1. 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 (December 2000)
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2. 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.
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3. 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
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