Peritoneal protein loss (PPL) through peritoneal effluent has been a well-recognized detrimental result of peritoneal dialysis (PD) treatment since its inception. Investigation has focused mainly on PPL quantitative and qualitative determinations and evaluation of its prognostic value. A comprehensive review of the pathophysiology of PPL (3-pore model revisited), methods of quantification, dialysate protein composition, and impact on clinical outcomes is presented herein. The author summarizes a brief analysis of associated cardiovascular disease and nutritional consequences, exploring the controversial cause-effect on mortality and technique failure. Therapeutic modalities aiming to reduce PPL (angiotensin-converting enzyme inhibitors [ACEI]s and vitamin D therapies) were explored, although it is unclear whether PPL represents a valid therapeutic target or, on the other hand, is solely a manifestation of endothelial dysfunction.

<b><i>Introduction:</i></b> Peritoneal protein loss (PPL) has been associated with mortality. Inflammation was assumed a putative cause with malnutrition as a consequence. Hydrostatic convection is a major drive for microvascular protein transport, but most studies in peritoneal dialysis (PD) patients overlooked this mechanism. An association between peritoneal protein clearance (PPCl) and venous congestion has been reported recently. The aim of this study was to explore the importance of fluid overload in PPCl in PD. <b><i>Methods:</i></b> Sixty-seven prevalent PD patients were assessed with peritoneal equilibration test and multifrequency bioelectrical impedance assessment (BIA). PPL and PPCl were calculated from simultaneously obtained 24-h peritoneal effluent. <b><i>Results:</i></b> PPL averaged 5.2 g/24 h. It was higher in patients on continuous treatment than in those without a long dwell. Significant associations between PPCl and BIA parameters of overhydration were found in both univariable and multivariable analyses. Lean mass index, partly dependent on hydration status, was associated with PPCl in univariable but not in multivariable analysis. A multiple linear model identified extracellular water excess and higher D/P creatinine as predictors of higher PPCl, independent of PD duration, type of PD, age, gender, albumin, cardiovascular disease, C-reactive protein, or lean mass index. <b><i>Conclusions:</i></b> The uni- and multivariable strong associations between fluid overload and PPCl support the importance of hydrostatic pressure-induced convection for PPCl. Also, peritoneal small solute transport was associated with PPCl. Both are amenable by adjusted dialysis prescription, especially focused on fluid status and avoidance of overhydration. The assumption of an association with inflammation and malnutrition was not confirmed.

Introduction Availability of assisted PD (asPD) increases access to dialysis at home, particularly for the increasing numbers of older and frail people with advanced kidney disease. Although asPD has been widely used in some European countries for many years, it remains unavailable or poorly utilised in others. A group of leading European nephrologists have therefore formed a group to drive increased availability of asPD in Europe and in their own countries. Methods Members of the group filled in a proforma with the following headings: personal experience, country experience, who are the assistants, funding of asPD, barriers to growth, what is needed to grow, and their top 3 priorities. Results Only 5 of the 13 countries surveyed provided publicly funded reimbursement for asPD. The use of asPD depends on overall attitudes to PD with all respondents mentioning need for nephrology team education and/or patient education and involvement in dialysis modality decision making. Conclusion and call to action Many people with advanced kidney disease would prefer to have their dialysis at home, yet if the frail patient chooses PD most healthcare systems cannot provide their choice. AsPD should be available in all countries in Europe and for all renal centres. The top priorities to make this happen are education of renal healthcare teams about the advantages of PD, education of and discussion with patients and their families as they approach the need for dialysis, and engagement with policy makers and healthcare providers to develop and support assistance for PD.

