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

Pretreatment with the thromboxane synthase inhibitor OKY-046 but not the cyclo-oxygenase inhibitor ibuprofen protects against ischemia-induced acute tubular necrosis. However, ibuprofen together with the vasodilating agent prostaglandin E1 is protective. This suggests that a high prostaglandin to thromboxane ratio is the major factor operative in preventing tubular necrosis, the subject of this study. Rats that had unilateral nephrectomy (n = 60) with the exception of rats that had sham operations (n = 8) underwent 45 minutes of left renal pedicle clamping. Thirty minutes before the operation, the rats received either a saline solution or a thromboxane synthase inhibitor that was given intravenously. The inhibitors OKY-046 (2 milligrams per kilogram, n = 10), UK38485 (1 milligram per kilogram, n = 9) and U63357A (10 milligrams per kilogram, n = 10) were given as a single bolus while the inhibitor CGS13080 (0.1 milligram per kilogram, n = 9, and 1.0 milligram per kilogram, n = 7) was given by constant infusion and continued for 60 minutes after reperfusion. With saline solution therapy, five minutes after reperfusion, thromboxane B2 increased from 154 to 2,537 picograms per milliliter (p less than 0.00001) and 6-keto-prostaglandin F1 alpha increased from 51 to 266 picograms per milliliter (p less than 0.004). At 24 hours, the creatinine level increased from 0.5 to 2.8 milligrams per deciliter (p less than 0.00001). Only OKY-046 yielded a creatinine level at 24 hours of 1.2 milligrams per deciliter, a value lower than that for those in the saline solution control group (p less than 0.002). Furthermore, OKY-046 led to the highest prostaglandin to thromboxane ratio (p less than 0.035). The five other ratios which occurred after drug therapy were inversely related to the decrease in the creatinine value (r = -0.93, p less than 0.02). Histologically, OKY-046 was the only thromboxane synthase inhibitor to prevent acute tubular necrosis (p less than 0.05). Results show that a high prostaglandin to thromboxane ratio protects against acute tubular necrosis.
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PMID:A high plasma prostaglandin to thromboxane ratio protects against renal ischemia. 367 99

Renal involvement in legionnaires' disease is a well-known, yet incompletely understood, complication. Manifestations of renal involvement include proteinuria, hematuria, pyuria, cylindruria, and azotemia. Previous cases of legionnaires' disease with renal involvement have shown pathophysiologic changes consistent with acute tubulointerstitial nephritis or acute tubular necrosis. A toxic metabolite produced by Legionella pneumophila has been theorized to produce a vasoconstrictive effect on the renal microvasculature, leading to ischemia and renal dysfunction. The case reported here is unique in that the patient presented with interstitial nephritis in the absence of pulmonary signs or symptoms.
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PMID:Interstitial nephritis in a patient with Legionnaires' disease. 380 71

Thromboxane (Tx) synthase but not cyclo-oxygenase inhibitors prevent acute tubular necrosis (ATN) after renal ischemia, a phenomenon believed to be due to stimulation of the endogenous production of vasodilating prostaglandins (PG). This study directly tests that vasodilating PG protect against the consequences of renal ischemia. Anesthetized, 500-g rats had right nephrectomy and 45 minutes of left renal pedicle clamping or sham clamping. The rats were treated with intravenous (I.V.) saline 1.9 mL/h starting 40 minutes after clamping or sham clamping. All rats except the sham group (N = 8) were pretreated 1 hour before ischemia with ibuprofen (12 mg/kg) to prevent prostanoid synthesis. Beginning 5 minutes before clamp release, the rats were treated intravenously for 2 hours with: saline vehicle (N = 9), PGE1 400 ng/kg/min (N = 6), nitroprusside 4 micrograms/kg/min (N = 8), or dopamine 3 micrograms/kg/min (N = 11). After 24 hours, sham rat creatinine level was 0.5 mg/dL and weight of the left kidney was 86.5% of the previously removed right kidney. Compared with sham rats, ischemia and saline treatment resulted in a rise in creatinine level to 2.7 mg/dL (p less than 0.05) and a rise in kidney weight to 101.9% (p less than 0.05); PGE1 led to a creatinine level of 1.1 mg/dL, a value lower than that of the rats treated with saline (p less than 0.05), and a kidney weight of 92.0%, a value similar to that of sham rats; nitroprusside and dopamine led to a rise in creatinine levels to 3.2 mg/dL (p less than 0.05) and 2.3 mg/dL (p less than 0.05), respectively, as well as a rise in kidney weight to 108.0% (p less than 0.05) and 105.4% (p less than 0.05), respectively. Histologic examination showed ATN in rats treated with saline, nitroprusside, and dopamine, but not in rats treated with PGE1. These results indicate that PGE1 protects the cyclo-oxygenase-treated kidney against ischemia-induced ATN.
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PMID:Vasodilator prostaglandins (PG) prevent renal damage after ischemia. 381 90

