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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of volume depletion and renal ischemia in the development of renal functional impairment in glycerol-induced ARF is not clear. This study was designed to evaluate the role of volume depletion in this model by determining the hemodynamic and functional alterations which occur between 3 and 18 hr after glycerol administration and the reversibility of these changes in response to Ringer loading. Three hours after glycerol, Cln and RBF, measured by flowmeter, were reduced 70% and 52%, respectively, in comparison with control values. FeNa was 0.04%. Ringer loading increased Clkn to 103% and RBF to 93% of control values. Qualitatively similar results were found 6 hr after glycerol. At 18 hr, Cln and RBF were 47% of control values. After Ringer loading, RBF rose to 100% of control. The response of Cln, however, was a function of the baseline FeNa. Cln incrased substantijally in rats with low FeNa but changed only slightly in animals in which this parameter was increased. These studies indicate that the early reduction in the Cln is dependent upon the fall in RBF. At 12 and 18 hr, however, the fall in Cln is not blood flow-dependent, and a second mechanism must be operative. FeNa seems to be a reliable index of the functional status of a given animal.
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PMID:Sequential studies on the pathophysiology of glycerol-induced acute renal failure. 740 Jun 68

Acute renal failure induced by the administration of gentamicin (GM) was studied enzymochemically in comparison with that in rats with tubular disorder resulting from postischemic reperfusion. Renal ischemia was caused by clamping the renal artery for 30 minutes to create complete ischemia and reflow. The activities of renal tissue glutathione peroxidase (GSH-Px) and the values to the renal contents of glutathione (GSH) and malondialdehyde (MDA) were measured in each sample. In order to confirm whether GSH plays an important role in the intrinsic anti-oxidant system in this model, buthionine sulfoximine (BSO), which is a gamma-glutamylcysteine synthetase inhibitor, was administered intraperitoneally to decrease the renal GSH content before the procedure in renal ischemia. On the other hand, the GM-induced ARF model was made by injection with GM 100 mg/kg during a period of 5 days. In the GM group, a significant increase in MDA and a reduction in the sphigomyelin (SPH)/phosphatidylcholine (PC) ratio and inactivation of PLA2 were observed. In the kidney tissue obtained 15 min. after reperfusion, the renal content of MDA was elevated markedly in the BSO-preadministered group. A reduction of SPH/PC ratio was also observed in the reperfusion model. PAL2 hydrolyzes the acyl group at the 2-position containing much of the highly unsaturated fatty acids that are easily oxidized. Further, PLA2 is considered to act directly on one of PC or phosphatidylinositol. Phospholipidosis thesauruses, noted in acute renal failure induced by GM, is considered to be caused by reduced liberation of lysosomal intramembranous phospholipid into the cytoplasm and accelerated peroxidation of intramembranous lipid.
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PMID:[Lipid peroxidation and tubular disorder in experimental acute renal failure-enzymochemical study in the rat kidney]. 807 17

Although the search for effective methods of renal prophylaxis during aortic surgery spans many decades, definitive answers are scarce. The literature is voluminous, yet the amount of work clearly relevant to the specific clinical situation of perioperative prophylaxis is small. Given the significant morbidity and subsequent mortality involved with perioperative ARF, it is difficult to sit back and do nothing when pharmacologic agents empirically are believed to possibly benefit the patient. Care must be taken to apply data from different clinical scenarios in the literature to the situation at hand. Drugs felt to be innocuous, even in low doses, may be insidiously counterproductive or damaging if they are not managed properly. Maintaining an adequate preload and stable hemodynamics seems to be the most logical universal approach at this time. Furosemide treatment without maintaining an adequate volume status once diuresis commences may be detrimental, which is true with the diuretic effects induced by mannitol or dopamine. The tachycardia resulting from a relative hypovolemia and from the beta effects of dopamine can cause myocardial ischemia from increased oxygen demand. Low urine output does not portend a negative outcome in the face of an adequate intravascular volume any more than an induced diuresis prevents renal injury. Currently, minimization of renal ischemia and maintenance of an adequate intravascular volume and renal hemodynamics are the keys to optimizing renal outcome during aortic surgery. Other maneuvers are not definitive and should be cautiously undertaken.
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PMID:Intraoperative management of renal function in the surgical patient at risk. Focus on aortic surgery. 1109 87

Most cases of ARF are secondary to volume depletion. In the literature, very few scientific publications address the problem of what to do when confronted with such a patient. As regarding the diagnosis of hypovolemia, an accurate history and physical examination can help to determine both the presence and etiology of volume depletion; postural hypotension (decrement in systolic blood pressure of more than 20 mmHg after standing from the supine position), associated with a pulse increment of 30 beats/min or more and dizziness are specific symptoms of hypovolemia. Laboratory indices are useful to diagnose volume depletion, but their interpretation is not simple, and they may not be available in the non-nephrologic environment. Fluid replacement therapy in hypovolemia is largely dependent upon the type of fluid that has been lost and concurrent electrolytic and acid-base disorders. Patients with hypernatremia and volume depletion should receive mild hypotonic solutions, whereas those with hyponatremia and hypovolemia should receive mild hypertonic solutions. The entity of reinfusion depends on daily losses. Conversely, monitoring of body weight can be considered an adequate index of fluid balance. Concerning the treatment of ARF, the use of loop diuretics in the early phases of pre-renal ARF decrease oxygen consumption in the tubular cells by inhibiting transcellular sodium transport, therefore preventing or limiting ischemic cell injury. The use of loop diuretics should also be evaluated in intermediate syndrome and ischemic NTA where diuretics can, respectively, reduce renal ischemia and convert oliguric ARF into the non-oliguric form.
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PMID:[Clinical management of the patient affected with acute renal failure (ARF) secondary to volume depletion]. 1452 97

Postischemic acute renal failure is worsened when occurs in a various conditions with impaired nitric oxide (NO) synthesis, such as arterial hypertension. Reoxygenation itself increases ischemic injury through the massive production of oxygen-free radicals. Therefore, we have directed our investigations to effects of both NO donor and antioxidant treatment on course of acute renal failure in experimental hypertension. Experiments were performed in anesthetized, adult male spontaneously hypertensive rats. In ARF groups the right kidney was removed, and rats were subjected to renal ischemia by clamping the left renal artery for 40 min. Experimental group received NO donor L-arginine (2 g/kg b.m.) (LArg group), or oxidant scavenger vitamin C (100 mg/kg b.m.) (Vit C group) during 3 days before the period of ischaemia. All parameters were measured 24 h after reperfusion. The mean arterial pressure was markedly reduced and renal vascular resistance significantly dropped in the ARF+L-Arg group vs. ARF group. Tubular injuries were similar between the ARF+L-Arg and ARF groups. Intensity of tubular necrosis and dilatation was markedly reduced in ARF+Vit C group in comparison to ARF. L-arginine failed to reduce tubular injury, despite its evident improvement of systemic and renal haemodynamic, thus NO seems to act as a double-egged sword, but reduction of tubular injury promotes vitamin C as an effective chemoprotectant against ishemia-reperfusion tubular injury in hypertension.
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PMID:Comparative effects of L-arginine and vitamin C pretreatment in SHR with induced postischemic acute renal failure. 1989 87