Abstract

Sirs, We have read with great interest the study by Spivacow et al. regarding metabolic risk factors in children with kidney stone disease [1]. The authors found biochemical abnormalities in 84.4% of 90 children, with hypercalciuria and hypocituria being the two most common causes. This high incidence of biochemical abnormalities matched with results reported in previous studies [2, 3] that had recommended screening for metabolic abnormalities in pediatric urolithiasis even in patients with documented urinary tract anomalies. A urinary tract anomaly has long been considered a predisposing condition for the formation of calculi, with the associated urinary stasis considered to promote crystal retention and stone formation. However, several recent reports have questioned this theory and have suggested that, in patients with urinary tract anomalies, stone formation is caused by underlying metabolic abnormalities [4, 5]. We would like to present a case which demonstrates the difficulty of immediate diagnosis of stone pathogenesis in patients with urinary tract abnormalities. We describe here a case of bilateral ureter stones in a 1-year-old boy in whom tortuosities of both ureters was observed. A 1-year-old boy was referred to our hospital because of diarrhea and oliguria. The boy was delivered uneventfully at 38 weeks of gestation and had a birth weight of 3190 g. Prenatal ultrasonography during the second trimester of pregnancy did not reveal any abnormalities, and a family history of stone disease in first-degree relatives was denied. Upon referral, the boy had been lethargic and anuric for 10 h after having had watery diarrhea for the previous 7 days. The results of blood analyses were as follows: tCO2, 12 mEq/L; blood urea nitrogen, 16.3 mg/dL; creatinine, 0.7 mg/dL. Urinalysis was not performed because of the anuria, which persisted despite isotonic saline infusion. At the 12-h follow-up examination, serum creatinine had increased to 1.1 mg/dL, and the acidosis persisted (pH 7.249; tCO2 13.7 mEq/L). Renal ultrasonography revealed hydronephrosis, and nonenhanced computed tomography showed bilateral proximal ureter stones with moderate attenuation. Percutaneous nephrostomy (PCN) of both kidneys using a 6-Fr pigtail catheter was performed to relieve the ureteral obstruction, and alkalinization of urine with an intravenous sodium bicarbonate infusion was initiated on hospital day (HD) 2. After the PCN procedure, serum creatinine level dropped rapidly from 1.9 to 0.8 mg/dL, and urinary flow through a Foley catheter was observed on HD 3. Antegrade pyelography (AGP) via a PCN catheter on HD 7 confirmed that both ureters were fluent and that calculi were absent, but it also revealed tortuosities of both ureters at the ureteropelvic junction. As the ureter calculi were lysed during alkalinization, stone analysis could not be conducted. Urine drained from the renal pelvis at the time of catheter insertion was acidic (pH 5.5), and there was a high ratio of uric Pediatr Nephrol (2009) 24:2077–2078 DOI 10.1007/s00467-009-1182-1

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