Is Poststreptococcal Glomerulonephritis (PSGN) included in the differential diagnosis for a patient with microscopic hematuria, subnephrotic proteinuria, and hypertension?

Poststreptococcal Glomerulonephritis in the Differential Diagnosis for Microscopic Hematuria, Subnephrotic Proteinuria, and Hypertension

Yes, poststreptococcal glomerulonephritis (PSGN) should definitely be included in the differential diagnosis for a patient presenting with microscopic hematuria, subnephrotic proteinuria, and hypertension. This clinical triad is highly characteristic of PSGN, which is a prototypical form of immune-mediated acute glomerulonephritis.

Clinical Presentation of PSGN

PSGN typically presents with the following features:

• Microscopic or gross hematuria (present in 89% of cases) 1
• Proteinuria that is usually moderate (1-3 g/day) 2
• Hypertension (present in 57-95% of cases) 1, 3
• Edema (present in approximately 59% of cases) 1
• Oliguria (present in about 35% of cases) 1

Diagnostic Considerations

When evaluating a patient with this clinical presentation, several key diagnostic elements should be assessed:

• Recent infection history: PSGN typically follows streptococcal infection of the pharynx (41%) or skin (45%) by 1-3 weeks 4, 2
• Laboratory findings:
  • Elevated antistreptolysin O (ASO) titer (present in 32% of cases) 1
  • Low serum complement levels, particularly C3 (present in 33% of cases) 1
  • Normal C4 complement levels in most cases 5
  • Urinalysis showing dysmorphic red blood cells and red cell casts 2
  • Elevated inflammatory markers may be present 5

Differential Diagnosis

The differential diagnosis for a patient with microscopic hematuria, subnephrotic proteinuria, and hypertension should include:

• PSGN 2
• IgA nephropathy (Berger disease) 2
• ANCA-associated vasculitis 2
• Membranoproliferative glomerulonephritis 2
• Lupus nephritis 2
• Thin basement membrane nephropathy 2
• Alport syndrome 2
• Hepatitis-associated glomerulonephritis 2
• Infective endocarditis-related glomerulonephritis 2

Diagnostic Algorithm

1. Urinalysis assessment:

   • Presence of dysmorphic red blood cells and red cell casts strongly suggests glomerular disease 2
   • Tea-colored urine with proteinuria (>2+ by dipstick) further supports glomerular origin 2

2. Serologic testing:

   • Check ASO titer, anti-DNase B, and throat/skin cultures 1
   • Measure complement levels (C3 and C4) - low C3 with normal C4 is characteristic of PSGN 5
   • Screen for ANCA antibodies to rule out vasculitis 2

3. Renal function assessment:

   • Measure serum creatinine, BUN, and eGFR 6
   • Quantify proteinuria with 24-hour collection if dipstick shows ≥1+ 6

4. Imaging:

   • Renal ultrasound may show enlarged kidneys with increased cortical echogenicity in acute glomerulonephritis 2

Prognostic Considerations

• PSGN generally has an excellent prognosis in children, even in cases with severe initial renal impairment 5
• High-degree proteinuria (≥2+) is significantly associated with elevated serum creatinine (>100 μmol/L) 4
• Persistent hypertension beyond the acute phase (found in 6.8% of patients during 2-5 year follow-up) may indicate a poorer prognosis 3
• Severe cases may require renal biopsy, which can show diffuse proliferative glomerulonephritis or crescentic changes 4

Management Approach

• Supportive treatment is the mainstay of therapy 5
• Appropriate antibiotic treatment (penicillin or erythromycin if penicillin-allergic) even in the absence of persistent infection 2
• Management of hypertension with diuretics (primarily furosemide) 3
• Close monitoring of renal function, proteinuria, and blood pressure 3
• Most cases of hypertension resolve within 3-5 days with normalization of glomerular filtration rate and plasma volume 3

Important Caveats

• Renal biopsy is generally not required for typical cases but should be considered in patients with persistent proteinuria ≥2+ for more than 2 weeks and elevated serum creatinine, as these patients may have atypical histological findings 4
• While PSGN typically has a self-limiting course, it has been linked to late-onset chronic kidney disease in some populations, particularly in cases with high levels of proteinuria 4
• Patients should be followed for at least 3 years to ensure complete resolution of urinary abnormalities, as approximately 25% may have persistent urinary findings 1