Case study reveals acute kidney injury and proteinuria in a child with pneumonia, suggesting underdiagnosis risk.
A previously healthy, 4-year-old girl was admitted with a two-day history of vomiting, diarrhea, fever and decreased urine output. At admission, she was dehydrated, blood pressure (BP) was 100/60 mmHg (95th percentile 108/70 mmHg), and she had crepitant rales in the upper lobe of the right lung. Lobar pneumonia was confirmed by chest X-ray ([Fig. 1a]). Initial laboratory findings ([Table 1]) revealed acute kidney injury (AKI, serum creatinine level 1.38 mg/dl), hypoalbuminemia (2.9 gr/dl), and hematuria and proteinuria in urine analysis. The day after, her urine became tea-coloured. Ultrasonography (USG) showed hyperechogenic kidneys. Serum complement 3 (C3) was 12.8 mg/dl (N:90–180), complement 4 (C4) was normal, and anti-nuclear antibody (ANA) and anti-double stranded DNA (anti-dsDNA) were negative. There was no history of recent pharyngeal or cutaneous infection. Firstly, fluid resuscitation, allopurinol and ceftriaxone treatments were initiated. The dehydration and AKI improved (serum creatinine level 0.36 mg/dl). During the follow-up, she had peripheral edema, her urine output decreased, and hypertension developed (BP 115/75 mmHg), so fluid restriction was applied, albumin and furosemide were administered. Teicoplanin and clindamycin were added because of persistent fever after the 3rd day of initial treatment and increased pneumonic infiltration. Macroscopic hematuria resolved on the 5th day of the antibiotics. Pneumonia treatment was completed, and she was discharged 3 weeks after admission with 0.30 mg/dl creatinine, 4.2 g/dl albumin and ongoing proteinuria (spot urine protein-to-creatinine ratio [UPCR] 0.72 mg/mg) and microscopic hematuria, and normal BP without antihypertensives. At the follow-up visit after 2 weeks, the C3 level was normal (90 mg/dl), spot UPCR was 0.25 mg/mg, and microscopic hematuria (22 red blood cells/hpf) continued. After 3 months, proteinuria and microscopic hematuria disappeared, and renal hyperechogenicity on USG also resolved.
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Öztürk et al. (2025) studied this question.
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