After a short literature survey, indicating the rarity of acute papillary necrosis in transplanted kidneys, the authors reported one of their patients, aged 32, with transplanted dead body kidney from a male, aged 30, with blood group compatibility and compatibility of two antigens in locus A. Two hemodialysis were necessiated because of acute tubular necrosis in the transplant. After the second one, performed 10 days after the transplantation, the patient felt very strong pains in the region of the transplant, edema around it and hypovolemic shock. The kidney was explanted and necrosis of the majority of the papillae in it--established, and around it--blood collection. After that incidence, the patients had three severe gastrointestinal hemorrhages with shocks, that necessitated profuse transfusion of blood. Their cause was a small erosion, about a lentil seed, at the pyloric opening, resulting from the cortico-therapy and periodic heparinization for dialysis. The patients was reanimated and returned to programmed chroniodialysis. The possible causes for papillary necrosis are discussed, most acceptable being two of them them--urostasis from 1200 ml urine in the urinary bladder, that required catheterization before the incidence and/or compression and ischemia of the transplanted kidney by the blood collection around it.
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PMID:[Acute papillary necrosis in transplanted kidney]. 391 82

An inordinately high rate of renal complications was encountered among 35 patients treated for thrombotic or thromboembolic occlusion of the leg by injection of streptokinase into a bypass graft or native artery. Five patients demonstrated massive myoglobinuria following restoration of flow to ischemic and necrotic tissues; acute tubular necrosis developed in 2 of them, and 1 patient died as a result of renal shutdown, electrolyte imbalance, hypofibrinogenemia, and mediastinal and retroperitoneal hemorrhage. Massive myoglobinuria was also noted in 5 out of 13 patients with compartment syndrome but no evidence of ischemic necrosis. This complication could be lessened by fasciotomy and resection of the upper third of the fibula. Although myoglobinuria and complications such as acute tubular necrosis are only rarely reported, they are not unexpected following muscular ischemia. Attempts to salvage irreparably damaged tissues by re-establishing circulation appear to carry an unacceptably high risk of renal complications and may even threaten the life of the patient.
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PMID:Streptokinase therapy: complications of intra-arterial use. 396 56

Post transplant acute tubular necrosis (ATN) is responsible for approximately 90% of acute renal failure episodes occurring within the first few weeks following renal transplantation. This phenomenon is observed in 34% of cadaver transplant recipients and 9% of those with live donor kidneys. Although the exact cause of post transplant ATN remains unknown, the following factors are thought to be associated with a higher incidence of ATN: 1) donor hypotension, 2) prolonged "warm ischemia time", 3) increased vascular resistance with poor perfusate flow, 4) presence of "ligandin" or excess lactate in the renal perfusate, 5) reduced allograft blood flow, 6) cold lymphocytotoxins in the patient's serum and 7) administration of nephrotoxic drugs particularly to the hypovolemic graft recipients. Therapeutic maneuvers such as hydration of the donors and recipients, harvesting the kidneys from heart beating cadavers, donor pretreatment with massive doses of corticosteroids and alpha-adrenergic blocking agents and warming of the graft immediately after vascular anastomosis, seem to reduce the incidence of ATN. Since the management differs significantly, post transplant ATN has to be distinguished from other causes of acute renal failure such as the renal artery thrombosis, hyperacute rejection and obstruction of the urinary tract. The tests which are of use in the differential diagnosis include, 131-I Hippuran renogram, transplant ultrasound, renal angiogram, retrograde pyelogram and renal transplant biopsy. Patients with established ATN should undergo every other day dialysis, under low dose or regional heparinization, until the creatinine clearance improves to 20 ml/min. The dose of azathioprine has to be reduced to prevent bone marrow toxicity. Even though there are short term disadvantages, the post transplant ATN does not appear to exert any detrimental effects in the long run. However, this issue remains controversial in the published reports.
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PMID:Post transplant acute renal failure: a review. 634 76

