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      Urinary Excretion of Vasoactive Factors following Contrast Media Exposure in Humans

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          Background: Radiographic contrast media (CM) induce renal vasoconstriction and may initiate induced nephropathy. Endothelin (ET), a vasoconstrictor, and nitric oxide (NO), a vasodilator, which are synthesized in the kidney by the vascular endothelium as well as by tubular epithelial and glomerular mesangial cells, are key modulators of renal circulation after CM administration. Intravascular CM, in addition, induces pronounced diuresis and natriuresis. The aim of the present study was to evaluate and compare changes in endogenous vasoactive mediators and contrast-induced natriuresis after CM administration. Methods: Diagnostic angiographic procedures were performed in 14 patients (9 males and 5 females) using the non-ionic CM Iopamidol. Before and immediately after angiography, venous blood and urine samples were obtained. The urinary excretion of ET-1 and nitrates/nitrites (NOx), and the fractional excretion of sodium (FENa) were measured and analyzed. Results: The urinary excretion of both ET-1 and NOx increased significantly (p < 0.05) after angiography, and urinary ET-1 and NOx excretion was correlated with an increase in FENa (p < 0.05). Conclusion: Exposure to CM in humans is associated with an increase in urinary ET and NOx. The excretion of sodium following CM administration is associated with an increase in urinary ET and NOx. ET and NO might be important in the renal change in humans after CM administration.

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          Most cited references 17

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          Hospital-acquired renal insufficiency: a prospective study.

          Twenty-two hundred sixty-two consecutive medical and surgical admissions were evaluated prospectively to determine the contribution of iatrogenic factors to the development of renal insufficiency in hospital. Of 2,216 patients at risk, some degree of renal insufficiency developed in 4.9 percent. Decreased renal perfusion, postoperative renal insufficiency, radiographic contrast media, and aminoglycosides accounted for 79 percent of the episodes. Iatrogenic factors, broadly defined, accounted for 55 percent of all episodes. Poor prognostic indicators included oliguria, urine sediment abnormalities and, most importantly, severity of renal insufficiency; with an increase in serum creatinine of 3 mg/dl or greater, the mortality rate was 64 percent. Age, admission serum creatinine levels, and the number of episodes of renal insufficiency did not significantly affect outcome. We conclude that there is a substantial risk of the development of renal failure in hospital and that the mortality rate due to hospital-acquired renal insufficiency remains high.
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            Salt-sensitive hypertension in endothelin-B receptor-deficient rats.

            The role of the endothelin-B receptor (ET(B)) in vascular homeostasis is controversial because the receptor has both pressor and depressor effects in vivo. Spotting lethal (sl) rats carry a naturally occurring deletion in the ET(B) gene that completely abrogates functional receptor expression. Rats homozygous for this mutation die shortly after birth due to congenital distal intestinal aganglionosis. Genetic rescue of ET(B)(sl/sl) rats from this developmental defect using a dopamine--hydroxylase (DBH)-ET(B) transgene results in ET(B)-deficient adult rats. On a sodium-deficient diet, DBH-ET(B);ET(B)(sl/sl) and DBH-ET(B);ET(B)(+/+) rats both exhibit a normal arterial blood pressure, but on a high-sodium diet, the former are severely hypertensive. We find no difference in plasma renin activity or plasma aldosterone concentration between salt-fed wild-type, DBH-ET(B);ET(B)(+/+) or DBH-ET(B);ET(B)(sl/sl) rats, and acute responses to intravenous L-NAME and indomethacin are similar between DBH-ET(B);ET(B)(sl/sl) and DBH-ET(B);ET(B)(+/+) rats. Irrespective of diet, DBH-ET(B);ET(B)(sl/sl) rats exhibit increased circulating ET-1, and, on a high-sodium diet, they show increased but incomplete hypotensive responses to acute treatment an ET(A)-antagonist. Normal pressure is restored in salt-fed DBH-ET(B);ET(B)(sl/sl) rats when the epithelial sodium channel is blocked with amiloride. We conclude that DBH-ET(B);ET(B)(sl/sl) rats are a novel single-locus genetic model of severe salt-sensitive hypertension. Our results suggest that DBH-ET(B);ET(B)(sl/sl) rats are hypertensive because they lack the normal tonic inhibition of the renal epithelial sodium channel.
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              Contrast-medium-induced acute renal failure.


                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                November 2005
                06 July 2005
                : 101
                : 3
                : c150-c154
                Department of Radiology, Nippon Medical School, Tokyo, Japan
                86715 Nephron Clin Pract 2005;101:c150–c154
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 2, References: 25, Pages: 1
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                Original Paper

                Cardiovascular Medicine, Nephrology

                Angiography, Endothelin, Contrast media, Nitric oxide, Sodium


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