No abstract

Decades after the introduction of chronic maintenance hemodialysis, the optimal means of quantifying dialysis dose remains controversial. Differences of opinion in the international dialysis community lead to substantial diversity in everyday clinical practice. Several studies suggest that the well-recognized international mortality differences in hemodialysis populations may result from these divergent approaches to dialysis care. One of the main areas of divergence is the different degree of reliance on dialysis clearance when prescribing dialysis. The "clearance approach" implies that treatment quality is primarily dependent on efficient removal of uremic toxins as estimated by dialytic urea clearance. Urea can be rapidly removed by high efficiency dialysis in a relatively short time. The main alternative to this strategy is the "time approach" based on the recognition that longer or more frequent dialysis provides benefits beyond increasing urea removal. Some of the putative benefits are more effective volume and blood pressure control, better maintenance of hemodynamic stability because of slower ultrafiltration and removal of uremic toxins that do not behave like urea. Recently, chronic inflammation has been proposed to be an important predictor of outcome in dialysis patients. Inflammatory markers are commonly elevated in chronic renal failure and levels of these seem to correlate with malnutrition, maintenance of residual renal function, and volume control. The relationships between dialysis clearance, treatment time, chronic inflammation, volume control, and hemodynamic stability are explored in this review. We propose that a better understanding of these complex relationships may provide opportunities for improving outcomes of maintenance hemodialysis patients.

In an era of evidence‐based medicine and dialysis performance measures, there is strong motivation to find specific, objective, quantifiable, and reproducible parameters to characterize the clinical condition of chronic kidney disease patients and to present population‐wide statistics that may describe quality of care in dialysis centers. Yet, in the last three decades, several studies demonstrated that while parameters including Kt/V urea, serum phosphorus, parathyroid hormone, serum cholesterol fulfill all these criteria, efforts to optimize these lab parameters failed to improve survival on dialysis. However, subjective assessments of nutrition including subjective global assessment and malnutrition–inflammation score, while not ideally suited for statistical analysis and not optimal from the point of view of scientific methodology due to their general, semi‐quantifiable, subjective nature have, nevertheless, proved themselves as some of the strongest predictors of clinical outcomes in the dialysis population. Where does this paradox leave us? We propose that a deeper understanding of relevance of these variables in the dialysis population may improve appreciation of the clinical situation of individual patients and may result in a paradigm shift from dialysis adequacy to quality dialysis.

The relationship between renal disease progression and genetic polymorphism of enzymes influencing endothelial function remains incompletely understood. We genotyped three cohorts of elderly Hungarian patients: 245 patients with end-stage renal disease (ESRD) on chronic hemodialysis (HD), 88 patients with mild chronic kidney disease (CKD), and 200 healthy controls. The underlying diagnoses of renal diseases were primary glomerulonephritis, interstitial nephritis, hypertension, diabetic nephropathy, and hereditary diseases. We examined genetic polymorphisms of eight candidate genes associated with endothelial function: endothelial constitutive nitric oxide synthase (ecNOS) T-786C, endothelin-1 G5727T, methylenetetrahydrofolate reductase (MTHFR) C677T, paraoxonase-1 Q192R and M55L, angiotensinogen M235T, angiotensin-converting enzyme (ACE) I/D and angiotensin II type 1 receptor A1166C gene. Six gene polymorphisms were detected by real-time polymerase chain reaction with melting-point analysis, and two via allele-specific amplification and gel electrophoresis. Control group patients were in Hardy-Weinberg equilibrium for all tested genotypes. In ESRD patients attributed to hypertension, the endothelin gene G5727T GG genotype occurred significantly less but GT genotype more frequently (P < 0.01 for both). In ESRD patients attributed to primary glomerulonephritis, more ACE DD and less ID genotypes were found (P < 0.02 for both) than in the controls. The underlying diagnosis may modify the association of genetic polymorphism and dialysis-dependent ESRD.

Background: The relationship between treatment time, ultrafiltration rate (UFR) and inflammation has received limited exploration so far. Methods: This is a cross-sectional cohort study of 12 hemodialysis clinics. Statistical models explored the association of multiple patient- and dialysis-specific covariates with low albumin (≤40 g/l) or high C-reactive protein (CRP) (>5 mg/dl) and calculated the ORs and 95% CIs. Results: 616 patients with a mean age of 60.9 ± 14.4 years participated in our study. Mean treatment time was 237.3 ± 23.8 min and mean UFR was 7.0 ± 4.0 ml/kg/h. In stepwise logistic regression, treatment time >4 h reduced the risk of low albumin (OR 0.397, 95% CI 0.235–0.672, p < 0.001). Congestive heart failure (OR 1.634, 95% CI 1.154–2.312, p = 0.006) and acute infection (OR 1.799, 95% CI 1.059–3.056, p = 0.03) were significant correlates of the risk of high CRP. There was no association between UFR and either CRP or albumin. Conclusion: Treatment time had a significant cross-sectional association with serum albumin but not with CRP.