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Radiocontrast-induced nephropathy (RCIN), a leading cause of in-hospital acute renal failure, is an acute decrease in renal function related to intravascular administration of iodinated radiocontrast agents. Though RCIN is relatively uncommon in patients without predisposing factors, patients with preexisting renal dysfunction, diabetes mellitus and severe congestive heart failure are at increased risk for acute renal failure following radiocontrast. Three recently developed animal models have provided important insights into the pathophysiology of RCIN. Specifically, these studies have implicated transient renal ischemia, direct renal tubular toxicity and changes in glomerular capillary permeability as possible mediators of RCIN, and these pathophysiologic mechanisms are not mutually exclusive. There is currently no effective treatment for RCIN. Assuring adequate hydration may reduce the risk of RCIN. In addition, synthetic atrial natriuretic factor and/or mannitol are promising, but as yet unproven, approaches to the prophylaxis of RCIN.
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PMID:Radiocontrast-induced nephropathy: current status and future prospects. 138 89

The need to support the distal circulation during aortic crossclamping and the subsequent effects on hemodynamics and organ perfusion prompted our review of 51 patients who underwent repair of aneurysm of the descending thoracic aorta from 1983 through 1987. Forty-three patients had aneurysms originating distal to the left subclavian artery, and eight had aneurysms involving the distal aortic arch and the proximal descending aorta; 10 patients had emergency operation for aneurysm rupture. Three different techniques were used: Seventeen patients had left atrial-distal aorta arterial bypass with a centrifugal pump, 18 patients had a Gott shunt, and 16 patients had no circulatory support during aneurysm repair. Location and type of aneurysm, age, sex, diabetes, preoperative hypertension, and serum lipid levels were similar in the three groups. Duration of crossclamping was 54 +/- 12 minutes for left atrial-aortic assist, 45 +/- 5 for the shunt group, and 34 +/- 4 for patients without circulatory support. With crossclamping, all groups had similar and significant increases in heart rate (p less than 0.03). Proximal systolic blood pressure did not change during left atrial-aortic assist, but a transient increase occurred in patients with shunts (p less than 0.01), and a sustained increase occurred in patients without circulatory support (p less than 0.05). With crossclamp release, arterial pH and capillary pulmonary wedge pressure decreased significantly (p less than 0.05) in patients without shunt or bypass. Postoperative renal function did not vary significantly when circulatory support was used, but serum creatinine rose transiently in patients with unsupported aortic crossclamping. We conclude that support of the distal circulation during thoracic aortic crossclamping stabilizes hemodynamics and prevents systemic acidosis and renal ischemia. Further, our data suggest that the centrifugal pump may provide better protection than a passive shunt.
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PMID:Circulatory support during crossclamping of the descending thoracic aorta. Evidence of improved organ perfusion. 235 21

RCIRF is a complex syndrome resulting in acute renal dysfunction following exposure to radiologic contrast media. It accounts for 10 per cent of all cases of acute renal failure. The pathogenesis appears multifactorial but most probably involves contrast-mediated renal ischemia and direct tubular toxicity. Significant risk factors include preexisting renal insufficiency, diabetes mellitus, advanced age, volume depletion, and presence of multiple myeloma. The diagnosis should be suspected with acute renal dysfunction temporally related to radiologic contrast administration. The prognosis for recovery is good in most cases. Key preventive measures include identification of high-risk patients, ensuring adequate hydration prior to contrast agent administration, avoiding excessive and repeated contrast exposure, and instituting prophylactic therapy in selected cases.
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PMID:Radiologic contrast-induced renal failure. 329 29

More than 40,000 new patients begin treatment for end-stage renal disease in the United States each year. The most frequent causes are diabetes and hypertension. The incidence rates for blacks and Native Americans are six- to sevenfold in excess of those for whites. Studies are seeking to determine the roles of atherosclerotic vascular disease, renal ischemia, and the amount of renal mass on the rate of progressive renal disease. Other studies seek to identify the factors that predict the development of nephropathy in patients with diabetes mellitus. Treatment of hypertension slows the rate of progressive renal disease by 40% to 50%. Meta-analysis of several European studies suggests that dietary protein restriction appears to delay the onset of end-stage renal disease.
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PMID:Epidemiology and prevention of renal disease. 792 79

