why the Other Options are Incorrect
A) Not the Most Common Cause of AKI
Acute glomerulonephritis accounts for only approximately 10% of AKI episodes in adults 3. The predominant causes of AKI in hospitalized patients are sepsis, major surgery, and nephrotoxic drugs—not glomerulonephritis 3. While infection-related glomerulonephritis remains a leading cause of acute GN specifically (particularly in children and low-middle income countries) 2, 1, it is not the most common cause of AKI overall.
B) Always Has an Immunological Basis
This statement is false because acute GN always involves immunological mechanisms. The disease can be classified by immune mechanism: immune-complex mediated (including infection-related GN, IgA nephropathy, lupus nephritis), ANCA-associated (pauci-immune), anti-GBM antibody-mediated, C3 glomerulopathy, or monoclonal immunoglobulin-associated 1. All forms involve immune activation, complement activation, and antibody-mediated injury 3.
D) Glomerular Hematuria is Essential
The absence of glomerular hematuria does not rule out acute GN. While hematuria is a cardinal feature, some patients may present with:
- Predominantly proteinuric presentations
- Subclinical disease detected incidentally
- Nephrotic syndrome without prominent hematuria 4
The diagnosis requires integration of clinical presentation, laboratory findings (including complement levels, serologies), and often kidney biopsy—not solely the presence of hematuria 2, 1.
E) Corticosteroids Have a Role
Corticosteroids do have a role in specific forms of acute GN. Immunosuppressive therapy including high-dose corticosteroids is indicated for:
- Crescentic glomerulonephritis or rapidly progressive GN 2, 3
- ANCA-associated vasculitis (combined with cyclophosphamide) 3
- Lupus nephritis (diffuse proliferative forms)
- Anti-GBM disease (with plasma exchange) 3
The AsPNA guidelines specifically recommend immunosuppressive therapy for patients with crescentic infection-related GN or rapidly progressive disease 2.
Clinical Management Approach
Supportive care remains the cornerstone for most acute GN cases, particularly post-infectious GN 2, 4:
- Fluid and salt restriction for patients with edema or hypertension
- Diuretics (loop diuretics for volume overload)
- Antihypertensives (calcium channel blockers preferred for stage 2 hypertension)
- Antibiotics when indicated (staphylococcus-associated GN, infective endocarditis, shunt nephritis)
- Renal replacement therapy for severe AKI, hyperkalemia, or pulmonary edema
Inpatient monitoring is required for patients with significant edema, severe hypertension, or acute kidney injury 2.
Key Diagnostic Pitfalls
The diagnosis of acute GN requires kidney biopsy in patients with:
- Atypical features
- Nephrotic-range proteinuria
- Persistently low C3 beyond 12 weeks
- Rapidly progressive GN 2
Common mistake: Assuming all acute GN is post-infectious and self-limiting. Adult patients increasingly present with non-streptococcal infections (particularly Staphylococcus), ongoing infections at diagnosis, and worse prognosis than childhood post-streptococcal GN 5. These patients require more aggressive evaluation and may need immunosuppression.