Chronic Inflammation in Peritoneal Dialysis: The Search for the Holy Grail?

Pécoits-Filho, Roberto; Stenvinkel, Peter; Wang, Angela Yee-Moon; Heimbürger, Olof; Lindholm, Bengt

doi:10.1177/089686080402400407

Cited by 88 publications

(64 citation statements)

References 122 publications

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“…The blockade of erythropoiesis from inflammation and less so from secondary hyperparathyroidism is well established and also shown in our results (25,26). In future, the usage of more biocompatible PD solutions should also be considered when studying the possible benefits in the reduction of low grade persistent (micro)inflammation and the reduction of epoetin resistance (27). In our study, the total weekly creatinine clearance and nPCR were found to have no influence on epoetin responsiveness.…”

Section: Discussionmentioning

confidence: 99%

“…In our study, the total weekly creatinine clearance and nPCR were found to have no influence on epoetin responsiveness. Inflammation and malnutrition are closely related (25,27), and as such inflammation could be a confounder in the previously reported significant influence of nPCR on ERI (9). In contrast to a previous report (10) in which data was controlled only for TSAT, folate and vitamin B12 levels, we could find no difference in ERI for diabetic and non‐diabetic patients.…”

Section: Discussionmentioning

confidence: 99%

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Epoetin Responsiveness in Peritoneal Dialysis Patients: A Multi‐center Slovenian Study

et al. 2005

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The objective of our study was to assess the influence of residual renal function and other factors on epoetin requirements in chronic peritoneal dialysis patients. Fifty-one stable patients (mean age +/- SD: 52 +/- 13 years; 20 women) without recent bleeding, bone marrow disease or malignancy were recruited in four Slovenian centers. The target hemoglobin was above 110 g/L. The peritoneal equilibration test results and relevant clinical and laboratory parameters were recorded. The epoetin resistance index was expressed as a weekly epoetin dose/body weight/hemoglobin concentration. Twenty-four percent of the patients did not need epoetin treatment, the rest were treated with epoetin-beta in a dose of 70 +/- 56 U/kg per week s.c.; the hemoglobin concentration was 124 +/- 15 g/L. Ferritin >100 microg/L and transferrin saturation >20% fulfilled 63% of patients whose epoetin resistance index was not significantly lower (0.43 +/- 0.5 U/kg per week per g/L vs 0.6 +/- 0.72 U/kg per week per g/L, P = 0.502). No difference was found between diabetic and non-diabetic patients. Treatment with angiotensin system antagonists, but not with aluminum phosphate binders, was associated with increased epoetin resistance index (0.56 +/- 0.59 vs 0.3 +/- 0.4 U/kg per week per g/L, P = 0.038). No correlation between epoetin resistance index and residual glomerular filtration rate was found (r = -0.2, P = 0.173). A multiple linear regression analysis showed C-reactive protein, intact parathormone level, female sex and treatment with angiotensin system antagonists to be the independent predictors influencing epoetin resistance index. Our results show that systemic inflammation, secondary hyperparathyroidism and angiotensin system antagonist treatment are the most important modifiable parameters affecting epoetin requirements in stable peritoneal dialysis patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Epoetin Responsiveness in Peritoneal Dialysis Patients: A Multi‐center Slovenian Study

et al. 2005

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“…It should be emphasised that in PD patients some specific causes of inflammation related to dialysis practice patterns (i.e. bio‐incompatibility of PD solutions, impurity of PD solutions, peritonitis and exit site infections) may also exist 64 …”

Section: Evaluation Of Elevated Crpmentioning

confidence: 99%

Inflammation in end‐stage renal disease: The hidden enemy (Review Article)

2006

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Cardiovascular disease (CVD) remains the major cause of morbidity and mortality in end-stage renal disease (ESRD) patients. As traditional risk factors cannot alone explain the unacceptable high prevalence and incidence of CVD in this high-risk population, inflammation (interrelated to insulin resistance, oxidative stress, wasting and endothelial dysfunction) has been suggested to be a significant contributor. Indeed, several different inflammatory biomarkers, such as high sensitivity C-reactive protein (hs-CRP), have been shown to independently predict mortality in ESRD patients. As CRP is so strongly associated with vascular disease it has been suggested that this hepatic-derived protein is not only a marker, but also a mediator, of vascular disease. Although in vitro data from studies on endothelial cells, monocytes-macrophages and smooth muscle cells support a direct role for CRP in atherogenesis, data from studies performed in vivo have been controversial. The causes of the highly prevalent state of inflammation in ESRD are multiple, including inflammatory signals associated with the dialysis procedure, decreased renal function, volume overload, comorbidity and intercurrent clinical events. As the prevalence of inflammation varies considerably between continents and races, dietary and/or genetic factors may have an impact on inflammation in ESRD. Elevated CRP in dialysis patients could be evaluated at three different levels: (i) national/regional level; (ii) dialysis unit level; and (iii) individual patient level.

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“…In PD, apart from systemic inflammation, intra‐peritoneal inflammation is high because of peritonitis, degraded glucose products and advanced glycation end products (Pecoits‐Filho et al . ). Systemic inflammatory markers associated with atherosclerosis such as TNF‐alpha, IL‐6 and CRP are also increased in patients on PD (Stenvinkel et al .…”

Section: Discussionmentioning

confidence: 97%