Key result
Haemodialysis acutely reduced plasma ADMA levels (0.98 to 0.58 micromol/l; P<0.01) but did not reverse impaired NO-dependent vasodilation compared to controls (82.7% vs 89.6%; P<0.01).
Why the study?
Does haemodialysis acutely improve NO-dependent vasodilation and reduce plasma ADMA in end-stage renal disease patients?
Observational (n=48)
Does haemodialysis acutely improve NO-dependent vasodilation and reduce plasma ADMA in end-stage renal disease patients?
Haemodialysis acutely normalizes plasma ADMA levels but fails to reverse impaired NO-dependent vasodilation in patients with end-stage renal disease, suggesting ADMA accumulation does not fully explain endothelial dysfunction in this population.
Answers are grounded in this paper and cite their sources.
Haemodialysis-mediated ADMA reduction fails to restore NO-dependent vasodilation; leaves open non-ADMA pathways of endothelial dysfunction in ESRD.
End-stage renal disease patients have endothelial dysfunction and high plasma levels of ADMA (asymmetric omega-NG,NG-dimethylarginine), an endogenous inhibitor of NOS (NO synthase). The actual link between these abnormalities is controversial. Therefore, in the present study, we investigated whether HD (haemodialysis) has an acute impact on NO-dependent vasodilation and plasma ADMA in these patients. A total of 24 patients undergoing maintenance HD (HD group) and 24 age- and gender-matched healthy controls (Control group) were enrolled. The increase in forearm SkBF (skin blood flow) caused by local heating to 41 degrees C (SkBF41), known to depend on endothelial NO production, was determined with laser Doppler imaging. SkBF41 was expressed as a percentage of the vasodilatory reserve obtained from the maximal SkBF induced by local heating to 43 degrees C (independent of NO). In HD patients, SkBF41 was assessed on two successive HD sessions, once immediately before and once immediately after HD. Plasma ADMA was assayed simultaneously with MS/MS (tandem MS). In the Control group, SkBF41 was determined twice, on two different days, and plasma ADMA was assayed once. In HD patients, SkBF41 was identical before (82.2+/-13.1%) and after (82.7+/-12.4%) HD, but was lower than in controls (day 1, 89.6+/-6.1; day 2, 89.2+/-6.9%; P<0.01 compared with the HD group). In contrast, plasma ADMA was higher before (0.98+/-0.17 micromol/l) than after (0.58+/-0.10 micromol/l; P<0.01) HD. ADMA levels after HD did not differ from those obtained in controls (0.56+/-0.11 micromol/l). These findings show that HD patients have impaired NO-dependent vasodilation in forearm skin, an abnormality not acutely reversed by HD and not explained by ADMA accumulation.
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Engelberger et al. (2009) conducted an observational in End-stage renal disease (n=48). Haemodialysis vs. Healthy controls and pre-haemodialysis state was evaluated on NO-dependent vasodilation (SkBF41 as percentage of vasodilatory reserve) (p=<0.01). Haemodialysis acutely reduced plasma ADMA levels (0.98 to 0.58 micromol/l; P<0.01) but did not reverse impaired NO-dependent vasodilation compared to controls (82.7% vs 89.6%; P<0.01).
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