Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of administering insulin-like growth factor I (IGF-I) were examined in a model of ischemic acute tubular necrosis in rats. Injury was induced by 75 min of bilateral renal artery occlusion. Compared to rats administered vehicle, rats administered IGF-I (100 micrograms/day via continuous subcutaneous infusion) had significantly lower serum creatinine and blood urea nitrogen levels over the course of 7 days postocclusion. Glomerular filtration rate as determined by inulin clearance was examined on day 2 postocclusion and was significantly increased in IGF-I-treated animals (0.16 +/- 0.02 ml per min per 100 g of body weight) compared to vehicle-treated controls (0.08 +/- 0.02 ml per min per 100 g of body weight). The weight loss that occurred during the course of acute tubular necrosis was ameliorated by IGF-I. Mortality was reduced from 36.7% in vehicle-treated rats to 7.1% in rats administered IGF-I. Histologically, there was much less renal injury evident at day 7 postocclusion in the IGF-I-treated rats compared to vehicle-treated controls. In contrast, growth hormone (200 micrograms administered subcutaneously for 4 days) did not affect recovery of renal function or reduce mortality postreperfusion. This report demonstrates a beneficial effect of IGF-I administration in the setting of acute tubular necrosis. Several properties of IGF-I render it a pharmacological agent with excellent potential for treatment of this condition in humans.
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PMID:Insulin-like growth factor I accelerates recovery from ischemic acute tubular necrosis in the rat. 146 11

Two college students who developed reversible acute deterioration in renal function following binge drinking of beer and the use of nonsteroidal antiinflammatory drugs (NSAIDs) are reported. Both patients presented with back and flank pain with muscle tenderness, but showed no evidence of overt rhabdomyolysis. The first case had marked renal failure, with a peak serum creatinine reaching 575 mumol/L (6.5 mg/dL), and acute tubular necrosis was documented by renal biopsy. The second case had only modest elevation in serum creatinine, and renal function rapidly improved on rehydration. The contribution of the potential muscle damage associated with alcohol ingestion to the changes in renal function in these two cases is not clear. However, the major mechanism for the acute renal failure was thought to be related to inhibition of renal prostaglandin synthesis in the face of compromised renal hemodynamics secondary to alcohol-induced volume depletion.
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PMID:Acute renal failure following binge drinking and nonsteroidal antiinflammatory drugs. 151 10

Results of studies on the accuracy of the resistive index as a predictor of acute renal transplant rejection have varied widely. Clinical evaluations are limited by the inability to control the numerous coincidental factors that affect vascular resistance. We performed a controlled study in dogs to isolate the effects of acute tubular necrosis, cyclosporine toxicity, and acute rejection on the resistive index, and to compare them with a population of normal control subjects. By doing so, we hoped to identify the patterns of change in the resistive index over time and possibly explain the wide spectrum of resistive index data reported in the literature. Resistive index, a parameter calculated from relative systolic and diastolic velocity, indicates parenchymal resistance to perfusion. Since an increase in renal length also has been reported useful in predicting rejection, we studied changes in length in each of the isolated conditions. The normal control group (four dogs) had heterotopic autotransplantation with minimal cold ischemic time. The acute tubular necrosis group (six dogs) had heterotopic autotransplantation with 1 hr of warm ischemic time. The cyclosporine toxicity group (four dogs) was allowed approximately 3 months to heal from heterotopic autotransplantation. Very high (toxic) doses of cyclosporine were then administered. The acute rejection group (five dogs) had heterotopic allografting with minimal cold ischemic time. No medications were administered. In all groups, the abnormalities induced were confirmed by biopsy. Creatinine levels were also used to monitor cyclosporine toxicity. In the normal control and acute tubular necrosis groups, resistive index increased immediately after surgery, returning to baseline within 10 days. Renal length increased slightly in both groups, but the duration of increase was longer in the acute tubular necrosis group. No significant change in resistive index or renal length was seen in the cyclosporine toxicity group. In the acute rejection group, an initial decrease in resistive index during the mild to moderate phase was followed by a rapidly progressive increase with worsening rejection. Renal length increased progressively beginning immediately after surgery. Our study determined the patterns of change in resistance and renal length over time as caused by the isolated pathologic states. Our finding that vascular resistance decreased in mild to moderate acute rejection was unexpected, since almost all the literature reports resistive index elevation. This may explain some of the conflicting results obtained in Doppler investigations of rejection. Our results on renal length reinforce the positive clinical reports of its predictive value in rejection.
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PMID:Sonography of renal transplants in dogs: the effect of acute tubular necrosis, cyclosporine nephrotoxicity, and acute rejection on resistive index and renal length. 154 94

