Background and objectives An environmental trigger has been proposed as an inciting factor in the development of anti-GBM disease. This multicenter, observational study sought to define the national incidence of anti-GBM disease during an 11-year period (2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014) in Ireland, investigate clustering of cases in time and space, and assess the effect of spatial variability in incidence on outcome.Design, setting, participants, & measurements We ascertained cases by screening immunology laboratories for instances of positivity for anti-GBM antibody and the national renal histopathology registry for biopsy-proven cases. The population at risk was defined from national census data. We used a variable-window scan statistic to detect temporal clustering. A Bayesian spatial model was used to calculate standardized incidence ratios (SIRs) for each of the 26 counties.Results Seventy-nine cases were included. National incidence was 1.64 (95% confidence interval [95% CI], 0.82 to 3.35) per million population per year. A temporal cluster (n=10) was identified during a 3-month period; six cases were resident in four rural counties in the southeast. Spatial analysis revealed wide regional variation in SIRs and a cluster (n=7) in the northwest (SIR, 1.71; 95% CI, 1.02 to 3.06). There were 29 deaths and 57 cases of ESRD during a mean follow-up of 2.9 years. Greater distance from diagnosis site to treating center, stratified by median distance traveled, did not significantly affect patient (hazard ratio, 1.80; 95% CI, 0.87 to 3.77) or renal (hazard ratio, 0.76; 95% CI, 0.40 to 1.13) survival.Conclusions To our knowledge, this is the first study to report national incidence rates of anti-GBM disease and formally investigate patterns of incidence. Clustering of cases in time and space supports the hypothesis of an environmental trigger for disease onset. The substantial variability in regional incidence highlights the need for comprehensive country-wide studies to improve our understanding of the etiology of anti-GBM disease.
♦ Background: The percutaneous Seldinger method of peritoneal dialysis catheter (PDC) insertion has gained favor over recent years whereas traditionally it was reserved for patients considered not fit for general anesthesia. This blind technique is believed to be less safe, and is hence avoided in patients with previous laparotomy incisions. Reports on the success of this method may therefore be criticized for selection bias. In those with no prior abdominal surgery the optimal method of insertion has not been established. ♦ Methods: We retrospectively reviewed the outcomes of first-time PDC placements comparing the percutaneous (group P) and surgical (group S) insertion techniques in patients without a history of previous abdominal surgery in a single center between January 2003 and June 2010. We assessed catheter survival at 3 and 12 months postinsertion and compared complication rates between the two groups. ♦ Results: A total of 63 percutaneous and 64 surgical catheter insertions were analyzed. No significant difference was noted in catheter survival rates between group P and group S (86.2% vs 80% at 3 months, p = 0.37; and 78.3% vs 71.2% at 12 months, p = 0.42 respectively). Early and overall peritonitis rates were similar (5% vs 5.3%; p = 1, and 3.5 vs 4.9 episodes per 100 patient-months; p = 0.13 for group P and group S respectively). There were also no significant differences between the two groups in exit site leaks (15.9% in group P vs 6.3% in group S; p = 0.15), poor initial drainage (9.5% in group P vs 10.9% in group S, p = 0.34) or secondary drainage failure (7.9% in group P vs 18.8% in group S, p = 0.09).
Colchicine is an approved agent in the management and prophylaxis of gout and familial Mediterranean fever but its therapeutic value is limited by its narrow therapeutic index. Multisystem toxicity is uncommonly reported; and is often associated with renal impairment and/or specific drug interactions. We report two cases of colchicine toxicity marked by severe neuromyopathy in a diabetic with stage 4 chronic kidney disease (CKD) and a renal transplant recipient. Both patients presented with diarrhea, acute on chronic kidney injury and progressive muscle weakness while on colchicine for several weeks or longer. In addition to kidney disease, risk factors for colchicine toxicity included maintenance therapy with simvastatin in the first patient and cyclosporine in the second. Creatine phosphokinase (CPK) was elevated in both cases at presentation and neurophysiologic studies showed a pattern of severe myopathy with axonal sensorimotor neuropathy. The first patient recovered from neurological weakness in a few weeks, but the second patient suffered an extraordinarily protracted and severe neuromuscular disability for a year. The two cases reinforce the need for extra vigilance in prescribing and monitoring colchicine therapy in renal patients with specific attention to drug interactions known to increase the risk of toxicity, thus avoiding such combinations in patients with renal impairment.
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