Ultrafiltration and solute kinetics using low sodium peritoneal dialysate.

Low sodium peritoneal dialysate has been reported to enhance sodium loss and alleviate signs of fluid overload in continuous ambulatory peritoneal dialysis patients. To elucidate the mechanisms involved, we compared ultrafiltration and solute kinetics using low sodium dialysate (LNaD; 105 mEq/liter sodium, 2.5% glucose, 348 mOsm/liter), conventional dialysate with equal osmolality (CD1.5; 132 mEq/liter sodium, 1.5% glucose, 348 mOsm/liter) and conventional dialysate with equal glucose concentration (CD2.5; 132 mEq/liter sodium, 2.5% glucose, 403 mOsm/liter). A 2 liter, six hour exchange of each dialysate was performed on separate days in 10 chronic peritoneal dialysis patients. Transperitoneal solute diffusion was assessed by calculating the permeability-area product (PA) of the peritoneal membrane from the dependence of plasma and dialysate solute concentrations on tie. Net fluid removed using LNaD of 190 +/- 90 (SEM) ml was similar to that using CD2.5 (250 +/- 90 ml) but higher (P < 0.01) than that using CD1.5 (-200 +/- 60 ml). Sodium loss was higher using LNaD (72 +/- 11 mEq, P < 0.01) and CD2.5 (41 +/- 12 mEq, P < 0.05) than using CD1.5 (-18 +/- 8 mEq). Changes in plasma sodium concentration were small during each dwell and were not different among the study dialysates. PA values for urea (23.4 +/- 1.6 ml/min), creatinine (10.0 +/- 1.0 ml/min), and glucose (10.3 +/- 1.3 ml/min) were similar when determined in each dialysate. The PA value for sodium (7.6 +/- 1.5 ml/min) could only be accurately determined in LNaD. We conclude that: (1) net fluid removed is greater using LNaD than CD1.5 despite similar osmolalities because LNaD has a higher glucose concentration and glucose is a more effective osmotic solute than sodium; (2) sodium loss when using LNaD is enhanced by both diffusion and convection; and (3) sodium diffuses across the peritoneum slower than urea, creatinine and glucose. These data suggest that LNaD alleviates signs of fluid overload by increasing net fluid removal and enhancing sodium loss.

Atherosclerosis in chronic renal failure.

Atherosclerotic cardiovascular disease is a significant cause of morbidity and mortality in patients with chronic renal failure. It is unclear, however, if atherosclerosis in fact occurs at a higher incidence compared with the nonuremic population matched for age, hypertension, and diabetes mellitus or if it occurs at an accelerated rate following the onset of end-stage renal disease. The extent of true atherosclerotic lesions, versus clinically diagnosed "atherosclerosis," in patients with chronic renal failure is equally unclear. Potentially, the uremic state per se, the dialysis treatment, and factors unrelated to renal failure may participate in atherogenesis. The relative contribution of each of these factors is unknown. In this review, we discuss the pathology of "atherosclerotic" lesions in patients with chronic renal failure and the putative factors involved in atherogenesis in this population and describe the results of available studies examining the issue of accelerated atherosclerosis in uremia.

Chemical peritonitis secondary to intraperitoneal vancomycin.

Although previously reported in the literature, the existence of chemical peritonitis due to vancomycin in patients on peritoneal dialysis remains controversial. We report four similar episodes of sterile peritonitis in three patients receiving intraperitoneal (IP) vancomycin. The prior report implicated a change in the brand of vancomycin preparation, from Vancocin to Vancoled, as a contributing factor. We noted the occurrence of such episodes following a switch from Vancocin to a generic preparation from Abbott Laboratories. High-performance liquid chromatographic (HPLC) profiles of the three preparations show Vancocin to have a lower level of impurities than the other two; the presence of certain contaminants in the other brands may be contributing to the clinical difference observed. We conclude that chemical peritonitis due to IP vancomycin administration does occur, and that increased awareness of this entity could allow other cases to be identified.

Cardiac arrest after hypertonic citrate anticoagulation for chronic hemodialysis.

The use of regional citrate anticoagulation as an alternative to standard therapy in hemodialysis patients at risk for bleeding complications has been well described. Recently, a method using hypertonic citrate has been reported as being safe and efficacious, and having several advantages over the usual techniques. Two patients who suffered cardiac arrests after dialysis using hypertonic citrate are discussed. Both received anticoagulation as described in the literature, although the citrate infusion rate was lower than recommended. Electrocardiograms obtained during the first such session showed no change in the Q-Tc interval with initiation of the infusion in either patient. Both were noted to have cardiac arrest within 5 minutes of discontinuation of dialysis, without warning symptoms, following the second and fifteenth treatments, respectively. The initial rhythm of ventricular fibrillation did not respond to standard advanced cardiac life support therapy, and the patients were not successfully resuscitated until they received intravenous calcium. The authors postulate that the loss of positive calcium flux from the dialysate, in conjunction with circulating unmetabolized citrate, caused an electrolyte imbalance leading to the potentially fatal arrhythmia. Caution is recommended in using this method of regional anticoagulation.