Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mannitol may be useful clinically both as a diuretic and as an obligate extracellular solute. As a diuretic it can be used to treat patients with intractable edema states, to increase urine flow and flush out debris from the renal tubules in patients with acute tubular necrosis, and to increase toxin excretion in patients with barbiturate, salicylate or bromide intoxication. As an obligate extracellular solute it may be useful to ameliorate symptoms of the dialysis disequilibrium syndrome, to decrease cerebral edema following trauma or cerebrovascular accident, and to prevent cell swelling related to renal ischemia following cross-clamping of the aorta. Largely unexplored uses for mannitol include its use as an osmotic agent in place of dextrose in peritoneal dialysis solutions, its use to maintain urine output in patients newly begun on hemodialysis, and its use to limit infarct size following acute myocardial infarction.
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PMID:Mannitol. 38 67

Brief renal ischemia-reperfusion is reported to precondition the myocardium; however, the underlying mechanisms are unknown. This phenomenon was, therefore, investigated using an in vivo rabbit model of acute myocardial infarction. Characterization of the mechanisms involved was performed using the nonselective adenosine receptor antagonist 8-(p-sulfophenyl)theophylline (8-SPT) and the ATP-sensitive potassium (KATP) channel blocker sodium 5-hydroxydecanoate (5-HD). Pentobarbital-anesthetized rabbits underwent a left thoracotomy and pericardiotomy. A laparotomy was then performed to expose the left renal artery. Animals were either preconditioned with a 10-min occlusion of the renal artery followed by 10 min of reperfusion or underwent a 20-min sham period of anesthesia. Subsequently, the left coronary artery was then occluded for 30 min and reperfused for 2 h. Infarct-to-risk ratio was limited from 32.7 +/- 4.0% (n = 12) in controls to 17.8 +/- 3.0% (n = 9; P = 0.002) in preconditioned hearts. Protection was abolished by 7.5 mg/kg iv 8-SPT (36.7 +/- 3.7%; n = 6) or 5 mg/kg iv 5-HD (33.1 +/- 4. 4%; n = 6) administered before preconditioning. 8-SPT (40.0 +/- 4. 4%; n = 6) or 5-HD (40.5 +/- 4.2%; n = 6) did not affect infarct-to-risk ratio in sham controls. Thus activation of both adenosine receptors and KATP channels appears to be involved in acute renal preconditioning of the myocardium.
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PMID:Renal ischemia preconditions myocardium: role of adenosine receptors and ATP-sensitive potassium channels. 981 59

The underlying mechanisms of myocardial preconditioning after a brief period of renal ischemia-reperfusion are unknown. The phenomenon itself and the involvement of AT(1) angiotensin receptors was therefore investigated using an in vivo rat model of acute myocardial infarction. Anesthetized rats underwent a left thoracotomy and pericardiotomy. A laparotomy was performed to expose the left renal artery. Animals were then preconditioned with four episodes, each consisting of 5 min of renal artery occlusion followed by 10 min of reperfusion, or underwent a 60 min sham period of anesthesia. Subsequently, the left coronary artery was occluded for 30 min and reperfused for 2 h. Area at risk and infarct size was estimated along with hemodynamic and temperature data recording. The infarct-to-risk ratio was limited from 56.36 +/- 2.36 and 50.65 +/- 4.71 in control to 12.0 +/- 0.48 and 12.57 +/- 0.44 in preconditioned hearts, by volume and weight methods. The protective effect of renal preconditioning on the myocardium was not abolished by losartan 1 mg/kg (10.11 +/- 0.12 and 11.2 +/- 1.4) pretreatment whereas it was completely attenuated by losartan 5 mg/kg (46.5 +/- 1.0 and 47.8 +/- 1.4) administration. Thus we can infer that angiotensin AT(1) receptors participate in renal preconditioning of the myocardium in in vivo rat hearts.
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PMID:Evidence of the role of angiotensin AT(1) receptors in remote renal preconditioning of myocardium. 1507 10

Renovascular hypertension is usually due to an atherosclerotic artery stenosis or a fibromuscular dysplasia. We describe an uncommon cause of renal ischemia. A 66-year-old woman was admitted for severe hypertension. During her stay, she presented an acute myocardial infarction with normal coronary angiography. After a flank pain, a contrast-enhanced abdominal computed tomography scan was performed which revealed a stenosis of the left main renal artery. However, renal angiography displayed a thrombosis. Transesophageal echocardiography showed a mobile mass attached to the mitral valve. A diagnosis of renal artery thrombosis and acute myocardial infarction both resulting from a cardiac tumour embolism was established.
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PMID:An uncommon cause of renovascular hypertension. 2250 78

Hypertension and kidney disease often coexist, further increasing the risk of future cardiovascular events. Treatment of hypertensive adults with an angiotensin converting enzyme inhibitor in case of concomitant kidney disease may slow disease progression. The third-generation liphophilic angiotensin converting enzyme inhibitor zofenopril, administered alone or combined with a thiazide diuretic, has proved to be effective in lowering blood pressure in hypertensive patients and to reduce the risk of fatal and non-fatal events in post-acute myocardial infarction and heart failure. In almost three-hundred hypertensive patients with kidney impairment zofenopril administered for 12 weeks showed a similar blood pressure-lowering effect irrespective of the stage of the disease, with larger effects in combination with a thiazide diuretic, particularly in patients with slightly or moderately impaired kidney function. In animal models, zofenopril produced a significant and long-lasting inhibition of kidney angiotensin converting enzyme inhibitor and prevented kidney morphological and functional alterations following kidney ischemia-reperfusion injury. Treatment of hypertensive patients for 18 weeks with a combination of zofenopril 30 mg and hydrochlorothiazide 12.5 mg resulted in a reduction in albumin creatinine ratio of 8.4 mg/g (49.6% reduction from baseline values) and no changes in glomerular filtration rate, variations in line with those obtained in the control group treated with a combination of irbesartan 150 mg and hydrochlorothiazide 12.5 mg. Thus, some preliminary evidence exists to support that relatively long-term treatment with the angiotensin converting enzyme inhibitor zofenopril alone or combined with hydrochlorothiazide is effective in controlling blood pressure and may confer some kidney protection due to ACE inhibition properties.
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PMID:Efficacy of Zofenopril Alone or in Combination with Hydrochlorothiazide in Patients with Kidney Dysfunction. 3036 Jul 26