Role of Adenosine in Contrast Media—Induced Acute Renal Failure in Diabetes Mellitus Axel Pflueger, MD, Timothy S. Larson, MD, Karl A. Nath, MB, CHB, Bernard F. King, MD, Jennifer M. Gross, Franklyn G. Knox, MD, PhD Mayo Clinic Proceedings Volume 75, Issue 12, Pages 1275-1283 (December 2000) DOI: 10.4065/75.12.1275 Copyright © 2000 Mayo Foundation for Medical Education and Research Terms and Conditions
Fig. 1 Pathways of adenosine metabolism in the kidney. Enzymes: (1) 5′-nucleotidase, (2) nonspecific phosphatases, (3) S-adenosylhomocysteine hydrolase (SAH), (4) adenosine kinase, and (5) adenosine deaminase A1 = adenosine receptortype I; A1α and A1β = adenosine receptor subtypes; AC = adenylyl cyclase; ADP = adenosine diphosphate; 5′-AMP = 5′ adenosine monophosphate; ATP = adenosine triphosphate; Ca2+ = calciumion; cAMP = cyclic adenosine monophosphate; DAG=diacylglycerol; ER =endoplasmicreticulum;G;=G-inhibitoryprotein; G, =nonspecified G protein; IP3 =inositol 1,4,5-triphosphate; PKA =protein kinase A; PKC =protein kinase C; PLC = phospholipase C; Prot.-Phos = protein phosphorylation. Mayo Clinic Proceedings 2000 75, 1275-1283DOI: (10.4065/75.12.1275) Copyright © 2000 Mayo Foundation for Medical Education and Research Terms and Conditions
Fig. 2 Renal autoregulatory effects of adenosine under physiologic conditions (dotted arrows). Increased tubular load (eg, sodium) increasesenergy metabolismand generationof adenosine which in turn provides a negative feedback for energy metabolism by decreasing renal blood flow (RBF) and glomerularfiltration rate (GFR). Proposedpathophysiologic renal effects of contrastmedia (solid arrows) by causing afferent arteriolevasoconstriction and adenosinerelease and leading to a decrease inRBFandGFR, renal ischemia, and eventuallyto acute renal failure. ATP= adenosinetriphosphate; NO = nitric oxide; PGI2 = prostaglandin 1.2 Mayo Clinic Proceedings 2000 75, 1275-1283DOI: (10.4065/75.12.1275) Copyright © 2000 Mayo Foundation for Medical Education and Research Terms and Conditions