Endothelial dysfunction in patients with kidney failure and vascular risk factors: acute effects of hemodialysis.
BACKGROUND
Patients with kidney failure present endothelial dysfunction, which was shown to be partly corrected by hemodialysis. No data exist on the effects of hemodialysis on endothelial dysfunction in kidney failure patients with associated vascular risk factors. The aim of this study was to evaluate the acute effects of hemodialysis on endothelial dysfunction in patients with kidney failure and associated vascular risk factors and to assess the role of endothelium-toxic substances.


METHODS
We assessed endothelial dysfunction in 13 patients with chronic renal failure and other vascular risk factors before and after hemodialysis and in 13 healthy controls and simultaneously measured nitric oxide (NO) synthesis and activity. Endothelial dysfunction was studied using an echographic method as flow-mediated dilation (FMD) of the brachial artery; plasma NO2- and NO3-, cyclic guanosine-5-monophosphate (cGMP), plasma homocysteine levels and low molecular mass-advanced glycation end-products (LMM-AGEs) were simultaneously measured.


RESULTS
As compared with healthy controls, patients with renal failure showed a reduced FMD (2.89 +/- 1.43 vs. 7.81 +/- 1.54%, p < 0.01) which was not corrected by dialysis (after dialysis 2.40 +/- 1.65%, p = NS vs. pre). Plasma NO2- and NO3- were normal or slightly increased and remained unchanged after dialysis. Plasma cGMP levels were reduced and remained unchanged after dialysis. Homocysteine and LMM-AGE plasma levels were raised and, although significantly reduced by dialysis, remained higher than in controls.


CONCLUSIONS
Patients with kidney failure and associated vascular risk factors show an endothelial dysfunction related to defective NO activity, which is not corrected by hemodialysis despite the reduction, though not to normal, in homocysteine and LMM-AGE levels. Endothelial dysfunction may contribute to the progression of atherosclerosis in patients with kidney failure and vascular risk factors.
Migliacci
Rino
R
Division of General Medicine, Civic Hospital, Cortona (AR), Italy.
Falcinelli
Francesca
F
Imperiali
Patrizio
P
Floridi
Ardesio
A
Nenci
Giuseppe G
GG
Gresele
Paolo
P
D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D006152:Cyclic GMP / Q000097:blood; D003971:Diastole / Q000502:physiology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006710:Homocysteine / Q000097:blood; D006801:Humans; D007668:Kidney / Q000098:blood supply / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000097:blood / Q000453:epidemiology* / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D012039:Regional Blood Flow / Q000502:physiology; D012079:Renal Circulation / Q000502:physiology; D006435:Renal Dialysis; D012307:Risk Factors; D013223:Statistics as Topic; D013599:Systole / Q000502:physiology; D013997:Time Factors; D016896:Treatment Outcome; D014652:Vascular Diseases / Q000097:blood / Q000453:epidemiology* / Q000503:physiopathology*; D014664:Vasodilation / Q000502:physiology
D015415:Biomarkers; D009566:Nitrates; D009573:Nitrites; D006710:Homocysteine; D006152:Cyclic GMP