Une traduction en français de ce résumé figure à la fin de l'article. Al final del artículo se facilita una traducción al español. املقالة. لهذه الكامل النص نهاية يف الخالصة لهذه العربية الرتجمة
♦ BACKGROUND: There are no large studies that have examined ultra-short break-in period with a blind, bedside, midline approach to Tenckhoff catheter insertion. ♦ METHODS: Observational cohort study of 245 consecutive adult patients who underwent percutaneous catheter insertion for chronic peritoneal dialysis (PD) at our center from January 2009 to December 2013. There were 132 (53.9%) diabetics and 113 (46.1%) non-diabetics in the cohort. ♦ RESULTS: The mean break-in period for the percutaneous group was 2.68 ± 2.6 days. There were significantly more males among the diabetics (103 [78%] vs 66 [58.4%], p = 0.001). Diabetics had a significantly higher body mass index (BMI) (23.9 ± 3.7 kg/m vs 22.2 ± 4 kg/m, p < 0.001) and lower serum albumin (33.1 ± 6.3 g/L vs 37 ± 6 g/L, p < 0.001) compared with non-diabetics. Poor catheter outflow was present in 6 (4.5%) diabetics and 16 (14.2%) non-diabetics (p = 0.009). Catheter migration was also significantly more common in the non-diabetic group (11 [9.7%] vs 2 [1.5%], p = 0.004). Primary catheter non-function was present in 17(15%) of the non-diabetics and in 7(5.3%) of the diabetics (p = 0.01). There were no mortality or major non-procedural complications during the catheter insertions. Among patients with 1 year of follow-up data, catheter survival (93/102 [91.2%] vs 71/82 [86.6%], p = 0.32) and technique survival (93/102 [91.2%] vs 70/82 [85.4%], p = 0.22) at 1 year was comparable between diabetics and non-diabetics, respectively. ♦ CONCLUSIONS: Percutaneous catheter insertion by practicing nephrologists provides a short break-in period with very low mechanical and infective complications. Non-diabetic status emerged as a significant risk factor for primary catheter non-function presumed to be due to more patients with lower BMI and thus smaller abdominal cavities. This is the first report that systematically compares diabetic and non-diabetic patients.
A 44-year-old male presented to the emergency ward with chief complaints of recurrent episodes of generalized tonicclonic seizures for the past 5 h. He had a history of right-sided focal seizures 3 years ago, and on evaluation was found to have multiple infarcts in his brain. The patient had been taking the tablet sodium valproate 200 mg twice daily, with good compliance. On admission, he was drowsy and disoriented. Central nervous system examination did not reveal any focal neurological deficits. Other systemic examinations were unremarkable. His bladder was catheterized and his urine showed reddish-orange discoloration (Figure 1). The urinary catheter and the urine bag showed bright orange-colored deposits. Serum uric acid level was found to be 9.4 mg/dl on admission (normal cutoff being 3.5-7.2 mg/dl). His 24-h urine uric acid level was 1362 mg/day (normal cutoff being 250-750 mg/day). The urine pH was 5.5 and specific gravity was 1.030. Microscopic examination of urine revealed rosettes and rhomboid-shaped crystals of uric acid (Figure 2). His renal functions remained normal. The patient was adequately
Rifampicin is a widely used drug to treat tuberculosis and leprosy. Its toxicity is predominantly hepatic and immunoallergic in character. While hepatic toxicity is dose-related, the immunoallergic effects are unpredictable and usually associated with intermittent therapy. These immunoallergic effects may be minor (a cutaneous, gastrointestinal, or influenza-like syndrome) or major (hemolytic anemia, shock, or acute renal failure). Herein, we report a case of rifampicin allergy in a patient who was on intermittent once monthly rifampicin therapy for neuritic leprosy and was on his 4
th
month of treatment. Rifampicin exposure led to sudden shock and acute renal failure, which eventually required hemodialysis support. The patient made a complete recovery over the subsequent days and his renal function returned to normal over the next 3 weeks. He continues his multidrug therapy of leprosy without rifampicin.
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