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Background: The hemodialysis (HD) population has a particularly high incidence of amputation, which is likely associated with decreased tissue oxygenation during HD. However, information about the risk factors leading to amputation in peritoneal dialysis (PD) patients is limited. Here, we have investigated the association between the use of hypertonic peritoneal dialysate (HPD) and subsequent amputation in PD patients., Methods: Based on the data from the Taiwan National Health Insurance research database, this observational cohort study enrolled 203 PD patients who had received HPD early during treatment and had not undergone amputation and 296 PD controls who had not undergone amputation. Subjects were followed through until the end of 2009 and the event rates of new non-traumatic amputation were compared between groups., Results: The incidence of amputation was 3 times higher for the HPD cohort than for the comparison cohort (23.68 vs. 8.01 per 1000 person-years). The hazard ratio (HR) for this group, estimated using a multivariable Cox model, was 2.48 (95% confidence interval [CI] = 1.06-5.79). The HR for patients with both diabetes and early adoption of HPD increased to 44.34 (95% CI = 5.51-357.03), compared to non-HPD non-diabetic PD controls., Conclusion: Early utilization of HPD in PD patients is associated with increasing risk of amputation; this risk considerably increases for those with concomitant diabetes.

Fleet enemas are hypertonic solutions with an osmotic action and a high concentration of phosphate. When retained in the human body they have a great toxic potential, causing severe hydro-electrolyte disorders in children, especially in newborns. We report the case of a previously healthy 8-day-old newborn who needed neonatal intensive care treatment after the inadvertent administration of an osmotically active hypertonic phosphate enema. Taking into account that phosphate removal by peritoneal dialysis (PD) strongly depends on total dialysate turnover, we chose continuous flow PD (CFPD) as the treatment option, with a successful outcome. Clinical experience with this dialytic modality is limited to a few case reports in pediatric and adult patients. To the best of our knowledge, we report here the first description of CFPD in the setting of acute phosphate nephropathy in the neonatal period. The modality of PD described here has potential as an alternative management option as it is a highly efficient, methodologically simple, and low-cost method without any need for sophisticated equipment. Physicians and parents should be aware of the adverse effects of a hypertonic phosphate enema and should never use these medications in infants and newborns.

Unlabelled: Sclerosing encapsulating peritonitis secondary to peritoneal dialysis has been associated to acetate-containing dialysis fluids, hypertonic glucose and disinfectants. Physiopathologic mechanisms of fibrotic proliferation that implicate those agents are not totally explained. With an experimental approach using cultured peritoneal fibroblasts, we have studied intracellular pH changes and Na+/H+ antiporter activity under cells perfusion with peritoneal dialysis liquids containing acetate, lactate, hypertonic glucose and interleukin-1. All experiments were performed at extracellular pH 7.4 and physiologic HCO3/CO2 concentration., Results: 35 mM acetate produced a huge intracellular acidosis (ipH = 6.80 +/- 0.08). Lactate effect was less important (6.95 +/- 0.07), with a slow ipH recovery in about 30 min in both cases. IL-1, 10(-6) M also reduced ipH to 7.10 +/- 0.03. Acidosis was linked to Ca2+ outflow via Ca/H exchange and was blocked with Cd 20 nM. Extracellular Na = 0 and amiloride totally inhibited ipH recovery after acetate, lactate, or interleukin-induced acidosis. Hypertonic glucose perfusion increased ipH (7.31 +/- 0.06) for 5-7 min. This increase was also inhibited by amiloride or extracellular Na absence. Na+/H+ exchanger activity increased to 58%, and kept activated after ipH recovery. In conclusion, acetate, hypertonic glucose and IL-1 showed the common effect of stimulating the sodium-proton exchanger by different mechanisms, giving a possibility of potentiation. Activated Na+/H+ exchanger may act as a signal-transduction increasing fibroblast proliferation and explaining the cellular mechanism of sclerosing peritonitis.

