Advances in peritoneal dialysis. Conference on Peritoneal Dialysis最新文献

There is increasing evidence that long-term peritoneal dialysis (PD) is associated with structural changes in the peritoneal membrane. Inhibition of the renin-angiotensin system has been demonstrated to lessen peritoneal injury and to slow the decline in residual renal function. Whether spironolactone affects residual renal function in addition to the peritoneal membrane is unknown. We evaluated 23 patients (13 women) with a glomerular filtration rate of 2 mL/min/1.73 m2 or more who were receiving PD. Patients with an active infection or peritonitis episode were excluded. Baseline measurements were obtained for serum high-sensitivity C-reactive protein (hs-CRP), vascular endothelial growth factor (VEGF), transforming growth factor beta (TGF-beta), and connective tissue growth factor (CTGF); for daily ultrafiltration (in milliliters); for end-to-initial dialysate concentration of glucose (4/D0 glucose), Kt/V, and peritoneal transport status; and for dialysate cancer antigen 125 (CA125). Spironolactone therapy (25 mg) was given daily for 6 months, after which all measurements were repeated. Mean age of the patients was 46 +/- 13 years. Duration of PD was 15 +/- 21 months (range: 2-88 months). After spironolactone therapy, mean dialysate CA125 was significantly increased compared with baseline (20.52 +/- 12.06 U/mL vs. 24.44 +/- 13.97 U/mL, p = 0.028). Serum hs-CRP, VEGF, TGF-beta, CTGF, daily ultrafiltration, D/Do glucose, Kt/V and peritoneal transport status were similar at both times. At the end of the study period, residual glomerular filtration rate in the patients was lower. In PD patients, treatment with spironolactone seems to slow the decline of peritoneal function, suppress the elevation of profibrotic markers, and increase mesothelial cell mass.

Exaggerated postprandial increase in blood glucose has been postulated to be associated with cardiovascular injury. The concentration of blood glucose is altered by glucose absorption from peritoneal dialysis (PD) fluids. In PD patients, we used continuous blood glucose monitoring (CGM) to analyze diurnal variations in blood glucose. Diurnal blood glucose was determined in 10 diabetic PD patients who used CGM (iPro2: Medtronic, Northridge, CA, U.S.A.) for 3 days. Blood glucose concentrations before and after glycemic control were monitored in 5 patients. Correlations between CGM parameters [standard deviation of blood glucose (SDG)], peritoneal function [dialysate-to-plasma ratio of creatinine (D/P Cr) and end-to-initial dialysate (D/D0) glucose], 24-hour peritoneal glucose absorption, and glycemic index were determined. In 5 patients, CGM was performed again after adjustments to antidiabetic drugs. A large diurnal variation, especially at night, was observed in this patient cohort. No correlation of HbA1c with mean blood glucose concentration was observed. Although SDG had no association with 24-hour peritoneal glucose absorption, it did show an association with D/P Cr and D/D0 glucose. The SDG was significantly lower after treatment with a dipeptidyl peptidase IV inhibitor or an increase in insulin dose. Results of the present study indicate that diurnal variations in glucose depend on the speed of peritoneal glucose absorption rather than the net glucose absorption.

Glucose-based peritoneal dialysis (PD) solutions dilate the parietal and visceral peritoneal microvasculature by endothelium-dependent mechanisms that primarily involve hyperosmolality. This PD-mediated dilation occurs by active intracellular glucose uptake and adenosine Al receptor activation, and by hyperosmolality-stimulated glibenclamide-sensitive potassium channels. Both pathways invoke NO as a second messenger for vasodilation. We hypothesized that during crystalloid-induced osmosis, the osmotic water flux through the transendothelial water-exclusive aquaporin 1 (AQP1) channels is the primary mechanism whereby the endothelium is being stimulated to instigate hyperosmolality-driven vasodilation. Four microvascular levels (diameters in the range 6 - 100 microm) were visualized by intravital videomicroscopy of the terminal ileum in anesthetized rats. Microvascular diameters and flow were measured after topical exposure to a 5% hypertonic mannitol or 2.5% glucose-based PD solution, at baseline and after brief tissue pre-treatment (with 0.1% glutaraldehyde for 10 seconds) or after combined tissue pre-treatment and pharmacologic blockade of AQP1 with HgCl2 (100 micromol/L). Vascular endothelial integrity was verified by the response to acetylcholine (10(-4) mol/L) and sodium nitroprusside (10(-4) mol/L). The hyperosmolar solutions both caused rapid and sustained vasodilation at all microvascular levels, which was not altered by tissue pre-treatment. Inhibition of AQP1 completely abolished the mannitol-induced vasodilation and markedly attenuated the PD fluid-mediated vasodilation. Neither glutaraldehyde pre-treatment nor HgCl2 affected tissue integrity or endothelial cell function. We conclude that the peritoneal microvascular vasodilation caused by hyperosmolar PD fluid is instigated by the osmotic water flux through AQP1. Clinical PD solutions have components other than hyperosmolality that can induce endothelium-dependent peritoneal microvascular vasodilation independent of the AQP1-mediated osmosis.

