Although chronic anticoagulation is commonly prescribed to prevent thrombosis and malfunction of hemodialysis tunneled cuffed catheters (TCC), there are only limited data regarding its efficacy. The aim of this prospective study was to evaluate whether anticoagulation with adjusted-dose warfarin targeting an international normalized ratio (INR) of 1.5-2.0 is associated with improved catheter outcome in long-term patients at high risk of TCC malfunction. Among the 65 patients included in the study, 35 were considered at high risk (i.e., patients with a history of previous TCC thrombosis requiring catheter replacement and/or with TCC malfunction occurring within 2 weeks after catheter insertion in the absence of mechanical problems) and were prescribed warfarin, whereas 30 low-risk patients did not receive anticoagulation. During follow-up, TCC malfunction, defined as the need for inversion of catheter lines and/or recombinant tissue-type plasminogen activator infusion, was observed in 61.5% of patients. Among patients receiving warfarin, 19 (54.3%) achieved adequate anticoagulation (i.e., > 80% of follow-up INR values and INR value at the time of malfunction within target range). Anticoagulation was considered inadequate in 16 patients (45.7%). Malfunction-free catheter survival at 9 months was 47.1% in patients with adequate anticoagulation compared with 8.1% in patients with inadequate anticoagulation (p = 0.01). This difference remained statistically significant after adjustment for aspirin intake. These results suggest that achieving adequate anticoagulation with target INR 1.5-2.0 may prevent TCC malfunction and improve catheter outcome.

A 44 year old woman on hemodialysis presented a sudden cardiorespiratory arrest at the end of an otherwise uneventful dialysis session. It occurred while disconnecting the circuit from her tunneled catheter. She was reanimated and then transferred to the intensive care unit; the endotracheal intubation had been difficult, and she had been severely hypoxic. It was noted that the external venous clamp of the tunneled catheter was broken and the hypothesis of a break during the reanimation process was entertained. The routine chest x-ray postintubation showed that the tip of the catheter was ruptured and visible in one branch of the right pulmonary artery. The catheter was changed over a guide wire, and the broken catheter was sent for analysis to the manufacturer. A selective angiography of the right pulmonary artery was performed with the purpose of removing the fractured catheter tip but was unsuccessful. The patient recovered neurologic function slowly over the next 4 months. The exact etiology of the arrest remains incompletely understood; it is unknown whether it was caused by the catheter tip embolization or if an air embolism occurred.

Background/Aims: Studies have proposed various polymorphisms of genes implicated in the physiopathology of chronic kidney disease as risk factors of progression and potential clinical tools. We sought to validate and simultaneously compare their predictive value in a prospective cohort of chronic glomerulopathies receiving recommended antihypertensive and antiproteinuric therapies. Methods: Using PubMed, we identified 9 polymorphisms previously associated with progression. These were mostly of the renin-angiotensin-aldosterone and inflammation pathways: MCP-1 A2518G, TGF-β₁ T869C and C-509T, ACE I/D, AGT M235T, AT₁R A1166C, TSC-22 A-396G, eNOS 4b/a and CYP11β₂ C-344T. We hypothesized that their determination would identify individuals at higher risk of progression. Results: We recruited 93 predominantly male and Caucasian patients with a mean age of 63 and baseline eGFR of 33 ml/min/1.73 m² followed prospectively over a median of 36 months. 61% of patients had diabetic nephropathy, almost all received RAA blockade (90%) and none immunosuppressive therapy. The average blood pressure during follow-up was 140/72 mm Hg, the urinary protein to creatinine ratio 0.15 g/mmol and the rate of renal function decline –3.2 ± 4.1 ml/min/1.73 m²/year. Proteinuria and blood pressure strongly predicted progression. However, under recommended therapy, none of the proposed polymorphisms predicted renal function decline. In addition, none showed simple or partial correlations with the severity of proteinuria or blood pressure. Finally, summation variable of risk polymorphisms did not predict progression. Conclusion: This study does not validate the use of these 9 polymorphisms as individual clinical tools in patients with chronic glomerulopathies on recommended antihypertensive and antiproteinuric therapies.