Hyewon Hahn

Ifosfamide nephrotoxicity in pediatric cancer patients.

Abstract. The renal functions in pediatric cancer patients who received ifosfamide (IFO) treatment were evaluated and the risk factors related to IFO nephrotoxicity were determined. The medical records of all children treated with IFO were reviewed, and 62 with normal renal function before IFO treatment were selected. Nephrotoxicity was diagnosed by measuring urine β2-microglobulin and glucose, and serum phosphate, bicarbonate, and creatinine. Forty-eight (77.4%) had a history of previous cisplatin treatment. Nephrotoxicity was detected in 20 patients (32.3%). β2-Microglobulinuria was observed in all 20, hypophosphatemia in 10 (16.1%), hypocarbia in 2 (3.2%), glucosuria in 5 (8.1%), and decreased creatinine clearance in 7 (11.3%). The cumulative dose of IFO and a history of previous cisplatin therapy were related to nephrotoxicity. Among the 20 patients with nephrotoxicity, the median cumulative dose of IFO in patients with a low (<500 mg/m2) and high (>500 mg/m2) cumulative dose of previous cisplatin was 80 g/m2 (73–102 g/m2) and 45 g/m2 (11–76 g/m2), respectively. Most of the nephrotoxicity persisted after cessation of IFO treatment. In conclusion, close monitoring of IFO nephrotoxicity should be started earlier in patients with high-dose cisplatin pretreatment. Tubular proteinuria, as indicated by β2-microglobulinuria, was the most-sensitive marker for IFO nephrotoxicity. Long-term follow-up study for reversibility of IFO nephrotoxicity is in progress.

Genetic Basis of Congenital and Infantile Nephrotic Syndromes

Note: Mutations are designated in terms of protein (p) or cDN frame ends in a stop codon ( ) n amino acids from the first affecte Conversion factors for units: SCr in mg/dL to mol/L, 88.4; eGF Abbreviations and definitions: CNF, congenital nephrotic sy estimated glomerular filtration rate (calculated using the Schwar segmental glomerulosclerosis; GA, genitalia anomaly; LAMB2, MesPGN, mesangial proliferative glomerulonephritis; ND, not do nephrosis 2, idiopathic, steroid-resistant (podocin); NS, nephrot (having female-type external genitalia and a 46,XY karyotype); W Novel mutations. These 2 cases have been reported previously.

Bilateral ureter stones in a 1-year-old boy

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

Renal and Renovascular Hypertension in Children

접수 : 년 월 일 수정 2011 3 25 , : 년 월 일 2011 4 13 승인 : 년 월 일 2011 4 14 책임저자 :한혜원 서울시 노원구 하계 동 , 1 280-1 을지대학교 의과대학 소아청소년과 Tel : 02)980-9222 Fax : 02)976-5441 E-mail : petercat67@gmail.com 만의 증가와 함께 일차성 고혈압의 빈도가 증가하면 서 소아 청소년 고혈압의 양상이 바뀌고 있는 추세이 다 죽상경화증이 청소년기에 이미 생성을 시작한다 . 는 보고가 많으며 고혈압 자체도 말기 신부전 진행 , 의 위험 인자이므로 소아 신장 영역에서는 혈압의 , 관리에 지속적인 관심과 연구가 필요하다 본 연구에 . 서는 최근 소아와 청소년 연령에서 고혈압의 변화를 살펴보고 그 중 신성 고혈압과 신 혈관성 고혈압을 중점적으로 논하고자 한다.