Oxidative stress and inflammation in hemodialysis patients

Spittle, Margaret; Hoenich, Nicholas A.; Handelman, Garry J.; Adhikarla, Rohini; Homel, Peter; Levin, Nathan W.

doi:10.1053/ajkd.2001.29280

Cited by 177 publications

(94 citation statements)

References 22 publications

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“…As previously described [9,10,11,12,13,14], CRP is higher in HD patients who are non-responders to rhEPO therapy, indicating that inflammation is related to resistance to this therapy. Additionally, CRP serum levels were positively correlated with the weekly rhEPO/kg dose, suggesting that CRP is a good predictor of resistance to rhEPO therapy in HD patients.…”

Section: Discussionsupporting

confidence: 58%

“…However, there is marked variability in the sensitivity to rhEPO, with up to 10-fold variability in dose requirements to achieve correction of anemia [4,5,6,7,8,9,10]. Approximately 5–10% of the patients show a marked resistance to rhEPO therapy [4,5,6,9,10,11,12,13,14,15,16,17]. This variability however remains relatively unexplained.…”

Section: Introductionmentioning

confidence: 99%

“…This variability however remains relatively unexplained. rhEPO resistance is associated with several conditions including iron deficiency, oxidative stress, infection, inflammation, blood loss, hyperparathyroidism, aluminum toxicity and vitamin B 12 and folate deficiencies [9,10,11,12,13,14,15,16,17]. However, exclusion of these factors does not eliminate the marked variability in the sensitivity to rhEPO therapy [9,10,11].…”

Section: Introductionmentioning

confidence: 99%

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Role of Prohepcidin, Inflammatory Markers and Iron Status in Resistance to rhEPO Therapy in Hemodialysis Patients

et al. 2008

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The aim of our study was to assess possible relations between prohepcidin, iron status and inflammatory markers in hemodialysis (HD) patients, as well as its association with resistance to recombinant human erythropoietin (rhEPO) therapy. Fifty HD patients and 25 healthy controls were enrolled in the study. Among HD patients, 25 were non-responders and 25 were responders to rhEPO therapy. Complete blood cell count, reticulocyte count, and circulating levels of ferritin, iron, transferrin saturation, C-reactive protein (CRP), soluble interleukin (IL)-2 receptor (s-IL2R), soluble transferrin receptor (s-TfR), IL-6 and prohepcidin were measured in all patients and controls. HD patients showed higher circulating levels of ferritin, s-TfR, CRP, IL-6, s-IL2R and prohepcidin, and lower levels of transferrin compared to healthy controls. Higher levels of s-TfR, CRP and lower levels prohepcidin were observed among non-responders compared to responders. Prohepcidin levels correlated negatively with s-TfR and reticulocyte count. The weekly rhEPO/kg dose was found to be positively correlated with CRP, hemoglobin and s-TfR. In conclusion, our data show that a close interaction exists between inflammation, iron status and prohepcidin serum levels that ultimately regulate intracellular iron availability. Prohepcidin and s-TfR, together with CRP, may prove to be good markers of resistance to rhEPO therapy in HD patients.

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Section: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Role of Prohepcidin, Inflammatory Markers and Iron Status in Resistance to rhEPO Therapy in Hemodialysis Patients

et al. 2008

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“…Production of chemokines is enhanced [116]. Such patients have a raised C-reactive protein [117] and are more liable to cardiovascular disease [118]. Nitrated proteins are elevated in the plasma [119].…”

Section: Pathophysiological Implicationsmentioning

confidence: 99%

Cellular Oxidative Processes in Relation to Renal Disease

Wardle¹

2005

Am J Nephrol

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“…The causes of inflammation in dialysis patients include both factors arising from dialysis itself (efficiency and biocompatibility issues) as well as other non-dialysis-related causes [5]. ESRD patients have increased levels of inflammation-related proteins, such as interleukin-6 (IL-6) and C-reactive protein (CRP), and are subjected to enhanced oxidative stress, as a result of both insufficient antioxidant defense mechanisms and excessive generation of oxidant compounds [3, 6].…”

Section: Introductionmentioning

confidence: 99%