Although the new nonionic contrast agents are safer than ionic agents, renal insufficiency and even death still occur occasionally. Therefore, we have explored the use of carbon dioxide (CO2) as an alternative angiographic contrast agent used in combination with digital subtraction angiography. Clinical observations have been made in over 800 patients. The images obtained are of equivalent diagnostic quality compared with those using conventional iodinated contrast agents. Recent advances in imaging, including "stacking," provide images comparable with iodinated contrast. Very small vessels, equivalent to third-order branches of the renal artery, can be imaged satisfactorily with CO2. Occasional studies with CO2 yield information not apparent with iodinated contrast agents, including excellent visualization of arteriovenous shunts, collateral circulations, malignant tumors, and minute amounts of arterial bleeding. Many of the advantages and disadvantages of CO2 derive from its special physical and chemical properties. The advantages include no allergic potentiation and no renal metabolism of CO2, because CO2 is cleared by the lungs and does not recirculate. Other advantages include delivery by very small catheters because of the low viscosity of CO2, minimal discomfort on injection, and very low cost. However, the low-density and compressibility of CO2 poses some special problems. Imaging requires digital subtraction angiography with electronic enhancement and injections require an experienced investigator and, ideally, a dedicated CO2 injector. The dedicated CO2 injector provides calculated, controlled dosing and rates for injection, while excluding the possibility of air contamination. The buoyancy of CO2 inhibits good filling of dependent vessels. Accordingly, CO2 does not normally produce good nephrographic images, although proximal renal arteries are normally shown clearly. Experimental studies in dogs, whose renal arteries have been injected repeatedly with very large doses of CO2, demonstrate only transient changes in renal blood flow and no endothelial cell damage. However, these studies also showed clearly that renal ischemia can occur due to a "vapor lock" phenomenon if the kidney is positioned vertically above the injection site, and recurrent injections are given without time for absorption of the arterially delivered CO2 boluses. Uncontrolled studies in over 800 patients have confirmed that CO2 likely has a very low renal toxicity. At the University of Florida, CO2 is the radiologic contrast agent of choice in patients with renal insufficiency, especially those with diabetes mellitus, and in those with pre-existing allergy to iodinated contrast agents. Further controlled clinical studies are required to define the true clinical utility and safety of CO2 compared with conventional radiologic contrast agents.
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PMID:CO2 digital angiography: a safer contrast agent for renal vascular imaging? 794 29

Contrast-media associated nephropathy (CMAN) consists in a sudden impairment of glomerular filtration rate following exposure to radiographic contrast materials. Damage may be limited to an asymptomatic mild increase of blood creatinine, or reach the highest levels of nitrogen retention compatible with acute renal failure. Some preexisting clinical conditions or pathologies may lead to CMAN: not only renal insufficiency, diabetes mellitus, multiple myeloma, congestive heart failure and severe hypertension, but also simple dehydration and a growing series of immunologic diseases are recognized as predisposing condition. The exact mechanism responsible for renal injury is still doubtful but recently animal models have shown substantial ischemic changes that may be added to the traditional presumed pathogenesis of direct tubular toxicity and intra-tubular obstruction. As renal ischemia stimulates both endogenous vasoconstrictor and vasodilator substances, it is now supposed that CMAN acts similarly to non-steroidal anti-inflammatory agents, selectively inhibiting the vasodilatory prostaglandin phase and therefore causing a derangement of the physiologic vasoconstriction/vasodilatation balance of renal circulation. The role of oxygen free radicals to contribute to renal dysfunction is considered. Low osmolality non ionic contrast media when compared to conventional high osmolality ionic contrast media have reduced but not eliminated CMAN. Simple but effective lines of prevention include the previous selection of patients predisposed to CMAN for concomitant pathology, suspension of FANS or any other recognized nephrotoxic substance, the least amount of contrast media compatible with radiologic visualization of the patient's problem, careful hydration of the patient before contrast injection and sustained diuresis afterwards. The usefulness of pre-treatment with Ca-channel blockers or atrial natriuretic factors remains sub judice.
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PMID:[Physiopathology, clinical aspects and prevention of renal insufficiency caused by contrast media]. 917 67

We examined the influence of renal ischemia in rats with diabetes mellitus (DM). Male Wistar rats were rendered diabetic by streptozotocin treatment. Two weeks later, 30 minutes of complete ischemia was induced in the left kidney of DM and non-DM animals. Both groups were evaluated functionally and morphologically four or eight weeks post-ischemia. In non-DM animals renal function and morphology showed almost complete recovery. In the DM animals, however, this comparatively short period of ischemia caused a substantial loss of renal function. Four weeks post-ischemia inulin clearance in the DM kidneys rendered ischemic was only 20% of that in the corresponding non-DM kidneys, and after eight weeks the DM kidneys were completely anuric. Extensive inflammation and tubulointerstitial fibrosis were evident in DM kidneys four weeks after ischemia and seemed to increase over time. After eight weeks, tubular atrophy was found in the ischemic DM kidneys, resulting in a substantial loss of kidney mass. We conclude that in diabetic rats renal ischemia causes rapidly progressive kidney damage that in several respects resembles diabetic nephropathy in humans. Since advanced renal lesions similar to those seen in human diabetic nephropathy never develop in the rat solely as a result of DM, the present study may provide an experimental model for further studies on renal failure in diabetes mellitus.
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PMID:Ischemia causes rapidly progressive nephropathy in the diabetic rat. 932 37

