Post-streptococcal Glomerulonephritis Presenting With Acute Pulmonary Edema and Critical Hyperkalemia: A Rare Pediatric Case Report From Yemen

Abstract

Background:

Post-streptococcal glomerulonephritis (PSGN) is a common cause of acute nephritic syndrome in children. Rarely, it may result in life-threatening complications, including acute pulmonary edema and critical hyperkalemia.

Case Presentation:

We report a 10-year-old Yemeni girl (25 kg) presenting with severe respiratory distress, irritability, and generalized pitting edema. Laboratory tests confirmed PSGN with markedly reduced complement C3 (42.2 mg/dL) and nephritic urine sediment containing numerous red blood cells and casts. The patient developed critical hyperkalemia (7.0 mmol/L) and acute pulmonary edema, requiring urgent intubation and mechanical ventilation using pressure-controlled mandatory ventilation (P-CMV).

Management:

Aggressive fluid mobilization and electrolyte stabilization were initiated. High-dose intravenous furosemide (4 mg/kg/day) and low-dose dopamine (per local institutional protocols) were applied. Despite critical hyperkalemia, standard protocols (calcium, insulin-glucose) were unavailable; thus, potassium-lowering relied on continuous salbutamol and rapid diuresis. Appropriate adjunctive sedation was utilized briefly to facilitate mechanical ventilation. The patient produced 1700 mL urine in 17 hours, demonstrating a strong diuretic response. Continuous cardiac monitoring was maintained throughout the acute phase to mitigate arrhythmic complications.

Conclusion:

Early recognition of severe extra-renal complications in PSGN is critical. Intensive supportive care—including mechanical ventilation, meticulous fluid and electrolyte management, and appropriate sedation—is essential for survival in cases of acute pulmonary edema and critical hyperkalemia.

Introduction

Post-streptococcal glomerulonephritis (PSGN) is an immune-mediated renal disorder triggered by nephritogenic Group A β-hemolytic streptococci. Clinical manifestations range from asymptomatic microscopic hematuria to severe acute kidney injury with systemic complications. In rare cases, children develop acute pulmonary edema and critical hyperkalemia, requiring intensive care management. This report illustrates such a high-acuity pediatric case, emphasizing the role of early recognition and comprehensive supportive care.

Case Presentation

Initial Assessment

A 10-year-old Yemeni girl (25 kg) was admitted to the Pediatric Intensive Care Unit (PICU) at Al-Mansoor Polyclinic with severe respiratory distress, irritability, and generalized pitting edema. Vital signs on admission: blood pressure 130/90 mmHg, heart rate 160 bpm, respiratory rate 56 bpm. Pulmonary auscultation revealed bilateral basal crackles. Urine initially appeared grossly hematuric, later turning smoky and tea-colored.

Diagnostic Investigations

Laboratory studies indicated acute kidney injury and critical electrolyte disturbance. Serum potassium reached 7.0 mmol/L. Serum creatinine was 1.5 mg/dL on admission, peaking at 2.5 mg/dL on day 2. Urinalysis showed numerous red blood cells throughout the microscopic field, urinary casts, and mild proteinuria (+1). Complement C3 was markedly reduced (42.2 mg/dL; reference > 90 mg/dL), confirming PSGN. Chest radiography revealed bilateral diffuse pulmonary opacities consistent with pulmonary edema (Figure 1).

Figure 1.

Chest radiograph (posteroanterior view) demonstrating bilateral diffuse pulmonary opacities (arrows), predominantly involving the perihilar and lower lung zones. Increased interstitial and alveolar markings with symmetric distribution are evident, consistent with pulmonary congestion or edema. No focal consolidation, pleural effusion, or pneumothorax is observed. The cardiac silhouette appears within normal limits.

Management and Clinical Course

Due to respiratory compromise and pulmonary edema, the patient was intubated and mechanically ventilated using P-CMV. Morphine sedation (0.1 mg/kg/dose) was utilized solely to ensure patient-ventilator synchronization and control agitation during the initial acute phase. It was administered every 4 hours during the first 24 hours, then every 8 hours for 12 additional hours. Morphine was withdrawn prior to extubation. This regimen effectively controlled irritability and ensured optimal patient–ventilator synchronization, facilitating stable ventilation.

Additional management included:

• Diuretics: High-dose IV furosemide (4 mg/kg/day)

• Renal support: Low-dose dopamine (5 μg/kg/min)

• Electrolyte management: Salbutamol nebulization and strict potassium restriction. Due to acute resource constraints, standard hyperkalemia protocols (intravenous calcium and insulin-glucose) were not administered. Clinical decision-making relied heavily on continuous cardiac monitoring, which fortunately revealed no malignant arrhythmias. Given the stable cardiac rhythm and the immediate onset of massive diuresis, the medical team prioritized rapid fluid mobilization. Fortunately, the aggressive diuresis led to rapid potassium clearance.

