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

The delayed onset of anuria/oliguria in acute tubular necrosis has been theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental as well as a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea, and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of one kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although three patients with polyuric failure died before split studies could be run and two others have been too recent for computer analysis to have been completed, nine of the remaining ten had significantly greater renal plasma flows (194 versus 121 ml/min M(2), p < .01) and significantly greater urine flows (.99 versus .18 ml/min M(2), p < .01) on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the tenth patient with renal failure and in the six survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (p < .01) in these 21 shock patients. Such data suggest that delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria and then to anuria.
 ...
PMID:Renal decapsulation in the prevention of post-ischemic oliguria. 40 54

Renal function and morphology were studied before and after 60 min of renal ischemia and contralateral nephrectomy in two groups of rabbits. The animals were pretreated with ginsenosides (n = 22) and saline (n = 22) respectively, the latter as control. Results showed that ginsenosides (30 mg/kg body wt.) pretreatment by intravenous injection 10 min before warm ischemia resulted in the survival of all the animals with better renal function, 1, 3 and 7 days after blood urea nitrogen, fraction of excreted sodium and urine protein were observed in the control rabbits and a less pronounced increase was noted (P less than 0.05) after pretreatment with ginsenosides. The appearance of kidney tissue taken from surviving rabbits with Ginsenosides pretreatment was found to be normal under light microscope. Severe tubular necrosis was observed in kidneys of the control group. Tissues were examined with a transmission electron microscope. ginsenosides have protective effects on the epithelial cells of the proximal convoluted tubules, and microvilli and mitochondria were less damaged by ischemia than those of the control animals. There was also a large amount of ribosome on rough surfaced endoplasmic reticulum in the cells of ginsenosides-treated kidney, reflecting their ability to stimulate ribonucleic acid and protein synthesis. This is considered to be the basis of improvement of renal function.
 ...
PMID:[Protective effects of ginsenosides on warm ischemic damages of the rabbit kidney]. 132 38

The effects of antioxidant therapy with probucol were evaluated in rats subjected to 1 h renal ischemia and to 24 h reperfusion. Probucol exerted significant antioxidant effects in renal cortical tubules in vitro when exposed to a catalase-resistant oxidant. At 24 h probucol treatment (IP) improved single nephron glomerular filtration rate (SNGFR) (28.1 +/- 3.3 nl/min) in comparison to untreated ischemic (I) rats (15.2 +/- 3.0), primarily as a result of improving SNGFR in a population of low SNGFR, low flow and/or obstructed nephrons. However, absolute proximal reabsorption remained abnormally low in IP rats at 24 h (5.9 +/- 0.8 nl/min), and cell necrosis was greater than in I rats. Kidney GFR remained low in IP rats due to extensive tubular backleak of inulin measured by microinjection studies. Evaluations after 2 h of reperfusion revealed a higher SNGFR in IP (36 +/- 3.1 nl/min) than I rats (20.8 +/- 2.7 nl/min). Absolute proximal reabsorption was essentially normal (11.6 +/- 1.3 nl/min) in IP rats, which was higher than IP rats at 24 h and the concurrent I rats. Administration of the lipophilic antioxidant, probucol, increased SNGFR and proximal tubular reabsorption within 2 h after ischemic renal failure. Although SNGFR remained higher than I rats at 24 h, absolute reabsorption fell below normal levels and tubular necrosis was more extensive in IP rats. Early improvement in nephron filtration with antioxidants may increase load dependent metabolic demand upon tubules and increase the extent of damage and transport dysfunction.
 ...
PMID:Ischemic acute renal failure and antioxidant therapy in the rat. The relation between glomerular and tubular dysfunction. 283 99

