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A thrombosed dialysis access can be declotted either through an open surgical procedure or a percutaneous one. In choosing how the access should be managed, a nephrologist should balance the experience and outcomes of local providers to ensure the efficient and safe salvage of the vascular access. Percutaneous procedures often offer less disruption to the schedule of the patient and dialysis clinic, give more information about the central vasculature, are less invasive, and ultimately are preferred. Nephrologist should encourage local vascular surgeons and interventional radiologists to become proficient in these procedures to avoid unnecessary open cases., (© 2016 Wiley Periodicals, Inc.)

While nontuberculous mycobacterial peritonitis is uncommon among peritoneal dialysis (PD) patients, these infections have serious consequences. They present a significant diagnostic and therapeutic challenge for clinicians. Diagnosis can be delayed due to the slow growth rate of some mycobacterial species. These organisms can also be overlooked when adequate culture media are not used in the microbiological evaluation process. The choice of antimicrobial therapy depends upon isolation and speciation of the infecting Mycobacterium species, and prompt catheter removal is essential. Because serious intra-abdominal complications may follow infection, identifying patient risk factors for nontuberculous mycobacterial peritonitis and initiating prompt diagnosis and treatment are essential. We report three cases of peritonitis associated with Mycobacterium chelonae and Mycobacterium gordonae, each with a unique presentation, and discuss the appropriate diagnosis and treatment strategies for the management of PD-associated mycobacterial infections.

Intravenous iron therapy is instrumental in the management of anemia in patients with end-stage renal disease (ESRD). Iron is available in several different preparations, with slight differences in the pharmacology of each. Given the importance of intravenous iron in the management of these patients, clinicians should be aware of the potential risks associated with it. Intravenous iron has effects on host immunity that raise concerns about clinical infection risk. Iron preparations appear to increase oxidative stress in these patients, which has important implications for cardiovascular disease states. Lastly, the effects of intravenous iron on liver disease are largely unknown.

Aim: In patients with end-stage renal disease (ESRD), hyperphosphataemia and an elevated calcium-phosphorus (Ca-P) product contribute to morbidity and mortality. Suggested target goals for serum phosphorus concentration and calcium-phosphorus product have recently been lowered. As a result, long-term comparative studies of the efficacy of phosphate binders are critical. This study compares the long-term efficacy of sevelamer hydrochloride to calcium-containing binders (CCB)., Methods: A retrospective chart review was conducted in 30 patients receiving sevelamer hydrochloride for >1 years and 25 patients receiving CCB., Results: Patients on sevelamer hydrochloride had lower serum bicarbonate concentration than those on CCB, 18.6 +/- 2.7 versus 20.3 +/- 1.8 mmol/L (P = 0.0017). Serum phosphorus concentration was higher in patients on sevelamer hydrochloride compared to CCB 2.10 +/- 0.87 versus 1.74 +/- 0.28 mmol/L (P = 0.0013), as was the Ca-P product 4.97 +/- 0.94 mmol2L2 (62.1 +/- 11.8 mg2/dL2) versus 3.97 +/- 1.18 mmol2/L2 (49.7 +/- 14.7 mg2/dL2), P = 0.0009). Only 36% of patients on sevelamer hydrochloride compared with 68% on CCB (P = 0.015) met the serum phosphorus goal of < or =1.78 mmol/L., Conclusion: Patients on sevelamer hydrochloride for >1 years compared to those on CCB had a lower serum bicarbonate concentration, a higher serum phosphorus concentration and a higher Ca-P product. Clinicians should balance the increase in calcium load with CCB versus the cost and effectiveness of sevelamer hydrochloride in choosing a phosphate binder for ESRD patients.

Background: Intravenous (i.v.) iron is employed to treat absolute and relative iron deficiency in end-stage renal disease patients. However, there exists the possibility that i.v. iron increases infection risk. This pilot study examines whether i.v. iron gluconate acutely increases tunnelled haemodialysis catheter colonization, microbial growth, or blood-borne infection., Methods: Nineteen patients with haemodialysis catheters who met criteria to receive an i.v. iron load entered the study. Six matched patients with catheters who did not receive iron were controls. Blood aspirated from the catheter prior to initiation of haemodialysis was sent for qualitative/quantitative cultures. The study consisted of three baseline cultures, five cultures during iron (125 mg of ferric gluconate per treatment), and three cultures following iron administration. Patients were monitored for infection for 30 days following iron., Results: Fifteen iron-treated patients and six controls completed the study. Thirty-three per cent of treated patients were colonized at baseline; 66% were colonized following iron. Thirty-three per cent of controls (2/6) were colonized at baseline; no new colonization developed during follow up. Neither treated patients nor controls had significant microbial growth within catheters; one patient in the iron-treated group developed candidaemia., Conclusion: Intravenous iron is not associated with acute microbial growth in catheters or clinical infection. However, a trend towards increased catheter colonization following iron administration exists.

Oral iron is typically insufficient for the iron deficiency of hemodialysis patients. Intravenous (IV) iron is well tolerated by most patients and non-dextran-containing iron preparations are associated with few allergic reactions. However, there is the potential for an increased risk of infection with IV iron that appears to increase bacterial growth as well as inhibit the host's innate immune response to bacterial infection. Clinical studies suggest a link between iron therapy and infection. Practicing nephrologists should be aware of this issue, but should not hesitate to use IV iron in iron-deficient patients while avoiding the development of iron overload and administration of iron to patients who have active infection.

Sertraline has shown promise in the treatment of dialysis-associated hypotension (DAH) in a limited number of end-stage renal disease patients. We undertook a study to evaluate the effect of adding sertraline to other therapies for patients with documented DAH. We also measured the effect of sertraline on intradialytic haemodynamics. We used the ultrasound dilution technique (HD01 monitor) to measure cardiac output (CO), central blood volume (CBV) and peripheral vascular resistance (PVR) in these patients. The study was performed in two phases. Phase 1 was a control, while the second phase consisted of treatment with sertraline (50 mg/day). Cardiac output and central blood volume were measured 30 min following the initiation of dialysis and 30 min prior to the termination of dialysis. Blood pressure (BP) was monitored during haemodynamic measurements and throughout dialysis. Eighteen patients with documented DAH completed the study. Cardiac output, CBV and PVR were no different in the sertraline phase as compared with the control phase. The declines in systolic BP, diastolic BP and mean arterial pressures from pre-haemodialysis (HD) to lowest intradialytic and pre-HD to post-HD were not significantly different for the sertraline phase versus the control phase. In conclusion, it appears that sertraline has no additive effect on intradialytic haemodynamics to improve blood pressure in patients with DAH who are under therapy (with sodium modelling, cool dialysate and midodrine).