Objective: Chronic peritoneal dialysis (PD) may eventually result in vascular alterations of varying degree, which lead to progressive reduction in dialytic efficacy. Although the pathogenesis has not been elucidated yet, vascular endothelial growth factor (VEGF) has been proposed to play a central role in the process leading to vascular alterations., Design: Rats were allocated to three groups: no treatment, intraperitoneal introduction of hypertonic PD solution alone, and intraperitoneal introduction of hypertonic PD solution plus octreotide. After 4 weeks, a 1-hour peritoneal equilibration test (PET) was performed. Dialysate-to-plasma urea ratio (D/P urea), glucose reabsorption (D1/D0 glucose), ultrafiltration volume (UF), and levels of dialysate protein and VEGF were determined. Peritoneal membrane histology was evaluated by light microscopy., Results: Compared with the control group, rats treated with hypertonic PD solution showed dramatically deranged peritoneal function tests (UF: 5.8 +/- 0.9 mL vs 1.3 +/- 0.6 mL; D/P urea: 0.49 +/- 0.1 vs 0.74 +/- 0.04; D1/D0 glucose: 0.55 +/- 0.05 vs 0.34 +/- 0.06) and morphology (thickness: 4.6 +/- 0.4 mu vs 62 +/- 12 mu; neovascularisation: 0.1 +/- 0.3 vessels per field vs 2.2 +/- 0.3 vessels per field). Similarly, a higher level of VEGF was found in the rats treated with hypertonic PD solution. In rats treated with hypertonic solution plus octreotide, peritoneal thickness was not completely reduced (25 +/- 5 mu), but peritoneal functions were protected (UF: 4.0 +/- 0.5 mL; D/P urea: 0.58 +/- 0.02; D1/D0 glucose: 0.51 +/- 0.02). Moreover, VEGF level and neoangiogenesis were significantly less in the octreotide group than in the group treated with hypertonic dextrose alone., Conclusion: Our data document that, by increasing the production of VEGF, a high glucose concentration can cause vascular alterations within the peritoneal membrane. Octreotide can protect against the vascular alterations and preserve peritoneal function by inhibiting overexpression of VEGF and regulating the inflammatory response in the peritoneum.

Peritoneal equilibration test (PET) employing a 2.27%/2.5% glucose exchange is the most widely used method of to evaluating peritoneal function and small solute transport. Hypertonic (3.86%/4.25% glucose) PET has been recently recommended for the evaluation of ultrafiltration and to study certain causes of ultrafiltration failure, such as aquaporin dysfunction, through the analysis of dialysate sodium. However, there is not enough information on the optimal way to express the changes in dialysate sodium concentration, the normal range of values for this parameter, and possible adverse effects of hypertonic PET in the general population of peritoneal dialysis patients. A hypertonic PET was performed in 22 patients. Ultrafiltration failure (ultrafiltration < 0.4 L) was present in seven patients. Patients with ultrafiltration failure had higher small solute peritoneal transport and dialysate sodium concentration and had been treated with peritoneal dialysis for longer periods of time. Dialysate sodium concentration at 60 and 240 minutes was directly correlated with small solute peritoneal transport calculated as D/PCr240 (r = 0.74, p = 0.0008 y r = 0.84, p < 0.0001) and inversely correlated with ultrafiltration (r = 0.64, p = 0.0016 y r = 0.72, p = 0.0002). An absence of a dip in dialysis sodium, suggestive of aquaporin dysfunction, was only observed in one patient with a high-average small solute peritoneal transport. Dialysate sodium concentration at 60 minutes is a better discriminator between ultrafiltration failure patients than parameters such as D/PNa or the absolute dip in dialysate sodium with respect to time zero. We observed the following adverse effects: symptomatic hypotension in 2 patients with preserved ultrafiltration. In conclusion, hypertonic PET allows to confirm the diagnosis of ultrafiltration failure, but monitoring dialysate sodium concentration offers additional information only in patients with severe aquaporin dysfunction. Hypertonic PET may have adverse effects in patients without ultrafiltration failure.

Previous in vitro studies have revealed that the currently used peritoneal dialysis fluids (PDFs) inhibit several functions of phagocytic cells. Glucose-mediated hypertonicity was demonstrated to be one of the major detrimental factors. To investigate the clinical relevance of these in vitro findings, we compared the in vivo effect of a PDF with 3.86% glucose (D386) and a PDF containing 1.36% of glucose (D136) on peritoneal macrophage (PMO) function in eight CCPD patients. In a randomized cross-over setting, each patient used exclusively D136 or D386 on day one. The next day the patients who used D136 were switched to D386 and vice versa. PMO were isolated from the effluents and studied for their phagocytic capacity and chemiluminescence response. PMOs obtained from D386 effluents were significantly less phagocytic as compared to PMOs obtained after the in vivo use of D136 (38 +/- 7.1 vs 63 +/- 8.3%, p less than 0.02). In addition PMOs exposed to D386 were less able to mount a respiratory burst (peak response 4 +/- 1.0 vs 15 +/- 1.4% of control cells, p less than 0.05). Thus, the in vivo use of D386 was accompanied by significantly decreased PMO functions. These findings further stress the need to search for alternative solutions that do not rely on glucose-mediated hypertonicity for ultrafiltration.