Between 1980 and 1988, 12 patients at the Cleveland Clinic had biopsy-proven acute tubulointerstitial nephritis. Etiologies of the disease included drugs, systemic illness, and idiopathic causes. Clinical features were nonspecific, and the diagnosis of acute tubulointerstitial nephritis was seldom entertained in these patients prior to biopsy. Seven patients had unrelated underlying renal disease. Treatment included discontinuation of the offending agent and/or a trial of steroids. All patients had final creatinine levels lower than at diagnosis. Because the condition is potentially reversible, this disease should be considered in all patients with new azotemia who do not exhibit prerenal factors, features typical of acute tubular necrosis, red blood cell casts heralding a glomerular process, or evidence of obstructive uropathy.
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PMID:Acute tubulointerstitial nephritis. 155 Dec 11

Six children (aged 1.3-6.9 years) were examined with serial duplex Doppler sonography and diethylenetriaminepenta-acetic acid (DTPA) isotope renography in the post-renal transplant period. The resistive index (RI) was derived from sonographic studies and the renal blood flow (RBF) calculated from the isotope scans. The clinical status of the child and the corresponding plasma creatinine level were assessed together with these two parameters. The RIs ranged from 40% to 100% and the RBF from 0% to 16.8%. There were six rejection episodes in four patients. A significant fall in RBF mirrored a rise in plasma creatinine on each occasion, but there was no significant change in RI recorded. There were two graft losses, both associated with renal venous thrombosis. In both cases no significant RBF could be detected on DTPA renography. In one patient, the RBF remained low throughout a period of primary non-function associated with acute tubular necrosis, and increased as primary function was established and the plasma creatinine fell. Throughout this period there was no significant change in the RI. From our preliminary data RBF reflects graft dysfunction more accurately than does the RI.
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PMID:The evaluation of paediatric renal transplants using resistive index and renal blood flow. 157 Dec 15

Retrospective study on the incidence of severe acute tubular necrosis (ATN), defined as the need for dialysis on the first week post-transplantation ruling out acute rejection or technical complication, in our series of 81 renal transplantations from corpse donor. It includes an evaluation of the influence on severe ATN presentation of parameters such as recipient and donor's age, level of plasma creatinine prior to extraction, whether the corpse had hypotension, duration of both vascular anastomosis and procedure, type of removal (single or multiorgan) and cold ischaemia. We conclude that in our experience, cold ischaemia of the graft is the only determining factor among the cases studied for ATN presentation conditioning a reduced long-term survival of the graft (0.758 vs 0.971 at 18 months: p.05). Peripheral blood typing of corpse donor would allow us to shorten cold ischaemia duration, and thus achieve a low rate of severe ATN (13.6%).
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PMID:[Predisposing factors for the development of acute severe tubular necrosis in the immediate post-transplantation period]. 162 48

Thirty-three consecutive cadaveric renal transplantations performed at the National Taiwan University Hospital from November 1985 to December 1989 were reviewed to determine the effect of early function on the 1-year patient and graft survival rates. Immediate function was present in 17 transplants; delayed graft function with acute tubular necrosis occurred in 16 cases. The 16 transplants with acute tubular necrosis (ATN) were treated with low dose cyclosporine. Among them, 13 patients had delayed function which resolved after 2 to 60 days of hemodialysis, but 3 grafts did not regain function. The allograft survival rate at 1-year was 68.7% for the delayed function group and 88.2% for the immediate function group. This difference was not statistically significant (p greater than 0.05). The 1-year patient survival rate was also not significantly different (87.5% vs 88.2%). There was no relationship between graft loss and duration of ATN. However, the graft survival rate in patients with a serum creatinine level below 2 mg/dL, after recovery either from ATN or non-ATN, was better than that for patients with a serum creatinine level of more than 2 mg/dL. The difference was statistically significant (95.8% vs 50.0%, p less than 0.02). It is concluded that delayed allograft function with acute tubular necrosis does not significantly alter the 1-year survival rates of patients and grafts in low-dose cyclosporine therapy. However, it is deleterious to the 1-year survival rate of an allograft when poor functional recovery occurs in an ATN or non-ATN condition.
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PMID:The outcome of delayed graft function in cadaveric renal transplants treated with low dose cyclosporine. 168 80

