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  • Meeting abstract
  • Open Access

Impact of treatment modality, biochemical parameters and apoptosis on polymorphonuclear cell (PMN) function in patients with renal failure

  • 1,
  • 1,
  • 1,
  • 1,
  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
Critical Care20015 (Suppl 3) :P34

https://doi.org/10.1186/cc1367

  • Published:

Keywords

  • Creatinine
  • Flow Cytometry
  • Treatment Modality
  • Propidium Iodide
  • Propidium Iodide

It has been suggested that PMN apoptosis is increased in dialysis patients and may contribute to cellular dysfunction. We investigated the effect of treatment modality and biochemical parameters on PMN apoptosis and function. Blood was drawn from 17 controls, 17 patients with chronic renal failure (CRF; creatinine clearance 28 ± 14 ml/min/1.73 m2), 10 hemodialysis (HD) and 11 CAPD patients. Upon collection, whole blood aliquots were incubated in RPMI-1640 with propidium iodide (PI)-labeled Saureus (SA), PMA, fMLP or LPS for 30 min. Cells were then stained with DCFH-DA and analyzed by flow cytometry, in order to quantify phagocytosis and H2O2 release by PMN. After separation by gradient centrifugation, PMN were stained with Annexin-V and PI in order to quantify apoptosis by flow cytometry. The results were correlated with blood levels of urea, creatinine, bicarbonate, albumin and PTH. Results are presented as means ± SD.

Among CRF and HD patients, there was an inverse correlation between apoptosis and SA- (r = 0.62, P = 0.01 and r = 0.89, P = 0.02, respectively) and LPS-stimulated H2O2 release (r = 0.68, P = 0.005 and r = 0.61, P = 0.058, respectively). No biochemical parameters correlated with apoptosis or cellular functions. In summary, PMN apoptosis contributes to cellular malfunction in uremia, but does not account for all the dysfunction. Hence, it is possible that other uremic toxins affect cell performance independently of apoptosis.

Table

 

Controls

CRF

HD

CAPD

P *

Apoptosis, %

9.0 ± 5.6

19.8 ± 16.8

13.6 ± 9.3

6.4 ± 4.0

0.01

Phagocytosis, %

83.8 ± 7.5

79.2 ± 16.9

49.9 ± 28

86.4 ± 7.1

<0.0001

H2O2 release, MFI

     

   SA-stimulated

357 ± 123.4

357.6 ± 30.6

90 ± 41.7

570.4 ± 41.5

0.012

   LPS-stimulated

44.6 ± 16.4

50.9 ± 30.0

48.5 ± 27.2

56.4 ± 33.1

0.77

   PMA-stimulated

110.6 ± 81.6

95.9 ± 93

37.7 ± 25

152.9 ± 79.6

0.023

   fMLP-stimulated

131.9 ± 75.7

72.9 ± 55.5

41.2 ± 16.4

189.2 ± 141.1

<0.001

MFI, mean fluorescence intensity. *ANOVA; P < 0.05 versus controls and CAPD; P < 0.05 versus other groups.

Authors’ Affiliations

(1)
Disciplina de Nefrologia, UNIFESP-EPM, São Paulo, Brazil

Copyright

© The Author(s) 2001

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