The essential arterial hypertension is the second (after diabetes mellitus) cause of chronic renal failure which means a great social and economic burden to the society. It is well known that hypertension is a metabolic syndrome resulting in tissue injury. We tried to investigate the possible influence of some metabolic disturbances on renal function in nontreated essential hypertension. We have compared 25 patients with nontreated essential hypertension (11 women, 14 men) with 14 healthy volunteers (7 women, 7 men) matched for age. The patients' group was characterized by significantly higher urine excretion of NAG (N-acetyl-beta-D-glucosaminidase) (2.75 +/- 1.69 vs 1.82 +/- 1.46 p < 0.05) and a tendency to significantly higher urine fractional sodium excretion without significant difference in albumin excretion. These findings suggest that the tubular damage is present. We noticed the negative linear correlation between mean arterial pressure and (MAP) and NAG urine excretion in the group of hypertensive patients which may reflect the renal ischemia in tubulo-interstitial pathology. Our data suggests that in nontreated arterial hypertension the renal blood flow disturbances are the important cause of the deterioration of tubular function (which are earlier to glomerular damage).
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PMID:[Does any relationship exist between metabolic disturbances and some markers of renal damage in patients with untreated essential hypertension?]. 1139 62

Fenoldopam is an interesting orphan drug that is a variant of dopamine. It differs significantly from dopamine in that it is a specific agonist for the type I (DA-1) receptor. The DA-1 receptors are particularly prominent in the renal vasculature, renal tubules, mesenteric vasculature, and peripheral vessels. The DA-1 receptor stimulation vasodilates renal and peripheral vessels, causing a decrease in blood pressure and an increase in renal blood flow (RBF). Stimulation of the DA-1 receptors in the tubules causes an increase in sodium excretion, which gives rise to an increase in urine volume on the basis of a sodium natriuresis. Animal testing with fenoldopam has indicated that it is 6 times more potent than dopamine in its ability to decrease renal vascular resistance and increase RBF; this suggests that it could be a much more selective and potent renal protective agent against any toxin or stimulus that causes renal dysfunction by reducing RBF or increasing renal ischemia. The clinical activity of fenoldopam, which is administered intravenously, begins almost immediately and is clearly noticeable after 5 minutes. The drug has no rebound effect, and its use can be stopped at any time. The protocol for the use of fenoldopam as a renal protective agent (performed at the University of Minnesota) involves starting an intravenous fenoldopam infusion 2 hours before the procedure at a rate of 0.1 microg/kg/min and increasing the dose in increments of 0.1 microg/kg/min every 20 minutes, until a rate of 0.5 microg/kg/min is reached or the systolic blood pressure falls more than 40 mm Hg (or below 110 mm Hg). Any infusion level at or above 0.1 microg/kg/min is considered acceptable because the response in individual patients varies so widely. The fenoldopam infusion is maintained at the maximum rate throughout the procedure and for up to 4 hours after the end of the contrast administration. At the University of Minnesota, we have had anecdotal experience using the drug in 29 patients. The drug was used for patients who were thought to be at the highest risk for contrast-induced nephropathy, ie, patients who have both diabetes and pre-existing renal failure. In this small group of patients in whom hydration and other variables were not controlled, there was a startling lack of contrast-induced creatinine increase at any point during the 24 to 48 hours after the administration of contrast in all but 1 patient. Our experience suggests that fenoldopam may be of distinct benefit to high-risk patients who need intravascular contrast, especially those who may receive a large contrast dose, such as patients undergoing peripheral or coronary angiography and intervention and/or computed tomography. Although it is impossible on the basis of simple anecdotal case reports to determine whether or not the drug was the primary reason that such a marked protective effect was seen, the results are promising enough to indicate that a careful, prospective, randomized trial of fenoldopam versus hydration is warranted.
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PMID:Preventing contrast-induced nephropathy with fenoldopam. 1198 89

The renin-angiotensin system is initiate by numerous pathological situations which release the renal ischemia: heart failure, arterial hypertension, renal pathology with or without diabetes mellitus. Therapeutic possibilities in renin-angiotensin system control are offered by angiotensin-converting enzyme inhibitors, angiotensin II type-1 receptors antagonists, angiotensin converting enzyme inhibitors and neutral endopeptidase inhibitors and angiotensin II type 2 receptors agonists.
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PMID:[The renin-angiotensin system:implications, pathology, therapeutic possibilities, perspectives]. 1209 17


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