Impaired Polymorphonuclear Neutrophil Function in End-Stage Renal Failure and Its Correction by Continuous Ambulatory Peritoneal Dialysis

Porter, Christine J.; Burden, Richard; Morgan, A. G.; Daniels, Ian; Fletcher, J.

doi:10.1159/000188700

Cited by 16 publications

(7 citation statements)

References 6 publications

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“…In agreement with our earlier report [ 1 ] we were able to confirm that some ESRF patient PMN demonstrate defec tive intracellular bacterial killing of 5. epidermidis which is statistically significant (table 1). Table 1 also shows that while the mean total amount of hydrogen peroxide gener ated (assayed by LCL) was similar in all three subject groups the amount of intracellular hydrogen peroxide (as sayed by DCF) was significantly reduced in the ESRF group compared to both the CAPD (p = 0.03) and normal PMN (p = 0.03).…”

Section: Resultssupporting

confidence: 93%

“…However, table 1 does suggest that CAPD therapy will restore PMN intracellular hydro gen peroxide generation to normal levels. This interpreta tion would be in agreement with our previous study that followed patients with ESRF through to treatment by CAPD and demonstrated that reduced bacterial killing is corrected by CAPD [1], Taken together, these observa tions provide more evidence to support the suggestion that altered PMN function in ESRF patients is, at least in part, due to circulating factor(s) which may be removed by CAPD.…”

Section: Resultssupporting

confidence: 91%

“…We have previously reported that polymorphonuclear leukocytes (PMN) isolated from a sub-group of patients with conservatively treated end-stage renal failure (ESRF) fail to kill ingested Staphylococcus epidermidis, and that this defect is corrected by continuous ambulatory perito neal dialysis (CAPD) [1], Intracellular killing (IK) by PMN is dependent upon the generation of toxic oxygen derivatives produced during a process known as the respi ratory burst. This process involves the reduction of molec ular oxygen to superoxide anion catalyzed by a multicom This article is also accessible online at: http://www.kargcr.ch http://BioMedNet.com/kargcr ponent NADPH oxidase.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Impaired Bacterial Killing and Hydrogen Peroxide Production by Polymorphonuclear IMeutrophils in End-Stage Renal Failure

Porter

Burden²,

Morgan³

et al. 1997

Nephron

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Polymorphonuclear leukocytes (PMN) isolated from a sub-population of patients with end-stage renal failure (ESRF) who were identified because they demonstrated impaired intracellular bacterial killing, were assayed for hydrogen peroxide activity using two different techniques capable of distinguishing between total and intracellular hydrogen peroxide generation. In an attempt to elucidate the mechanism of impaired intracellular bacterial killing further, hydrogen peroxide activity was compared to PMN isolated from patients receiving continuous ambulatory peritoneal dialysis and a control group of healthy normal volunteers. PMN from conservatively treated ESRF patients demonstrated reduced production of intracellular hydrogen peroxide (mean 37.7 ± 4.3 fluorescence units), compared to PMN from both ESRF patients treated with continuous ambulatory peritoneal dialysis (mean 57.9 ± 6.6 fluorescence units) and normal controls (mean 60.4 ± 3.5 fluorescence units). This suggests that the probable mechanism of impaired bacterial intracellular killing by the PMN of conservatively treated ESRF patients involves the production of intracellular hydrogen peroxide.

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Section: Resultssupporting

confidence: 93%

Section: Resultssupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Impaired Bacterial Killing and Hydrogen Peroxide Production by Polymorphonuclear IMeutrophils in End-Stage Renal Failure

Porter

Burden²,

Morgan³

et al. 1997

Nephron

Self Cite

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“…These toxins are readily dialyzable. 32 In this study, we identified that small-(represented by urea), medium-and large-MW uremic toxins within uremic serum inhibit normal MDC and PDC functions, comparable to the effects of uremic serum on these cells. However, it is possible that drugs including vitamin D analogues such as calcitriol are present within the sera of HD patients, which may also contribute to the inhibitory effects of uremic serum on DC functions.…”

Section: Discussionmentioning

confidence: 71%

Uremia impairs blood dendritic cell function in hemodialysis patients

Lim

Kireta

Russ

et al. 2007

Kidney International

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Patients on hemodialysis have a general immunodeficiency involving both innate and adaptive responses. As the mechanisms contributing to this defect are uncertain, we sought to study the effects of uremia on circulating dendritic cells (DC) in hemodialysis patients. Immunomagnetic beads were used to isolate myeloid and plasmacytoid DCs from healthy donors. Immune-related functions were determined in these cells cultured in either a complete media containing ABO-compatible serum or media containing sera from uremic patients. The myeloid cells were analyzed for costimulatory molecule expression and allo-stimulatory capability following lipopolysaccharide stimulation. The production of interferon-alpha following herpes-simplex virus stimulation by the plasmacytoid cells was also measured. Myeloid DCs incubated with uremic sera demonstrated impaired maturation and decreased allo-stimulatory capacity. Similarly, herpes virus-stimulated plasmacytoid DCs incubated with uremic sera produced significantly less interferon-alpha compared with cells incubated in the complete media. Both small and large molecule uremic toxins inhibited DC functions in vitro. Use of more efficient dialysis to improve small molecule clearance reversed the inhibition of uremic sera on myeloid but not plasmacytoid DC function. We have shown that the immunodeficiency of hemodialysis patients is due to dialyzable uremic toxins.

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“…Polymorphonuclear leukocyte function improved in CRF patients following the commencement of peritoneal dialysis, which suggested that the soluble uremic toxins were removed by dialysis [27]. Functional MBL levels were significantly higher at 6 and 12 months than at the start of HD therapy.…”

Section: Discussionmentioning

confidence: 99%

Functional Mannose-Binding Lectin Levels in Patients with End-Stage Renal Disease on Maintenance Hemodialysis

Satomura¹,

Fujita

Yanai

et al. 2012

J Innate Immun

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Background: Innate immunity is generally impaired in chronic renal failure (CRF). Mannose-binding lectin (MBL) has an important role in first-line host defense against pathogens via the lectin pathway. We recently reported that functional MBL was significantly lower in CRF patients than in healthy subjects. In this study, we aimed to determine whether functional MBL would be improved following hemodialysis (HD) therapy. Methods: This study included 22 patients with end-stage renal disease (ESRD) on maintenance HD. Functional MBL was measured every 6 months for 1 year after HD using an enzyme-linked immunosorbent assay. Results: Median serum functional MBL levels of ESRD patients were significantly higher after 6 and 12 months than at the start of HD therapy (p < 0.05 and p < 0.01, respectively). Furthermore, median functional MBL levels at 12 months were significantly higher than those at 6 months (p < 0.05). Conclusions: We found significant increases in serum functional MBL levels in patients on HD. Our results indicated that HD tailored to remove uremic toxins could improve functional MBL levels in these patients.

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Impaired Polymorphonuclear Neutrophil Function in End-Stage Renal Failure and Its Correction by Continuous Ambulatory Peritoneal Dialysis

Cited by 16 publications

References 6 publications

Impaired Bacterial Killing and Hydrogen Peroxide Production by Polymorphonuclear IMeutrophils in End-Stage Renal Failure

Impaired Bacterial Killing and Hydrogen Peroxide Production by Polymorphonuclear IMeutrophils in End-Stage Renal Failure

Uremia impairs blood dendritic cell function in hemodialysis patients

Functional Mannose-Binding Lectin Levels in Patients with End-Stage Renal Disease on Maintenance Hemodialysis

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