We analyzed the survival results of 300 consecutive kidney transplants (TXs) performed at Hennepin County Medical Center, Minneapolis, Minnesota, between March 1965 and April 1980. The graft survival result were compared between three sequential time periods, each comprising 100 renal TXs. The proportion of live donor TXs decreased from 27% in period 1 to 16% in period 2 and 5% in period 3, while the number of older patients, diabetic and multiple TX patients increased steadily. A comprehensive patient care scheme utilizing clinical protocols was developed in period 2 and carried out effectively in period 3. The Cox multivariate regression models used in this analysis allowed us to assess the influence of each variable on the graft survival results, while the effects of all others were held constant. Among the nondiabetic patients who received antilymphocyte globulin, the 1 and 5 year graft survival rates were 59.7 and 38.8% in period 1, 85.3 and 74.3% in period 2, 90.4 and 83.1% in period 3 (periods 1 versus 2: P = 0.008, periods 1 versus 3: P less than 0.0001). This improvement in graft survival was independent of the effects of the following variables, that is, the recipient's age, donor source, prior dialysis, co-existing medical problems, splenectomy, previous TXs, blood transfusions, cytotoxic antibodies, cold ischemia time, HLA mismatches, and post-TX acute tubular necrosis. Our observations indicate that reduced immunosuppression, frequent use of biopsy specimens and comprehensive patient care, played an important role in minimizing the loss of renal transplants in the later time periods and contributed indirectly for the improved graft survival results of our institution.
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PMID:Factors contributing for improved graft survival in recipients of kidney transplants. 635 14

The experiments were made to determine whether alpha-adrenergic blockade would reverse the vascular spasm in kidney grafts exposed to a warm ischaemia time of 30 min and 24 hr cold storage. Total vascular resistance per unit kidney mass, hematocrit, urinary flow, plasma and urine concentrations of creatinine, [Na+] and [K+], blood gases, renal O2 consumption and acid-base balance were studied in 21 anaesthetized dogs before and after kidney transplantation and administration of the blocking agent. Seven dogs were used to evaluate the effects of warm and cold ischemic stress on graft circulation and function without blockade (group 1). In the remaining dogs the blockade was induced by infusion of phentolamine (100 micrograms/kg/min) over 20 min. Controlled normal level of blood pressure was maintained throughout the experiments by infusion of 10% dextran 40 in saline (group 2) or by blood transfusion (group 3). Despite of interruption of neural pathways phentolamine induced a marked decrease in graft vascular resistance ranging from 89.2% +/- 5.9 (group 2) to 78.5% +/- 6.7 (group 3) in relation to the difference between the resistances before and after transplantation. In contrast, the decrease in vascular resistance of untreated grafts amounted only to 10.7% +/- 7.8 within a recirculation period of 4 1/2 hours. The increased renal blood flow following the blockade was associated with a considerable rise in urine flow and urinary excretion of creatinine, [Na+] and [K+] and a significant decrease in their plasma levels. The reduced O2 utilization by the grafts and the metabolic acidosis remained unchanged. These results indicate that phentolamine caused an effective suppression of vasoconstriction in kidney grafts exposed to warm ischemia and cold storage reflecting the intensive sympathetic activity under these conditions. Although the recovery of ischemic damaged tubular cells in this way was not acutely effected, the pharmacological enhancement of the cortical and medullary blood supply in the early posttransplant period may be helpful for overcoming the acute tubular necrosis and for preventing the development of hypertension due to the augmented release of vasodepressive medullary hormones.
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PMID:[Hemodynamic effects of an alpha-adrenergic blockade following experimental kidney transplantation]. 637 12

Rhabdomyolysis leading to acute renal failure necessitating hemodialysis is described in three chronic alcoholics. In each case an acute medical or surgical event, but not alcoholic intoxication, was implicated. Renal biopsies demonstrated acute tubular necrosis with intraluminal deposits consisting of Tamm-Horsfall protein and myoglobin. After recovery all three patients were demonstrated to have proximal muscle weakness with similar electromyographic abnormalities but nerve-conduction was impaired in only two. Muscle biopsies showed mixed, but predominantly type II fiber atrophy and reduced muscle phosphorylase levels. In the one patient tested the lactate response to forearm muscle ischemia was abnormal. It is postulated that chronic alcoholics may be predisposed to rhabdomyolysis and acute renal failure following acute medical and surgical stress as well as acute alcohol abuse. The muscle damage in these patients may be due to impaired intra cellular glycogen metabolism.
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PMID:Rhabdomyolysis and acute renal failure in chronic alcoholics with myopathy, unrelated to acute alcohol ingestion. 673 97

A case involving immediate postoperative prolonged warm ischemia in a transplanted kidney from a living related donor is presented. Repair of the renal artery after 3 hours 15 minutes of complete occlusion resulted in an 18-day course of acute tubular necrosis followed by full return of normal renal function. Significant collateral circulation has been present in all previously salvageable cases of transplant renal artery obstruction. This case demonstrates that a kidney from an optimally prepared donor can withstand more than 3 hours of posttransplant warm ischemia despite the absence of collateral circulation. An aggressive surgical approach to restoring circulation is indicated.
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PMID:Successful revascularization of early posttransplant renal arterial occlusion. 703 93


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