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(Circulation. 2009;120:1749-1751.)
© 2009 American Heart Association, Inc.

Editorial

Prostaglandin-Based Renal Protection Against Contrast-Induced Acute Kidney Injury

Peter A. McCullough, MD, MPH; James A. Tumlin, MD

From the Department of Medicine, Division of Nutrition and Preventive Medicine, Department of Cardiology, William Beaumont Hospital, Royal Oak, Mich (P.A.M.), and Department of Internal Medicine, Division of Nephrology, University of Tennessee College of Medicine, Chattanooga (J.A.T.).

Correspondence to Peter A. McCullough, MD, MPH, Divisions of Cardiology, Nutrition, and Preventive Medicine, William Beaumont Hospital, 4949 Coolidge, Royal Oak, MI 48073. E-mail peteramccullough@gmail.com

Key Words: Editorials • contrast media • coronary disease • kidney • prostaglandins • vasodilation

An extract of the first 250 words of the full text is provided, because this article has no abstract.

It has been known for >3 decades that the kidneys rely considerably on a group of prostaglandins that are locally produced in both a constitutive and inducible fashion, primarily in the medulla, to regulate renal blood flow and a variety of functions in tubular cells that occupy that region of the kidney. Arachidonic acid released from phospholipids is converted by cyclooxygenase (COX-1 constitutively, COX-2 inducibly) in the kidney to PGI₂, PGE₂, PGF₂, PGD₂, and thromboxane A₂. PGE₂ and PGF₂ are produced predominantly but not exclusively in the renal medulla, whereas degradative enzymes are present in both the cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron, with urinary levels reflecting renal synthesis. In response to ischemia, vasoconstriction, norepinephrine, or angiotensin II, the kidney increases prostaglandin synthesis to modulate renal vascular resistance with a predominance of PGI₂ and PGE₂, which are vasodilatory, in contrast to PGF₂ and thromboxane, which are vasoconstricting.¹ These actions may be more pronounced in patients with diabetes mellitus because both the endothelial isoform of nitric oxide synthase and the COX-1 and COX-2 enzymes lose their normal regulation in the outer medulla of diabetic rats.^2,3 In addition to these effects in diabetic patients, prostanoids appear to offset the vasoconstrictive effects of iodinated contrast agents. For example, Agmon and coworkers⁴ examined the effects of vasodilatory prostaglandins on outer medullary blood flow in a rat model of contrast nephropathy and demonstrated . . . [Full Text of this Article]

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