Stefanie M. Bode-Böger

TL;DR: In PAOD patients, there is a progressive reduction in urinary nitrate and cGMP excretion rates, which may be caused in part by accumulation of ADMA, an endogenous inhibitor of NO synthase.

TL;DR: Systemic ADMA infusion is responsible for a short-term, modest decrease in cardiac output with comparable decrease in effective renal plasma flow while increasing systemic vascular resistance and blood pressure in a dose-related manner.

TL;DR: In contrast to several traditional cardiovascular risk factors, markedly increased blood concentrations of ADMA, a putative biochemical marker of atherosclerosis, are present even in nonsmoking patients without diabetes with incipient primary renal disease, and may be of relevance for the excess cardiovascular morbidity and mortality due to arterio- and atherosclerotic complications in patients with renal disease.

TL;DR: Lowering plasma ADMA concentrations may be a novel therapeutic target to prevent progressive renal impairment in patients with nondiabetic kidney diseases.

TL;DR: Recent findings suggest that large, prospective, randomized clinical trials might be needed to identify those patients who are the most likely to benefit from L-arginine, and testing patients for ADMA and L- arginine plasma levels for calculating the L- Arginine/ADMA ratio might be an adequate strategy.