Abstract: PUB176
From Sore Throat to Nephritis: Acute Post-Streptococcal Glomerulonephritis in a Young Female Patient
Session Information
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Sharma, Sharda L., San Fernando General Hospital, San Fernando, Trinidad and Tobago
- Mahabir, Jezron J., San Fernando General Hospital, San Fernando, Trinidad and Tobago
- Basdeo, Ravindra Suraj, San Fernando General Hospital, San Fernando, Trinidad and Tobago
- Moonilal, Sawyer A., San Fernando General Hospital, San Fernando, Trinidad and Tobago
- Narine, Vishnu, San Fernando General Hospital, San Fernando, Trinidad and Tobago
- Mohammed, Zara Tiffany Sharana, San Fernando General Hospital, San Fernando, Trinidad and Tobago
- Browne, Ariel Kyle, San Fernando General Hospital, San Fernando, Trinidad and Tobago
Introduction
Acute post-streptococcal glomerulonephritis (APSGN) is an immune-mediated renal disorder that follows nephritogenic group A β-hemolytic streptococcus infection.Typical features include hematuria,edema,hypertension,and acute kidney injury from glomerular inflammation. APSGN is usually self-limiting with supportive care.
Case Description
A 16-year-old female presented to San Fernando General Hospital with two weeks of exertional dyspnea, two days of pedal edema, and two pillow orthopnea, preceded by a productive cough and subjective fever one week earlier. Exam revealed bilateral pitting edema to the tibial tuberosity and hypertension. Urinalysis showed 2+ protein and 4+ blood. 24-hour urine:667mg protein/24h (volume 1,000 mL). Urine microscopy showed granular casts and red blood cells. Labs showed normal C4, LFTs, CRP, electrolytes, complete blood count and negative ANA. Notable abnormalities included creatinine 1.1 mg/dL (baseline 0.7–1.0), ESR 81 mm/h, Anti-streptolysin O (ASO) titer 1966 IU/mL and low C3. Normal Echocardiography supported a renal etiology for volume overload. A differential of APSGN was made. Management included an ACE inhibitor and fluid restriction.
Discussion
This case highlights an atypical APSGN presentation in an adolescent with marked nephritic features and fluid overload. APSGN results from an immune response to nephritogenic streptococcal antigens, forming circulating immune complexes or glomerular deposition activating the alternate complement pathway, producing low C3 with normal C4. The inflammatory cascade drives glomerular injury, typically presenting with nephritic syndrome. Dialysis in pediatric APSGN is rare and reserved for refractory hyperkalemia, uncontrolled hypertension, or severe overload. Elevated ASO with low C3 and preserved C4 aided early diagnosis, while negative ANA argued against lupus nephritis. Management is mainly supportive, emphasizing blood pressure and fluid status control. The patient improved with fluid restriction and ACE inhibition, with planned outpatient monitoring of renal function, proteinuria, and blood pressure.