Hemodialysis and the Acute-Phase Response in Chronic Uremic Patients

Trznadel, K; Luciak, M; Paradowski, Mariusz; Kubasiewicz-Ujma, B

doi:10.1177/039139888901201205

Cited by 17 publications

(7 citation statements)

References 19 publications

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“…This may be a response to the increased hepatocyte growth factor seen in liver damage [32]. The inverse correlations between fibrosis and α2-macroglobulin (positive) and haptoglobin (negative) can be explained by acute phase reaction induced by the dialysis procedure [33,34]. Data in the literature concerning the relationship between the FT accuracy and hemodialysis are very scarce.…”

Section: Discussionmentioning

confidence: 99%

Validation of Biochemical Markers for the Prediction of Liver Fibrosis and Necroinflammatory Activity in Hemodialysis Patients with Chronic Hepatitis C

et al. 2010

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Background: Liver biopsy is an imperfect gold standard for assessing the disease severity in hemodialysis patients with chronic hepatitis C. Our purpose was to compare the accuracy of the FibroTest (FT) and ActiTest (AT) with liver biopsy and the AST-to-platelet ratio index (APRI) in determining hepatic fibrosis and necroinflammatory activity in hemodialysis patients with hepatitis C virus (HCV). Methods: The FT-AT index combining 6 biochemical markers was assessed in 33 hemodialysis patients with HCV. Liver fibrosis and necroinflammatory activity was staged and graded according to the METAVIR scoring system. Results: The accuracy of FT-AT versus biopsy was 0.46 for significant fibrosis and 0.36 for severe necroinflammatory activity. The FT index had a positive predictive value of 20% for scores greater than 0.6 and a negative predictive value of 45% for scores less than 0.2. Eleven of the 33 patients had scores ≤0.2, 6 had significant fibrosis on biopsy. Four out of 5 patients with FT scores >0.6 had mild fibrosis. APRI correlated well with the biopsy. Conclusion: The FT-AT test does not seem to be a reliable noninvasive marker for the prediction of necroinflammatory activity and fibrosis in hemodialysis patients with HCV and cannot be used as an alternative to either liver biopsy or APRI.

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Section: Discussionmentioning

confidence: 99%

Validation of Biochemical Markers for the Prediction of Liver Fibrosis and Necroinflammatory Activity in Hemodialysis Patients with Chronic Hepatitis C

et al. 2010

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“…Lymphokines [e.g., tumor necrosis factor-· (TNF-·) and interleukin (IL)-1] [43], as well as a group of acutephase reactive proteins [44,45] (· 1 -acid glycoprotein, ceruloplasmin, and C4 complement component), have been found to be increased in hemodialysis patients when compared to other patients with chronic renal failure. Cytokine levels were recently reported to correlate with albumin levels in hemodialysis patients and, like albumin, predicted survival [46].…”

Section: Albumin Metabolism In End-stage Renal Disease (Esrd)mentioning

confidence: 99%

Albumin Turnover in Renal Disease

Kaysen

1997

Mineral Electrolyte Metab

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Hypoalbuminemia is found in patients both with the nephrotic syndrome and with end-stage renal disease (ESRD) treated either with continuous ambulatory peritoneal dialysis (CAPD) or hemodialysis. In nephrotic patients the primary causes of hypoalbuminemia are urinary albumin losses, an inappropriate increase in the fractional catabolic rate (FCR) of albumin and an insufficient increase in the rate of albumin synthesis to replace these losses. Nevertheless, the albumin synthetic rate is increased significantly. In patients on CAPD, albumin losses into the urine and across the peritoneal membrane contribute significantly to hypoalbuminemia. In contrast to nephrotic patients, albumin FCR decreases as serum albumin falls and serum albumin levels are significantly greater than in nephrotic patients with the same external losses of albumin. CAPD patients, like nephrotic patients with normal renal function, can increase albumin synthesis to replace losses. Thus ESRD does not directly suppress albumin synthesis. In contrast, hypoalbuminemia in hemodialysis patients results from reduced albumin synthesis. The cause of decreased albumin synthesis is a combination of response to inflammation (acute-phase response) and, to a lesser extent, inadequate nutrition. There is no evidence that shifts of albumin to the extravascular space or that dilution of the plasma by volume expansion play any role in causing hypoalbuminemia in ESRD or nephrotic patients.

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“…(4) Other events of possible clinical relevance in the proinflammatory effect of HD are the secretion of acute-phase molecules including complement components, C-reactive protein and serum amyloid A [13, 14]. …”

Section: Introductionmentioning

confidence: 99%