Withdrawal of steroid therapy in renal transplant recipients is associated with a risk of acute allograft rejection. To define clinical risk factors for rejection associated with steroid withdrawal, we analyzed the clinical characteristics of 107 patients with drawn from steroid therapy at various times after transplantation. Both univariate and multivariate analyses suggested that the timing of steroid withdrawal is an important predictor of steroid withdrawal failure. Withdrawal of steroids was successful in only 13 of 32 patients (41%) in whom prednisone was discontinued shortly after transplantation. In contrast, steroid withdrawal has been successful in 59 of 75 patients (79%) in whom prednisone was discontinued at least 6 months after transplantation. Black race and donor-recipient racial mismatch also were significant predictors of rejection associated with steroid withdrawal. In patients undergoing steroid withdrawal at least 6 months posttransplant, serum creatinine concentration also correlated independently with the risk of rejection. Neither age, sex, HLA match, pretransplant PRA, source of the allograft (cadaver vs. living relative), acute tubular necrosis, nor the presence of diabetes was predictive of the outcome of steroid withdrawal.
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PMID:Withdrawal of steroids after renal transplantation--clinical predictors of outcome. 173 83

The hepatorenal syndrome (HRS) is a well-known complication of liver failure, and medical treatment is usually not successful unless liver function can be improved. The authors review their experience with 130 adults undergoing orthotopic liver transplantation (OLT) over a 20-month period to determine the incidence of HRS and its effects on patient outcome, need for hemodialysis (HD), and the degree of recovery of renal function. The clinical diagnosis of HRS preoperatively was made by using criteria to exclude prerenal azotemia, acute tubular necrosis, and primary renal diseases. Nineteen patients were identified as having the HRS for a preoperative incidence of 15.1 per cent. Overall, 41 of the 126 patients reviewed required postoperative HD, and the mortality in this group was 54 per cent. Fifty-eight per cent of the HRS patients were dialyzed postoperatively vs 28 per cent of non-HRS patients. The mean posttransplant creatinine improved over time in the HRS patients while it worsened slightly in the non-HRS group. At 12 weeks posttransplant, there was a significant difference in the mean creatinine levels (1.8 +/- 0.3 mg/dl vs 1.2 +/- 0.04 mg/dl, P = .001). However, at 24 weeks the small difference was not statistically significant between the two groups (1.6 +/- 0.15 mg/dl vs 1.3 +/- 0.06 mg/dl, P = NS). The current survival of the hepatorenal group is comparable to the nonhepatorenal patients at a follow-up of 6 to 25 months: 68 per cent vs 78 per cent, P = NS. The authors conclude that liver transplantation reverses the HRS, and that hepatorenal patients can undergo liver transplantation with outcomes comparable to nonhepatorenal patients.
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PMID:The hepatorenal syndrome in liver transplant recipients. 174 99

Bilateral renal artery occlusion (RAO) for 120 minutes in dogs results in acute tubular necrosis (ATN) and peritubular capillary (PTC) congestion with rapidly deteriorating renal function. We have shown that prior splenectomy minimizes RAO-induced renal functional and histopathologic changes. The purpose of this study was to examine whether this renal protection is due to prevention of red blood cell echinocyte formation and resultant renal PTC congestion. Echinocytes (burr cells) are poorly deformable, impart high viscosity to the blood, and may hinder reperfusion by increasing resistance to renal capillary blood flow. Splenectomized (SPLX) or sham-SPLX dogs were treated with bilateral RAO for 120 minutes. After RAO, renal function and renal blood flow were monitored, and peripheral blood red blood cells were examined at 1 hour and at 24-hour intervals for 96 hours. Renal biopsies were taken 1 hour after RAO and the kidneys removed 96 hours after RAO. The RBCs and renal tissues were studied using scanning electron microscopy. Renal function was assessed by endogenous creatinine clearance. Sham-SPLX animals showed a marked and sustained decrease in creatinine clearance, consistently elevated serum creatinine levels and fractional excretion of sodium, and diffuse ATN and PTC congestion with echinocytes. These animals had a peak in circulating echinocytes 1 hour after RAO (p less than 0.05), which showed an excellent negative correlation with creatinine clearance (r = -0.999; p less than 0.001). On the contrary, SPLX animals had essentially no change in serum creatinine or fractional excretion of sodium, minimal tubular changes, no PTC congestion, and no rise in circulating echinocytes during the 96-hour observation. In vitro treatment of the postischemic red blood cells from sham animals with adenosine-inosine or fresh postischemic plasma from the SPLX animals showed almost complete reversal to discocytes (normal red blood cells), whereas in vitro treatment of postischemic red blood cells from the SPLX animals with fresh postischemic plasma from the sham animals resulted in a marked echinocytic response. We conclude that 1) a marked echinocyte response in the immediate postischemic period is an important mechanism in initiating ischemic ATN, 2) an echinocyte inducing factor may reside in the plasma of spleen-intact animals, and 3) mitigation of ATN and PTC congestion by splenectomy is, at least in part, consequential to attenuated echinocytic response in the immediate postischemic period.
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PMID:Erythrocyte deformation in ischemic acute tubular necrosis and amelioration by splenectomy in the dog. 175 6


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