Peritoneal dialysis (PD) solutions dilate microvessels by undefined mechanisms. This vasodilation directly affects ultrafiltration and solute exchange during a PD dwell and is thought to account for the variable mass transfer area coefficient for small solutes during a glucose-based hypertonic dwell. We hypothesized that PD-mediated vasodilation occurs by endothelium-dependent mechanisms that involve endothelium energy-dependent K+ channels (K(ATP)), adenosine A1 receptor activation, and NO release. We used intravital videomicroscopy to study 3 levels of microvessels (A1 inflow arterioles about 100 microm diameter to pre-capillary A3 arterioles 10 - 15 microm diameter) in the terminal ileum of anesthetized rats under control conditions in vivo in a tissue bath. Ileum was bathed with hypertonic mannitol or 2.5% glucose-based PD solution (Delflex: Fresenius Medical Care North America, Waltham, MA, U.S.A.) with or without topical application of individual or combined specific inhibitors of the endothelium-dependent dilation pathways.: NO (L-NMMA), prostaglandin I2 (mefenamic acid), endothelium hyperpolarizing factor (glibenclamide), and adenosine A1 receptor antagonist (DPCPX). The mannitol and PD solutions induced rapid and sustained peritoneal vasodilation whose magnitude depended on microvascular level and osmotic solute. Combined inhibition of endothelium-dependent dilation pathways completely abolished the mannitol-induced hyperosmolality-mediated dilation at all microvascular levels, but selectively eliminated the PD solution-mediated A3 dilation. The K(ATP) and adenosine receptor antagonists, individually or combined, remarkably attenuated dilation in the smaller pre-capillary arterioles; NO inhibition, alone or combined with K(ATP) and adenosine receptor antagonists, eliminated the PD solution-induced dilation. The cyclooxygenase pathway is not involved in PD-induced dilation. Solutions for PD dilate the visceral peritoneal microvasculature by endothelium-dependent mechanisms, primarily the NO pathway. Adenosine receptor-activated NO release and K(ATP) channel-mediated endothelium hyperpolarization significantly contribute to vasodilation in the smaller peritoneal pre-capillary arterioles.

Conventional automated peritoneal dialysis (APD) is prescribed as a repetition of the same dwell time and the same fill volume delivered by the cycler during the dialysis session. Nevertheless, it is well recognized that a cycle with a short dwell time and a small fill volume favors ultrafiltration (UF), while a cycle with a long dwell time and a large fill volume favors uremic toxin removal. The use of varied dwell times and dwell volumes, called adapted APD, allows for an optimized peritoneal dialysis prescription with better volume control--that is, both an increased UF volume at a lower metabolic cost [UF per gram of glucose absorbed (mL/g)] and increased dialytic sodium removal resulting in improved removal of uremic toxins (urea, creatinine, phosphate) during dialysis.

Studies have shown that a single-item question might be useful in identifying patients with limited health literacy. However, the utility of the approach has not been studied in patients receiving maintenance peritoneal dialysis (PD). We assessed health literacy in a cohort of 31 PD patients by administering the Rapid Estimate of Adult Literacy in Medicine (REALM) and a single-item health literacy (SHL) screening question "How confident are you filling out medical forms by yourself?" (Extremely, Quite a bit, Somewhat, A little bit, or Not at all). To determine the accuracy of the single-item question for detecting limited health literacy, we performed sensitivity and specificity analyses of the SHL and plotted the area under the receiver operating characteristic (AUROC) curve using the REALM as a reference standard. Using a cut-off of "Somewhat" or less confident, the sensitivity of the SHL for detecting limited health literacy was 80%, and the specificity was 88%. The positive likelihood ratio was 6.9. The SHL had an AUROC of 0.79 (95% confidence interval: 0.52 to 1.00). Our results show that the SHL could be effective in detecting limited health literacy in PD patients.

