End-stage kidney disease due to haemolytic uraemic syndrome - outcomes in 241 consecutive ANZDATA Registry cases

Extent: 11p.Background: The aim of this study was to investigate the characteristics and outcomes of patients receiving renal replacement therapy for end-stage kidney disease (ESKD) secondary to haemolytic uraemic syndrome (HUS). Methods: The study included all patients with ESKD who commenced renal replacement therapy in Australia and New Zealand between 15/5/1963 and 31/12/2010, using data from the ANZDATA Registry. HUS ESKD patients were compared with matched controls with an alternative primary renal disease using propensity scores based on age, gender and treatment era. Results: Of the 58422 patients included in the study, 241 (0.4%) had ESKD secondary to HUS. HUS ESKD was independently associated with younger age, female gender and European race. Compared with matched controls, HUS ESKD was not associated with mortality on renal replacement therapy (adjusted hazard ratio [HR] 1.14, 95% CI 0.87-1.50, p = 0.34) or dialysis (HR 1.34, 95% CI 0.93-1.93, p = 0.12), but did independently predict recovery of renal function (HR 54.01, 95% CI 1.45-11.1, p = 0.008). 130 (54%) HUS patients received 166 renal allografts. Overall renal allograft survival rates were significantly lower for patients with HUS ESKD at 1 year (73% vs 91%), 5 years (62% vs 85%) and 10 years (49% vs 73%). HUS ESKD was an independent predictor of renal allograft failure (HR 2.59, 95% CI 1.70-3.95, p < 0.001). Sixteen (12%) HUS patients experienced failure of 22 renal allografts due to recurrent HUS. HUS ESKD was not independently associated with the risk of death following renal transplantation (HR 0.92, 95% CI 0.35-2.44, p = 0.87). Conclusions: HUS is an uncommon cause of ESKD, which is associated with comparable patient survival on dialysis, an increased probability of renal function recovery, comparable patient survival post-renal transplant and a heightened risk of renal transplant graft failure compared with matched ESKD controls.Wen Tang, Janaki Mohandas, Stephen P McDonald, Carmel M Hawley, Sunil V Badve, Neil Boudville, Fiona G Brown, Philip A Clayton, Kathryn J Wiggins, Kym M Bannister, Scott B Campbell and David W Johnso

Long-term follow-up of children with vesicoureteral reflux with and without antibiotic prophylaxis

The aim of the present study was to obtain data on the outcome of children with persistent vesicoureteral reflux (VUR) after cessation of antibiotic prophylaxis. Children with VUR who had been on antibiotic prophylaxis for at least 2 y and were free of urinary tract infections (UTI), had normal voiding patterns, and no hydronephrosis or new kidney scarring, had antibiotic prophylaxis discontinued, were followed up prospectively with urine cultures, voiding cystourethrography, and technecium-99m dimercaptosuccinate renal scintigraphy. The findings were compared with those of the same patients while they were on antibiotic prophylaxis. In 54 children (39 girls and 15 boys), antibiotic prophylaxis was discontinued. The mean follow-up time on and off antibiotic prophylaxis was 4.4±2.1 and 4.4±2.2 y, respectively. Nine UTI episodes occurred during the on- and 8 during the off-prophylaxis period. In 80 of 96 and in 68 of 74 ureters the reflux resolved or downgraded during the on- and off-prophylaxis periods, respectively. No new scar lesions were detected in any of the children. In conclusion, in children with persistent VUR and certain characteristics, antibiotic prophylaxis can be safely discontinued. © 2005 Taylor &amp; Francis

Delayed Administration of Pyroglutamate Helix B Surface Peptide (pHBSP), a Novel Nonerythropoietic Analog of Erythropoietin, Attenuates Acute Kidney Injury

In preclinical studies, erythropoietin (EPO) reduces ischemia-reperfusion–associated tissue injury (for example, stroke, myocardial infarction, acute kidney injury, hemorrhagic shock and liver ischemia). It has been proposed that the erythropoietic effects of EPO are mediated by the classic EPO receptor homodimer, whereas the tissue-protective effects are mediated by a hetero-complex between the EPO receptor monomer and the β-common receptor (termed “tissue-protective receptor”). Here, we investigate the effects of a novel, selective-ligand of the tissue-protective receptor (pyroglutamate helix B surface peptide [pHBSP]) in a rodent model of acute kidney injury/dysfunction. Administration of pHBSP (10 μg/kg intraperitoneally [i.p.] 6 h into reperfusion) or EPO (1,000 IU/kg i.p. 4 h into reperfusion) to rats subjected to 30 min ischemia and 48 h reperfusion resulted in significant attenuation of renal and tubular dysfunction. Both pHBSP and EPO enhanced the phosphorylation of Akt (activation) and glycogen synthase kinase 3β (inhibition) in the rat kidney after ischemia-reperfusion, resulting in prevention of the activation of nuclear factor-κB (reduction in nuclear translocation of p65). Interestingly, the phosphorylation of endothelial nitric oxide synthase was enhanced by EPO and, to a much lesser extent, by pHBSP, suggesting that the signaling pathways activated by EPO and pHBSP may not be identical