The role of asymmetric and symmetric dimethylarginines in renal disease.
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The role of asymmetric and symmetric dimethylarginines in renal disease. / Schwedhelm, Edzard; Böger, Rainer.
In: NAT REV NEPHROL, Vol. 7, No. 5, 5, 2011, p. 275-285.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - The role of asymmetric and symmetric dimethylarginines in renal disease.
AU - Schwedhelm, Edzard
AU - Böger, Rainer
PY - 2011
Y1 - 2011
N2 - Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases. By inhibiting nitric oxide formation, ADMA causes endothelial dysfunction, vasoconstriction, elevation of blood pressure, and aggravation of experimental atherosclerosis. Levels of ADMA and its isomer symmetric dimethylarginine (SDMA), which does not inhibit nitric oxide synthesis, are both elevated in patients with kidney disease. Currently available data from prospective clinical trials in patients with chronic kidney disease suggest that ADMA is an independent marker of progression of renal dysfunction, vascular complications and death. High SDMA levels also negatively affect survival in populations at increased cardiovascular risk, but the mechanisms underlying this effect are currently only partly understood. Beyond glomerular filtration, other factors influence the plasma concentrations of ADMA and SDMA. Elevated plasma concentrations of these dimethylarginines might also indirectly influence the activity of nitric oxide synthases by inhibiting the uptake of cellular L-arginine. Other mechanisms may exist by which SDMA exerts its biological activity. The biochemical pathways that regulate ADMA and SDMA, and the pathways that transduce their biological function, could be targeted to treat renal disease in the future.
AB - Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases. By inhibiting nitric oxide formation, ADMA causes endothelial dysfunction, vasoconstriction, elevation of blood pressure, and aggravation of experimental atherosclerosis. Levels of ADMA and its isomer symmetric dimethylarginine (SDMA), which does not inhibit nitric oxide synthesis, are both elevated in patients with kidney disease. Currently available data from prospective clinical trials in patients with chronic kidney disease suggest that ADMA is an independent marker of progression of renal dysfunction, vascular complications and death. High SDMA levels also negatively affect survival in populations at increased cardiovascular risk, but the mechanisms underlying this effect are currently only partly understood. Beyond glomerular filtration, other factors influence the plasma concentrations of ADMA and SDMA. Elevated plasma concentrations of these dimethylarginines might also indirectly influence the activity of nitric oxide synthases by inhibiting the uptake of cellular L-arginine. Other mechanisms may exist by which SDMA exerts its biological activity. The biochemical pathways that regulate ADMA and SDMA, and the pathways that transduce their biological function, could be targeted to treat renal disease in the future.
KW - Humans
KW - Risk Factors
KW - Arginine/analogs & derivatives/metabolism
KW - Kidney/metabolism
KW - Renal Insufficiency, Chronic/epidemiology/metabolism
KW - Humans
KW - Risk Factors
KW - Arginine/analogs & derivatives/metabolism
KW - Kidney/metabolism
KW - Renal Insufficiency, Chronic/epidemiology/metabolism
M3 - SCORING: Journal article
VL - 7
SP - 275
EP - 285
JO - NAT REV NEPHROL
JF - NAT REV NEPHROL
SN - 1759-5061
IS - 5
M1 - 5
ER -