Patients with chronic kidney disease (CKD) experience serious adverse cardiovascular (CV) consequences. Cardiovascular disease is the leading cause of morbidity and mortality in patients with CKD, being secondary not only to an increased prevalence of traditional CV risk factors, but also to the presence of a wide array of nontraditional risk factors unique to patients with CKD. Pathogenesis includes both functional and structural alterations in the CV system. Those alterations give rise to a wide range of clinical CV syndromes, including ischemic heart disease, heart failure, and sudden cardiac arrest. As an increasingly prevalent disease, CKD, together with consequent CV disease, imparts major health and economic burdens to the community. In this review, we discuss traditional and nontraditional risk factors for CV disease, the pathogenesis of CV clinical syndromes, and prevention of CV syndromes in patients with CKD.

A recent study indicated that, compared with glycated hemoglobin (HbA1c), glycated albumin (GA) provides a more accurate assessment of glycemic control in diabetic patients on hemodialysis. However, the suitability of GA for this purpose in peritoneal dialysis (PD) patients is questionable. We measured blood glucose, GA, HbA1c, serum albumin, protein losses in urine and dialysate, protein catabolic rate, hemoglobin, and dose of erythropoiesis-stimulating agents in 71 PD patients [20 with diabetes (DM), 51 without DM]. In both DM and non-DM patients, blood glucose levels correlated significantly with HbA1c (r = 0.47, p < 0.001), but not with GA (r = 0.18, p = 0.19). In patients with high serum albumin (> 3.2 g/dL), blood glucose levels correlated significantly with GA (r = 0.32, p = 0.047). Further, low protein losses in urine and dialysate (< 5.9 g daily) also significantly correlated with GA (r = 0.37, p = 0.041). In PD patients, HbA1c is better than GA as an indicator of blood glucose levels. Glycated albumin can be used as an indicator of glycemic control in PD patients with normal serum albumin and low protein losses in urine and dialysate.

Urea clearance (Kt/V urea), adjusted for total body water (TBW) using the Watson formula (TBW(Watson)), is widely used to guide peritoneal dialysis (PD) prescription and to ensure dialysis adequacy. The impact of body composition on the determination of TBW(Watson) is well established, but the effect of hydration and nutrition status on TBW(Watson) is not understood. We therefore studied the effects of hydration and nutrition status on TBW(Watson) in PD patients. Our study enrolled 195 PD patients and 33 healthy control subjects. Multiple-frequency bioelectrical impedance spectroscopy (MF-BIS) was used to measure TBW and the result was compared with TBW(Watson). Patients were divided into three groups according to their degree of overhydration [deltahydration status (OH) in liters]: normally hydrated group (OH: < 2.0 L), mildly overhydrated group (OH: 2.0 - 4.0 L), and severely overhydrated group (OH: > 4.0 L). Compared with MF-BIS, the Watson formula overestimated TBW in normally hydrated patients, but underestimated TBW in severely overhydrated patients. In addition, of the normally hydrated patients, 22 were malnourished by subjective global assessment, and the TBW(Watson) overestimation was much greater in them than in the well-nourished patients. Our study suggests that hydration and nutrition status both strongly affect TBW(Watson) in PD patients.

Fournier gangrene (FG), a form of necrotizing fasciitis of the perineum and genitals, with high morbidity and mortality in the general population, carries the additional risk of involvement of the peritoneal catheter tunnel and peritoneal cavity in patients on chronic peritoneal dialysis (PD). We describe two men with diabetes who developed FG in the course of PD. Computed tomography showed no extension of FG to the abdominal wall, and spent peritoneal dialysate was clear in both patients. Broad-spectrum antibiotic therapy with anaerobic coverage and early aggressive debridement followed by negative-pressure wound therapy and repeated debridement led to improvements in clinical status in both cases. Surgical closure and healing of the wound was achieved in one patient; the wound of the second patient is healing, but remains open. Both patients experienced prolonged hospitalization, with a serious decline in nutrition status. In patients on PD, FG can be treated successfully. However, additional measures are required to evaluate for potential involvement of the PD apparatus and the peritoneal cavity in the infectious process; and prolonged hospitalization, worsening nutrition, and multiple surgical interventions can result.