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

We compared the clinical outcomes of patients with (n = 71) and without (n = 185) diabetes mellitus enrolled into the placebo arm of a large, multicenter clinical trial of patients with acute tubular necrosis (ATN). Compared with the nondiabetic patients, diabetic patients were older (65.5 +/- 12.9 versus 60.7 +/- 18.0 years, P < 0. 05), had higher usual serum creatinine concentration (1.7 +/- 0.6 versus 1.4 +/- 0.5 mg/dL, P < 0.001), and had a higher prevalence of underlying hypertension, coronary artery disease, and congestive heart failure (all P < 0.007). By day 21 after enrollment, neither mortality nor dialysis-free survival was different between the groups. Length of stay for surviving patients, in both the intensive care unit and the hospital, were significantly shorter for the diabetics. Among acute comorbidities predicting mortality or the need for dialysis, sepsis was more prevalent among the nondiabetic patients (18% versus 35%, diabetics versus nondiabetics, P < 0.05). In conclusion, clinical outcomes for diabetic patients with ATN were no worse than for nondiabetic patients, despite their older age and worse underlying renal function. Patients with diabetes mellitus had more chronic cardiovascular disease but were less acutely ill. We speculate that cardiovascular disease is a risk factor for ATN in patients with diabetes mellitus. These results fail to implicate the increasing prevalence of diabetes mellitus in the persistently poor prognosis of patients with ATN.
Am J Kidney Dis 1999 Dec
PMID:Acute tubular necrosis in patients with diabetes mellitus. 1058 9

It is not known whether a kidney with chronic structural and functional changes is more vulnerable to an acute renal insult, and whether its regeneration capacity after injury is altered. To study this question, Lewis rats were submitted 10 wk after 5/6 nephrectomy to an ischemic insult of 60 min (remnant kidney [RK] group). Functional and morphologic data of the RK group were compared with data obtained in 10-wk uninephrectomized (1K) and normal (2K) Lewis rats with unilateral and bilateral renal ischemia, respectively. The acute postischemic decrease in creatinine clearance was smallest in the RK group, followed by the 2K and 1K groups, respectively. At days 1 and 3, fewer proximal tubules in the outer stripe of the outer medulla of the RK and 2K groups had undergone acute tubular necrosis compared with the 1K group. The mean percentage of tubules with signs of regeneration was maximal at day 3 in the three experimental groups. At day 10, regeneration was almost complete in the three groups. The number of leukocytes (OX1+ cells) present in the RK before ischemia did not increase after ischemia/reperfusion injury (377 +/- 146 cells/mm2 at day 0) in contrast to the 1K and 2K groups. In the latter groups, the number of leukocytes had increased gradually, reaching a maximum at day 15 (1K: 960 +/- 308 cells/mm2) and day 10 (2K: 668 +/- 164 cells/mm2), respectively. In conclusion, this study has shown that an RK exhibiting chronic morphologic changes of interstitial fibrosis and tubular atrophy is protected against ischemia/reperfusion injury, and that its regeneration capacity is preserved. The reperfusion injury is not followed by further accumulation of leukocytes, which were already present in the RK before ischemia.
J Am Soc Nephrol 1999 Dec
PMID:Chronic reduction in renal mass in the rat attenuates ischemia/reperfusion injury and does not impair tubular regeneration. 1058 94

Immunosuppressant-induced nephrotoxicity, in particular chronic progressive tubulointerstitial fibrosis/arteriopathy induced by the calcineurin inhibitors cyclosporin and tacrolimus, has become the 'Achilles heel' of immunosuppressive agents. The use of calcineurin inhibitors as primary immunosuppressants in hepatic and cardiac transplantation has led to end-stage renal disease and dialysis. Calcineurin inhibitor-induced acute renal failure may occur as early as a few weeks or months after initiation of cyclosporin therapy. The clinical manifestations of acute renal dysfunction are caused by vasoconstriction of renal arterioles, and include reduction in glomerular filtration rate, hypertension, hyperkalaemia, tubular acidosis, increased reabsorption of sodium and oliguria. The acute adverse effects of calcineurin inhibitors on renal haemodynamics are thought to be directly related to the cyclosporin or tacrolimus dosage and blood concentration. However, new clinical data indicate that calcineurin inhibitor-induced chronic nephropathy can occur independently of acute renal dysfunction, cyclosporin dosage or blood concentration. Several strategies have been evaluated to attenuate cyclosporin-induced nephropathy, but their efficacy remains unknown. Cytokine release syndrome associated with the use of muronomab-CD3 (OKT-3) can also contribute to the pathogenesis of transient acute tubular necrosis and renal dysfunction following renal transplantation. Continued research and clinical experience should provide information regarding the aetiology of cyclosporin-induced chronic progressive tubulointerstitial fibrosis/arteriopathy and its potential treatment.
Drug Saf 1999 Dec
PMID:Immunosuppressant-induced nephropathy: pathophysiology, incidence and management. 1061 71