• Fluid balance: Input calculated including insensible losses (400 mL/m²) plus prior urine output

• Antimicrobials: IV ampicillin/sulbactam (100 mg/kg), followed by oral azithromycin

A robust diuretic response was observed: 1700 mL urine in 17 hours. By day 2, serum potassium normalized to 4.2 mmol/L and creatinine improved to 1.9 mg/dL. The patient was successfully extubated and transitioned to nasal cannula oxygen.

Following extubation, the patient continued to show remarkable clinical improvement. Her fluid overload and respiratory distress resolved completely. She was subsequently discharged from the hospital in a stable condition with normalized serum potassium and improving renal function. Subsequent follow-up confirmed full clinical recovery without residual complications

Discussion

PSGN is an immune-complex–mediated disorder triggered by nephritogenic Group A β-hemolytic streptococci, commonly after pharyngitis or impetigo.^1,2 Immune complexes deposit in glomeruli, activate complement, and trigger inflammation, reducing GFR.^1,3-5 Hypocomplementemia, particularly low C3, is a hallmark.

Severe pediatric cases may develop massive intravascular volume expansion, precipitating pulmonary edema. ⁶ Reduced GFR also impairs potassium excretion, causing critical hyperkalemia (⩾7.0 mmol/L), a medical emergency.

Ventilatory Support

Mechanical ventilation was the primary and life-saving intervention for acute respiratory failure in this patient. As a minor temporary adjunct, basic sedation was utilized to ensure patient-ventilator synchronization and reduce the work of breathing, allowing the mechanical ventilation to effectively reverse the hypoxia caused by pulmonary edema.

Renal Hemodynamics and Diuresis

Fluid overload was managed with high-dose loop diuretics, producing rapid diuresis (1700 mL/17 hours) and improved renal function. Low-dose dopamine (5 μg/kg/min) was administered concurrently based on older local institutional protocols. However, we acknowledge that contemporary pediatric nephrology literature and current evidence do not support the use of “renal-dose dopamine” for nephroprotection or enhanced renal perfusion. Its use reflects localized clinical practice rather than an evidence-based standard.

Electrolyte Management

Critical hyperkalemia was addressed with salbutamol nebulization and diuresis. While standard emergency management of critical hyperkalemia dictates the use of intravenous calcium for myocardial protection and insulin-glucose infusion for intracellular shifting, these were not utilized due to setting limitations. The rapid and massive diuretic response (1700 mL/17 hours) was the primary mechanism that safely and rapidly normalized serum potassium.

Diagnostic Reliability and Prognosis

Despite unavailable ASO titers, the nephritic triad (hypertension, edema, hematuria), urinary casts, and low C3 strongly supported PSGN diagnosis. Early recognition and intensive supportive care ensured excellent outcomes.^1,3,5,6

Conclusion

PSGN may rarely present with life-threatening complications such as acute pulmonary edema and critical hyperkalemia. This case highlights that even in resource-limited settings where ideal critical care modalities and standard emergency protocols may be constrained, prompt recognition, mechanical ventilation, and aggressive diuresis can lead to rapid recovery and excellent outcomes in pediatric patients. Prompt recognition and intensive supportive care—including diuretics, electrolyte correction, mechanical ventilation, and appropriate sedation—are essential. With timely intervention, full recovery is achievable in most pediatric patients.

The primary clinical insight of this report lies in demonstrating the feasibility of reversing critical hyperkalemia and acute pulmonary edema using exclusively basic pharmacological interventions and diuresis. While similar PSGN presentations exist, this case highlights a successful survival strategy for practitioners in austere or severely resource-limited environments where standard advanced critical care modalities—including dialysis and standard hyperkalemia protocols—are inaccessible.

Limitations

Serological confirmation (ASO, anti-DNase B) was unavailable. Quantitative proteinuria assessment was not performed. Furthermore, due to the acute emergency presentation and severe resource constraints in our setting, essential objective clinical details—including Arterial Blood Gas (ABG) analysis, continuous electrocardiographic (ECG) findings, detailed ventilator settings, and specific renal function indices (eg, fractional excretion parameters)—were not documented. Management relied heavily on clinical assessment and basic laboratory monitoring. However, clinical presentation, nephritic urinary findings, hypocomplementemia, and disease course strongly support PSGN, consistent with pediatric literature.^1,3,6