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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diuretics have found wide application in critical care medicine. The use of mannitol and loop diuretics in a variety of life-threatening disorders is reviewed. The combined venodilatory and natriuretic effects of bumetanide, furosemide and ethacrynic acid relieve congestive symptoms in pulmonary edema. Although commonly administered to prevent development of acute tubular necrosis or in varying stages of evolving disease, few data are available to demonstrate the efficacy of mannitol or loop diuretics. An approach to the oliguric patient with acute tubular necrosis is described. The dangers of hyponatremia are reviewed, and the rational use of loop diuretics and hypertonic saline is outlined. The 3 loop-active agents inhibit calcium reabsorption in the thick ascending limb of Henle's loop and therefore have proved useful in treating hypercalcemia. A practical approach to the diuretic-saline treatment of severe hypercalcemia is outlined. The kaliuretic effect of loop diuretics can be used to advantage in patients with acute or chronic hyperkalemia. A guide to such therapy is described.
Am J Cardiol 1986 Jan 24
PMID:Diuretic use in critical care. 351 55

Contrast-induced nephropathy (CIN) is the third leading cause of acute kidney injury in hospitalized patients and is associated with significant patient morbidity. The pathogenesis of CIN is complex and not fully understood, but iodinated contrast agents induce intense and prolonged vasoconstriction at the corticomedullary junction of the kidney. Moreover, high-osmolar dyes directly impair the autoregulatory capacity of the kidney through a loss of nitric oxide production. These effects, coupled with direct tubular toxicity of contrast media, lead to overt acute tubular necrosis and the syndrome of CIN.
Am J Cardiol 2006 Sep 18
PMID:Pathophysiology of contrast-induced nephropathy. 1694 76

Contrast induced nephropathy (CIN) remains a common complication of coronary angiography. There is no specific treatment once contrast induced acute renal failure develops, and management must be as for any cause of acute tubular necrosis, with the focus on maintaining fluid and electrolyte balance. The best treatment of CIN is prevention. A variety of preventive measures including the administration of intravenous saline or possibly sodium bicarbonate and the antioxidant acetylcysteine may reduce the risk of CIN.
Int J Cardiol 2009 May 29
PMID:The value of hydration and acetylcysteine in the prevention of contrast-induced nephropathy: a potentially catastrophic complication of the percutaneous coronary interventions. 1765 30

Contrast media induce various factors that may increase vasoconstriction and decrease vasodilatation in the renal medulla, leading to hypoxia and acute tubular necrosis known as contrast-induced nephropathy (CIN) that tends to occur in diabetics and patients with preexisting renal insufficiency. Contrast media inhibit mitochondrial enzyme activities and subsequently increase adenosine through hydrolysis of ATP. Both catabolism of adenosine and medullary hypoxia generate reactive oxygen species (ROS) that scavenge nitric oxide (NO). Released along with endothelin and prostaglandin from endothelial cells exposed to contrast media, adenosine activates the A1 receptor that mainly constricts afferent arteriole at the glomerulus but not the medullary vasculature. Adenosine also activates the A2 receptor that increases NO production, leading to medullary vasodilatation which is induced by activation of endothelin-B receptor and G-protein coupled E-prostanoid receptor 2, and 4 of prostaglandin PGE2 respectively as well. Conversely medullary vasoconstriction is mediated by activating endothelin-A receptor and G-protein coupled E-prostanoid receptor 1, and 3 of prostaglandin PGE2 respectively. The osmotic load of contrast media increases interstitial pressure and sodium transport and thus oxygen consumption. Risking hypoxia, increased medullary oxygen consumption may also result from stimulating Na(+)-K(+)-ATPase activity by endothelin-A receptor. N-acetylcysteine (NAC) scavenges ROS and therefore preserves NO that not only dilates medullary vasculature but also reduces sodium reabsorption and oxygen consumption, tipping the balance against medullary vasoconstriction, hypoxia, and thus CIN. While prostacyclin and its analog, iloprost, prevent CIN by inducing medullary vasodilatation, atrial natriuretic peptide (ANP) may do so by inhibiting renin secretion.
Int J Cardiol 2012 Jul 12
PMID:Pathophysiology of contrast-induced nephropathy. 2302 89

Contrast-induced acute kidney injury (CI-AKI) refers to acute kidney injury (AKI) after intravenous or intra-arterial administration of contrast media (CM). The 2 key mechanisms related to AKI are acute tubular necrosis and prerenal azotemia. Although the pathophysiology of AKI is complex, modern frameworks show that AKI has 3 major pathways: hemodynamic injury, systemic inflammation, and toxic injury. In the pathophysiology of CI-AKI, 3 major distinct, but potentially interacting pathways are recognized: hemodynamic effects, increase in oxygen free radicals, and direct CM molecule tubular cell toxicity. This article reviews the pathophysiology of CI-AKI by describing and explaining these pathways.
Interv Cardiol Clin 2014 Jul
PMID:Pathophysiology of Contrast-Induced Acute Kidney Injury. 2858 21

Contrast-induced nephropathy, or contrast-induced acute kidney injury (AKI), is an acute impairment of renal function as manifested by an increase in serum creatinine. Different urinary and serum proteins have been intensively investigated as possible biomarkers for the early diagnosis of AKI. Promising candidate biomarkers have the ability to detect an early and graded increase in tubular epithelial cell injury and to distinguish prerenal causes of AKI from acute tubular necrosis. In this article new, emerging biomarkers of contrast-induced AKI are presented and described, of which serum neutrophil gelatinase-associated lipocalin appears to be the most promising.
Interv Cardiol Clin 2014 Jul
PMID:Biomarkers of Contrast-Induced Nephropathy: Which Ones and What Is Their Clinical Relevance? 2858 23