Ethylene glycol intoxication is a rare but dangerous type of poisoning. It causes a severe acidosis with high anion and osmolal gaps. Clinical manifestations of the ethylene glycol intoxication can be divided in three phases: a neurologic stage, with hallucinations, stupor and coma; the second stage is cardiovascular with cardiac failure. Renal failure characterizes the third stage, due to acute tubular necrosis. After aggressive gastric emptying, the main treatment is ethanol or 4-methypyrazole, which can be given either orally or intravenous, with supportive measures for all symptoms or diseased organ.
Acta Clin Belg 1999 Dec
PMID:Diagnosis and treatment of an unusual cause of metabolic acidosis: ethylene glycol poisoning. 1103 83

Hepatic steatosis is associated with significant morbidity and mortality after liver resection and transplantation. Although apoptosis is a key mechanism of reperfusion injury in the normal liver, the pathway leading to cell death in steatotic hepatocytes is unknown. A model of hepatic ischemia and reperfusion injury in fatty and lean Zucker rats was used. Fatty animals had increased aspartate aminotransferase (AST) release and decreased survival after 60 minutes of ischemia compared with lean animals. Apoptosis was the predominant form of cell death in the lean rats (82%), whereas necrosis was minimal. In contrast, fatty animals developed only moderate amounts of apoptosis but showed massive necrosis (73%) after 24 hours of reperfusion. Intracellular mediators of apoptosis, such as caspase 8, caspase 3, and cytochrome c, were significantly lower in the steatotic than in the lean liver indicating dysfunction in activation of the apoptotic pathway. The high percentage of necrosis in the steatotic rats was associated with renal acute tubular necrosis after 24 hours of reperfusion in the fatty, but not in lean rats. Caspase inhibition significantly decreased reperfusion injury in lean animals, but was ineffective in fatty animals. The results indicate that the increased susceptibility of fatty livers to reperfusion injury is associated with a change from an apoptotic form of cell death to necrosis. We conclude that new therapeutic strategies are necessary in the fatty liver.
Hepatology 2000 Dec
PMID:Mechanisms of ischemic injury are different in the steatotic and normal rat liver. 1109 35

Focal tubular cell multiplication at sites on an injured nephron is a critical event in the recovery phase following acute tubular necrosis. During this process, numerous viable tubular cells exfoliate and are shed into the urine. Lysophosphatidic acid (LPA) is generated in the plasma membrane of injured cells and acts as an intercellular mediator of various biological processes, including inflammation, proliferation and repair. In the present study, exfoliated proximal tubule (PT) cells were isolated from human urine and the mitogenic effects of LPA were investigated as a model of repair and proliferation following renal injury. LPA stimulated a 23. 5% increase in DNA synthesis, a 29.4% increase in cell number and an 86.6% decrease in cAMP content. All of these responses were pertussis toxin sensitive, indicating the involvement of G(i)-type G-proteins in LPA signalling. Conversely, the LPA-induced DNA synthesis and the decrease in intracellular cAMP content were insensitive to wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K), suggesting a mitogenic response via PI3K-independent mechanisms. Furthermore, we detected specific mRNA transcripts for the recently cloned human LPA-receptors, endothelial differentiation gene (Edg)-2 and Edg-4 (Edg-2>>Edg-4) by reverse transcription-PCR in PT cells. Our data suggest that LPA may behave as a local growth factor in PT cells following tubular injury.
Clin Sci (Lond) 2000 Dec
PMID:Mitogenic action of lysophosphatidic acid in proximal tubular epithelial cells obtained from voided human urine. 1109 1