Experiments were performed on rats subjected to renal ischemia and various treatment procedures to determine the origin and functional consequences of vascular obstruction. To this end, its occurrence and severity was assessed qualitatively and quantitatively in the outer medulla, where it is particularly prominent. The incidence of medullary hyperemia was not influenced by inhibiting thrombocyte aggregation with 5 or 70 mg/kg of acetyl salicylic acid or preventing fibrin deposition with 100 IE/kg of heparin before ischemia, and these substances produced no improvement renal function. The incidence and degree of hyperemia, however, could be substantially reduced or completely eliminated by acutely raising blood pressure after ischemia or by decreasing the number of circulating erythrocytes before ischemia. These procedures were effective in raising filtration rate and tubular reabsorption from 20% to 60% of normal, in restoring renal blood flow and vascular resistance to completely normal, and in diminishing epithelial damage both three and 18 hours after ischemia. The following conclusions are drawn: first, vascular obstruction, which is not lessened by inhibiting thrombus formation but is easily reversed or prevented by raising perfusion pressure or decreasing hematocrit, is probably caused by erythrocyte aggregation during ischemia. Second, vascular obstruction, which appears to raise renal vascular resistance and lower blood flow and filtration rate, cannot be limited to the medulla but must also be present in the cortex. Finally, reversing or preventing vascular obstruction can fully restore renal perfusion, partially restore glomerular and tubular function, greatly reduce tubular necrosis and thus prevent renal failure.
 ...
PMID:The contribution of vascular obstruction to the functional defect that follows renal ischemia. 356 Jun 46

In a restrospective study of 220 patients with melioidosis admitted to the hospital over a period of 3.5 years, acute renal failure was noted in 77 patients. Interesting clinical features included hypercatabolism, hypoalbuminemia, hyponatremia, jaundice and multisystem involvement. Prognosis was poor especially when associated with jaundice, lung involvement and the presence of underlying diseases. Mortality rate was 89.6%. Renal failure is believed to the due to renal ischemia from multiple nonspecific factors. In a limited pathological study renal changes consisted of tubular necrosis, microabscesses, interstitial nephritis and mild tubular degeneration.
 ...
PMID:Renal failure in melioidosis. 360 Sep 25

Sprague-Dawley rats were injected with known nephrotoxic doses of tobramycin and then subjected to varying amounts of warm renal ischemia. Analysis of serum creatinine at the time of sacrifice revealed no statistically significant difference among controls and the two doses of tobramycin at any given duration of ischemia. Light microscopy revealed no worsening of tubular necrosis with increasing doses of tobramycin.
 ...
PMID:Tobramycin and renal ischemia. 378 4

Since prostacyclin (PGI2) is known to regulate renal cortical blood flow and since ischemia stimulates thromboxane (Tx) A2 synthesis, the role of these prostanoids in moderating the response to renal ischemia was studied in the rat. At baseline, plasma TxB2 concentration in untreated animals (n = 13) was 357 pg/ml. The left renal pedicle was clamped for 45 minutes after a right nephrectomy (n = 16), which led after 5 minutes of reperfusion to a rise in TxB2 to 2825 pg/ml (p less than 0.001), but there was no change in 6-keto-PGF1 alpha. After 24 hours creatinine levels rose from 0.4 to 3.0 mg/dl (p less than 0.001), and left renal weight rose from 94% to 117% (p less than 0.001) relative to the weight of the right kidney. In nephrectomized but nonischemic sham control rats (n = 7), creatinine level was 0.9 mg/dl and kidney weight 91% after 24 hours. Pretreatment with OKY 046 (n = 13) (2 mg/kg administered intravenously) blocked ischemia-induced TxB2 synthesis, while 6-keto-PGF1 alpha levels rose from 96 to 302 pg/ml (p less than 0.001). There was no increase in creatinine levels or kidney weight relative to the sham group. Pretreatment with ibuprofen (n = 10) (12 mg/kg) or OKY 046 and ibuprofen (n = 9) inhibited TxB2 and 6-keto-PGF1 alpha synthesis, but creatinine levels and renal weight rose (p less than 0.001). Renal histology in OKY 046-pretreated animals was equal to that in nephrectomized controls, while all other ischemic groups showed tubular necrosis. Results indicate that a high PGI2/TxA2 ratio protects against renal ischemia.
 ...
PMID:Prostacyclin and thromboxane A2 moderate postischemic renal failure. 389 35