Peritoneal protein loss (PPL) has been correlated with mortality, malnutrition and inflammation. More recently overhydration was brought to the equation. This study aims to review classic and recent factors associated with PPL. Prevalent and incident peritoneal dialysis (PD) patients were included. Dialysate and serum IL-6 was obtained during PET. Hydration and nutritional status were assessed by bio-impedance. Linear regression and Cox regression were performed. The 78 included patients presented median values of PPL 4.8 g/24 h, serum IL-6: 5.1 pg/mL, and IL-6 appearance rate 153.5 pg/min. Mean extracellular water excess (EWexc) was 0.88 ± 0.94 L, and lean body mass index (LBMI) 17.3 ± 2.4 kg/m2. After mean follow-up of 33.9 ± 29.3 months, 12 patients died. Linear univariable analysis showed positive associations between PPL and small solute transport, body composition (LBMI and EWexc), comorbidities and performing CAPD (vs. cycler). PPL correlated positively with dialysate appearance rate of IL-6, but not with serum IL-6. Linear multivariable analysis confirmed positive association between PPL and EWexc (p = 0.012; 95%CI: 4.162–31.854), LBMI (p = 0.008; 95%CI: 1.720–11.219) and performing CAPD (p = 0.023; 95%CI: 4.375–54.190). In survival analysis, no relationship was found between mortality and PPL. Multivariable Cox regression showed Charlson Comorbidity Index (HR: 1.896, 95%CI: 1.235–2.913), overhydration (HR: 10.034, 95%CI: 1.426–70.587) and lower PPL (HR: 0.576, 95%CI: 0.339–0.978) were predictors for mortality. Overhydration, was a strong predictor of PPL, overpowering variables previously reported as determinants of PPL, namely clinical correlates of endothelial dysfunction or local inflammation. PPL were not associated with malnutrition or higher mortality, emphasizing the importance of volume overload control in PD patients.

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Atherosclerotic cardiovascular disease is the main cause of morbidity and mortality in chronic kidney disease patients. There is a raft of evidence showing that in the general population dyslipidaemia is associated with an increased risk of cardiovascular events, as well as with a greater prevalence of chronic kidney disease. Consequently, the use of statins in the general population with dyslipidaemia is not controversial. Nevertheless, the benefits of statins in patients with chronic kidney disease are more elusive. The authors review the possible effects of statins on the progression of renal disease and cardiovascular events in chronic kidney disease patients.

Background/Aims: Peritoneal protein loss (PPL) is associated with cardiovascular disease and mortality in peritoneal dialysis (PD). Controversial results have been published about the effect of paricalcitol in PPL among PD patients. This study intends to analyze the relationship between paricalcitol and PPL in PD. Methods: In a retrospective study, prevalent PD patients were divided into 2 groups: “with paricalcitol” and “without paricalcitol”. X²-test, Student’s t test, Pearson correlation coefficient and Logistic Regression analysis were applied. Results: Eighty-two patients were included. PPL was lower among patients medicated with paricalcitol (5.17 ± 1.71 vs. 6.79 ± 2.10 g/24 h, p = 0.0001). In multivariate analysis, paricalcitol and dialysate/plasma ratio of creatinine (D/P creatinine) were independently related to PPL (OR 4.270 [1.437–12.684], p = 0.009 and OR 0.205 [0.064–0.659], p = 0.008, respectively), adjusted for diabetes. Conclusion: Paricalcitol and D/P creatinine were independently related to PPL. Paricalcitol may have an effect on PPL in PD patients

Kidney graft survival has been mainly evaluated using an up to 10-year threshold. Instead, in this study our aim was to evaluate predictive variables that impact long-term kidney graft survival (≥10 years). We enrolled 892 patients in our analysis: 638 patients with functioning graft at 10 years PT and 254 patients with graft failure at 10 years PT (considering patient death with a functioning graft <10 years PT as graft failure). Between groups comparisons were done using Mann-Whitney and chi-square test. To determine independent predictive variables for long-term graft survival a multivariate-adjusted logistic regression was performed. Significant predictors of long term graft survival were lower 12-month PT creatinine (OR = 0.26, P < 0.001), lower donor age (OR = 0.98, P = 0.004), shorter time on dialysis (OR = 0.93, P = 0.044), recipient positive CMV IgG (OR = 1.59, P = 0.040), absence of AR episodes (OR = 1.57, P = 0.047), 0 to 1 (versus 2) HLA-B mismatch (OR = 1.80, P = 0.004), and recipients male gender (OR = 1.84, P = 0.005). Our results show that an early KT, younger donor age, and an optimal first year graft function are of paramount importance for long-term graft survival. Measures that address these issues (careful donor selection, preemptive KT, and effective immunosuppressive protocols) are still warranted.