Acute renal failure is commonly due to acute tubular necrosis (ATN), the latter representing an acute, usually reversible loss of renal function incurred from ischemic or nephrotoxic insults occurring singly or in combination. Such insults instigate a number of processes-hemodynamic alterations, aberrant vascular responses, sublethal and lethal cell damage, inflammatory responses, and nephron obstruction-that initiate and maintain ATN. Eventually, reparative and regenerative processes facilitate the resolution of renal injury and the recovery of renal function. Focusing mainly on ischemic ATN, this article reviews evidence indicating that the inordinate or aberrant generation of reactive oxygen species (ROS) may contribute to the initiation and maintenance of ATN. This review also discusses the possibility that ROS may instigate adaptive as well as maladaptive responses in the kidney with ATN, and raises the possibility that ROS may participate in the recovery phase of ATN.
Am J Med 2000 Dec 01
PMID:Reactive oxygen species and acute renal failure. 1109 87

Idiopathic acute renal failure (IARF) is an uncommon but severe complication in children with relapsing nephrotic syndrome and may require long-term dialytic support until recovery of renal function takes place. Due to limited understanding of the pathophysiology of IARF, specific guidelines for its prevention and therapy have not been developed. Among triggering factors, peritonitis was present in half of all pediatric patients with this complication described in the English literature over the past 15 years. We report an additional nephrotic child who developed IARF following spontaneous bacterial peritonitis. The renal biopsy showed tubular epithelial changes consistent with acute tubular necrosis. A discussion of related literature and possible pathogenesis of this association is presented.
Pediatr Nephrol 2000 Dec
PMID:Peritonitis as a risk factor of acute renal failure in nephrotic children. 1114 20

The current disparity of viable organs and patients in need of a transplant has been an impetus for innovative measures. Live donor renal transplantation offers significant advantages compared with cadaveric donor transplantation: increased graft and patient survival, diminution in incidence of delayed graft function, acute tubular necrosis (ATN), and reduction in waiting time. Notwithstanding these gains live donors continue to be underutilized and account for only approximately one quarter of all renal transplants performed in the United States. It has been felt that inherent disincentives to live donation have slowed its growth. These include degree and duration of postoperative pain and convalescence, child care concerns, cosmetic concerns, and time until return to full activities and employment. In an attempt to curtail the disincentives to live donation, laparoscopic live donation (laparoscopic donor nephrectomy; LDN) was developed. The purpose of this study was to compare the results of our first 25 laparoscopic nephrectomies (performed over a 10-month period from September 1998 through July 1999) with the previous 25 standard open donor nephrectomies (ODNs) completed over the past 3 years. We conducted a retrospective review of all donor nephrectomies and recipient pairs performed over the past 3 years. End points included sex, operative time, length of stay, immediate and long-term renal function, and willingness to donate. There were no differences in demographics of the ODN versus the LDN group. The average length of stay was 2.48+/-0.72 days for the LDN versus 4.08+/-0.28 days for the ODN. ODN and LDN have comparable short- and long-term function with no delayed graft function and no complications. Growth of living donor transplant has increased from 16 per cent of all kidney transplants performed in 1995 to 23 per cent in 1999. We conclude that LDN is a viable alternative to the standard donor operation. LDN has had a positive impact on the donor pool by minimizing disincentives to live donation. With the initiation of our laparoscopic program the number of LDNs has increased. Presently the live donor pool is the most viable alternative to significantly increase the number of kidneys for transplantation.
Am Surg 2000 Dec
PMID:Laparoscopic donor nephrectomy: impact on an established renal transplant program. 1114 84

A 61-year-old Caucasian man presented with acute renal failure after multiple wasp stings. The patient required dialysis support temporarily. Work-up failed to show rhabdomyolysis or hemolysis and a kidney biopsy revealed acute allergic interstitial nephritis. The patient's renal function recovered completely after a short course of steroid therapy. Acute renal failure after wasp stings is typically caused by acute tubular necrosis in the setting of hemolysis or rhabdomyolysis. Compared with previously reported cases of acute renal failure associated with bee stings, our patient is unique in that his renal failure was caused by a hypersensitivity reaction apparently to the wasp venom.
Am J Kidney Dis 2001 Dec
PMID:Acute tubulointerstitial nephritis after wasp stings. 1172 93


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