To examine the role of the renal vascular receptor in the control of renin secretion in the rat, a denervated, nonfiltering kidney model (DNFK) was developed. The left kidney was subjected to a 2-hr period of total renal ischemia followed by ureteral ligation and section Denervation was accomplished by stripping all visible nerves and painting the renal vessels with 5% phenol. Forty-eight hours later lissamine green dye was injected iv and failed to appear in either the cortical or medullary tubules, indicating that glomerular filtration had ceased. Histological study of these kidneys revealed diffuse tubular necrosis with extensive intratubular cast formation. Norepinephrine content of the DNFK was reduced 91% compared to the contralateral normal kidney (P less than 0.001). In another group of anesthetized rats with a single DNFK, 15 min of suprarenal aortic constriction (SAC) increased plasma renin activity (PRA) from 3.4 +/- 0.6 to 11.5 +/- 1.6 ng AI/ml/hr; in a time control series, PRA was unchanged. To exclude the influence of adrenal catecholamines in this response, bilateral adrenalectomy was performed in a separate group of animals with a DNFK. In this series, SAC also markedly increased PRA. The present data indicate that in the rat the macula densa, the renal nerves, and adrenal catecholamines were not essential for the hyperreninemia induced by a reduction in renal perfusion pressure.
 ...
PMID:A denervated nonfiltering kidney preparation in the rat: a model for study of renin release. 634 93

The high blood flow rate/gram of kidney tissue supplies mainly the renal cortex. The net effect of the interaction of the renin-angiotensin system, the kallikrein-kinin system and prostaglandins is to autoregulate renal blood flow within a narrow range. Drugs and neurogenic factors also influence renal hemodynamics. The renal circulation responds to changes in extracellular fluid volume, and in cardiac output. Renal ischemia occurs readily as these parameters decrease and prompt correction of circulatory dynamics can restore renal blood flow and prevent tubular necrosis. With hypovolemia or heart failure, angiotensin II is a mediator of efferent arteriolar constriction promoting a proportionately greater fall in renal plasma flow than in glomerular filtration rate, thereby augmenting sodium reabsorption. With renal failure, glomerulotubular balance is affected conversely promoting sodium loss. Appreciating these distinctions allows recognition of inappropriate sodium retention or loss. With such data, prognosis can be estimated more accurately and attempts to restore circulatory dynamics can be guided.
 ...
PMID:Pathophysiology of renal hemodynamics. 726 10

Xanthine oxidase (XO) activity and hydroxyl radical (.OH) formation are widely proposed mediators of renal reperfusion injury, potentially altering the severity of, and recovery from, postischemic acute renal failure. The goal of this study was to ascertain whether combination XO inhibitor (oxypurinol) and .OH scavenger (Na benzoate) therapy, given at the time of renal ischemia, alters the extent of: (1) tubular necrosis and filtration failure; (2) DNA fragmentation/apoptosis (assessed in situ by terminal deoxynucleotidyl transferase reactivity); (3) early tubular regenerative responses (proliferating cell nuclear antigen expression; (3H)thymidine incorporation); and (4) the rate and/or degree of functional and morphologic repair. The effects of XO inhibition, .OH scavengers, and "catalytic" iron (FeSO4) on human proximal tubular cell proliferation in vitro were also assessed with a newly established cell line (HK-2). Male Sprague-Dawley rats were subjected to 35 min of bilateral renal arterial occlusion with or without oxypurinol/benzoate therapy. These agents did not alter the extent of tubular necrosis or filtration failure, proliferating cell nuclear antigen expression or thymidine incorporation, or the rate/extent of renal functional/morphologic repair. DNA fragmentation did not precede tubular necrosis, and it was unaffected by antioxidant therapy. By 5 days postischemia, both treatment groups demonstrated regenerating epithelial fronds that protruded into the lumina. These structures contained terminal deoxynucleotidyl transferase-reactive, but morphologically intact, cells, suggesting the presence of apoptosis. Oxypurinol and .OH scavengers (benzoate; dimethylthiourea) suppressed in vitro tubular cell proliferation; conversely, catalytic Fe had a growth-stimulatory effect. These results suggest that: (1) XO inhibition/.OH scavenger therapy has no discernible net effect on postischemic acute renal failure; (2) DNA fragmentation does not precede tubular necrosis, suggesting that it is not a primary mediator of ischemic cell death; and (3) antioxidants can be antiproliferative for human tubular cells, possibly mitigating their potential beneficial effects.
 ...
PMID:An evaluation of antioxidant effects on recovery from postischemic acute renal failure. 791 60


1 2 3 4 5 6 7 8 Next >>