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One of the major goals in investigating children with urinary tract infection (UTI) is to recognize patients at risk of further UTI-related problems. This study reports the clinical features of 19 pediatric patients with UTIs in whom associated hepatic and/or pulmonary nodules were incidentally diagnosed by the imaging tests performed for the UTI. Hepatic nodules in five patients were detected on ultrasound scans, and pulmonary nodules and both hepatic and pulmonary nodules were detected in 12 and two children by dimercaptosuccinic acid scintigraphy. The mean age of the patients was 24.5 months. Vesicoureteral reflux (VUR) was detected in nine of 17 patients (52.9%), acute pyelonephritis was identified in nine of 18 patients, and renal scarring was found in 57.1% patients with pyelonephritis. On follow-up, the hepatic and/or pulmonary nodules regressed in all patients. About 85.7% of patients experienced a recurrence of UTI within 1 year. In comparison with age- and sex-matched controls with UTIs without pulmonary or hepatic nodules, the presence of VUR and the recurrence of UTI within 1 year were higher in patients with UTIs and nodules (P

The renin-angiotensin system plays an important role in renal growth and development. Exposure of the neonate to angiotensin converting enzyme (ACE) inhibitors increases mortality and results in growth retardation and abnormal renal development. It has been demonstrated that ACE inhibition in the developing kidney reduces the renal expression of growth factors, which may account for renal growth impairment. This study was designed to investigate the relationship between renal growth impairment and the expression of transforming growth factor-beta1 (TGF-beta1), TGF-beta receptor I [TbetaRI, activin-like kinase (ALK)-1 and ALK-5], and TGF-beta receptor II (TbetaRII). Newborn rat pups were treated with enalapril (30 mg/kg per day) or vehicle for 7 days, and kidneys were removed for Western blotting of TGF-beta1, ALK-1, ALK-5, and TbetaRII, and for RT-PCR of ALK-5 and TbetaRII. TGF-beta1, ALK-1, ALK-5, and TbetaRII were also detected by immunohistochemistry. Enalapril treatment resulted in an increased mortality (30.4%) by day 7, and reduced body weight and kidney weight ( P

Sirs, Sjogren’s syndrome is very rare in children. Here, we introduce the reader to a case of primary Sjogren’s syndrome (pSS) with mesangial proliferative glomerulonephritis and IgA deposits, an uncommon renal manifestation in boys. Although we thought his prognosis was not good, his response to steroid therapy was good regarding renal problems of pSS. An 11-year-old boy was admitted to the hospital for intermittent gross hematuria and mild proteinuria, which he had had for the past year. He complained of dry eyes and dry mouth, and this had been aggravated 6 months previously. He had no family history of any kidney disease or autoimmune disease. The vital signs were stable and the physical examination revealed no abnormalities, including the lack of parotid gland swelling. Laboratory findings were as follows: hemoglobin 12.2 g/dL, white blood cell count 7,100/μL, platelet count 327,000/μL, blood urea nitrogen (BUN) 10 mg/dL, creatinine 0.7 mg/dL, C3 134 mg/dL, C4 15.4 mg/dL, C1q 15.5 mg/dL, CH50 46.2 U/mL, IgA 196 mg/dL, IgG 1,230 mg/dL, and IgM 71.9 mg/dL. The blood gas results showed mild metabolic acidosis. The electrolytes, liver function tests, protein, albumin, antineutrophil antibody, and the glomerular filtration rate were also unremarkable. The cryoglobulin and anti-Ro/ SSA Ab tests were remarkably positive. Urine analysis showed microscopic hematuria (RBC > 60/high power field) and the 24-h urine protein was 154.9 mg/day. The radiological findings, including abdominal ultrasound, a Tc-dimercaptosuccinic acid scan and intravenous pyelography, were unremarkable. Ophthalmological consultation showed a positive Schirmer’s test, and distal renal tubular acidosis (RTA) was detected by a bicarbonate loading test. A diagnosis of pSS was made on the basis of the xerostomia, the xerophthalmia, the positive Schirmer test and the positive tests for anti-RO/SSA Ab. He underwent a kidney biopsy under local anesthesia. On the conventional light microscopy biopsy, our patient’s specimen showed increased mesangial cellularity (Fig. 1). On immunofluorescence microscopy, IgA (1+) deposits were seen in the mesangial regions. He was started on oral steroid (Deflazacort 1 mg/kg) and artificial tears. After 4 months, the patient’s hematuria and cryoglobulinemia subsided, yet the anti-RO/SSA Ab was still positive. The characteristic histological features of the kidney in patients with pSS are chronic interstitial nephritis with a diffuse or focal plasmacytoid lymphocytic infiltration. In addition, it has been reported that a few patients with pSS display glomerulonephritis (GN), including membranous nephropathy, membranoproliferative GN or mesangial proliferative GN. It has been reported that the glomerular lesions in pSS are related to systemic lupus erythematosus or combined cryoglobulinemia [1]. The pathogenesis of glomerular lesions remains unclear, yet circulating immune complex deposits might be an important factor. Our patient also had cryoglobulinemia and we can strongly suggest that it might have been related to GN. Regarding the clinical and biochemical manifestations and the immune abnormalities between the interstitial S. K. Jung :K. H. Park :H. E. Yim :K. H. Yoo (*) : Y. S. Hong : J. W. Lee Department of Pediatrics, Guro Hospital, Korea University Medical Center, #80, Guro-Dong, Guro-Gu, Seoul 152-703, Korea e-mail: guroped@korea.ac.kr

Here, we report on a boy with acute tubulointerstitial nephritis (ATIN), who developed it following ingestion of Chlorella tablets as a food supplement. He was incidentally detected to have glucosuria, proteinuria, and leukocyturia during school mass screening. He had had a history of ingestion of Chlorella tablets for 3 months. Laboratory studies showed anemia, increased levels of creatinine, decreased glomerular filtration rate (GFR), hypokalemia, hypo-uricemia, hypophosphatemia, hypergammaglobulinemia, proteinuria, leukocyturia, and glucosuria. ATIN was diagnosed by renal biopsy. The patient's renal function improved after initiation of corticosteroid therapy and discontinuation of Chlorella for 6 months. Chlorella may be a causative allergen inducing tubulointerstitial injury in kidney.