Search

Background Low birth weight (LBW)/prematurity have been proposed as risk factors for the development of kidney disease in adulthood. Whether there is an association between LBW/prematurity and poor renal outcomes in childhood onset nephrotic syndrome remains unknown. Methods Children with nephrotic syndrome diagnosed between 1 and 18 years of age were followed prospectively from 1996 to 2016 at The Hospital for Sick Children (N = 377). LBW/prematurity was defined as birth weight < 2500 g or gestational age < 36 weeks. Normal birth weight (NBW) was defined as birth weight [greater than or equal to] 2500 g. Measures evaluating clinical course of nephrotic syndrome include initial steroid-resistant nephrotic syndrome (SRNS), time to first relapse, and frequently relapsing nephrotic syndrome. Kaplan-Meier survival analysis, logistic regression, and Cox proportional hazards regression were used to determine the association of LBW/prematurity with clinical outcomes. Results Median birth weights in LBW/premature (n = 46) and NBW (n = 331) children were 2098 g (interquartile range [IQR] 1700-2325 g) and 3317 g (IQR 2977-3685 g), respectively. Odds of having SRNS were 3.78 (95% confidence interval [CI] 1.28-11.21) times higher among LBW/premature children than NBW children. An 8% decrease in odds of developing SRNS was observed for every 100 g increase in birth weight (adjusted odds ratio [OR] 0.92; 95% CI 0.86-0.98). Median time to first relapse did not differ (hazard ratio [HR] 0.89; 95% CI 0.53-1.16). Conclusions LBW/premature children were more likely to develop SRNS but did not have a difference in time to first relapse with NBW children. Understanding the impact and mechanism of birth weight and steroid-resistant disease needs further study., Author(s): Natalia Konstantelos [sup.1] [sup.2] , Tonny Banh [sup.1] , Viral Patel [sup.2] , Jovanka Vasilevska-Ristovska [sup.1] , Karlota Borges [sup.1] , Neesha Hussain-Shamsy [sup.2] , Damien Noone [sup.2] [sup.3] [...]

Byline: David Raveh (1,3), Ovadia Shemesh (1), Yaakov Jack Ashkenazi (1), Robert Winkler (1), Vivian Barak (2) Keywords: Nephrotic syndrome; Tumor necrosis factor-[alpha] Abstract: We report a 13-year-old boy with refractory nephrotic syndrome (minimal change with mesangial proliferation) who failed the standard treatment protocols. There was some temporary response to large steroid doses, but even the Mendoza protocol could not induce remission. We show suppression of the proteinuria with Infliximab (Remicade) with tapering of steroids. Serial serum levels of tumor necrosis factor (TNF)-[alpha] are shown and discussed. We suggest studying the TNF-[alpha] blocking agents as optional treatment for nephrotic syndrome. Author Affiliation: (1) Division of Internal Medicine, Shaare Zedek Medical Center, Jerusalem, Israel (2) Immunology Laboratory, Oncology Department, Hadassah Medical Center, Jerusalem, Israel (3) Infectious Disease Unit, Shaare Zedek Medical Center, Jerusalem, Israel Article History: Registration Date: 18/06/2004 Received Date: 08/04/2003 Accepted Date: 12/05/2004 Online Date: 25/08/2004 Article note: Editorial comment Before the decision was made to accept this report for publication, it was carefully considered by both medical and ethical experts with special regard for the acknowledged relationship between the patient and one of the treating physicians. We believe that this "hypothesis paper" may be of interest to our readership.

Byline: M. I. Lilova (1), I. G. Velkovski (2), I. B. Topalov (3) Keywords: Key wordsaThromboembolic complications; Nephrotic syndrome; Treatment; Outcome; Prophylaxis Abstract: Over a period of 22 years, 447 children with nephrotic syndrome (NS) have been retrospectively studied for clinically apparent thromboembolic complications (TEC). The incidence of TEC is 2% (9/447) 16 clinically apparent TEC were registered in 9 children. The incidence of TEC was 1.5% among patients with steroid-sensitive NS and 3.8% among those with steroid-resistant NS. TEC were predominantly venous (81% venous vs. 19% arterial). The most commonly affected vessels were deep leg veins, followed by inferior vena cava (IVC). Rare locations of TEC were also observed -- superior vena cava (SVC), mesenteric artery, IVC, and hepatic veins with the development of Budd-Chiari syndrome Depending on the location of the TEC, imaging techniques used were: X-ray, computed tomography, and Doppler sonography. The major iatrogenic risk factor was furosemide, administered to 7 of the 9 children with TEC. In some patients additional predisposing factors were infections, dehydration, trauma, venepuncture, and immobilization. Treatment with heparin was followed by oral anticoagulation. Fibrinolytic therapy was effective in 3 of 4 patients. No new TEC occurred under oral anticoagulant prophylaxis. The outcome was a full recovery in 6 patients and a partial recovery in 1 patient. Two children died -- 1 with SVC thrombosis and the other with recurrent TEC affecting cerebral vessels. Although rare, TEC are among the most serious life-threatening complications in children with NS and require intensive care. Author Affiliation: (1) University Children&apos;s Hospital, Clinic of Pediatric Nephrology, 11 "D. Nestorov," 1606 Sofia, Bulgaria e-mail: lilovsk@phys.uni-sofia.bg Tel.: +359-2-542347, BG (2) National Center for Cardiovascular Diseases and Cardiac Surgery, Clinic of Pediatric Cardiology, Sofia, Bulgaria, BG (3) Military Medical Institute, Clinic of Cardiovascular Surgery, Sofia, Bulgaria, BG Article note: Received: 11 February 1999 / Revised: 26 October 1999 / Accepted: 26 October 1999