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)

In this study we have analyzed incidence, causes and clinical course of ARF due to primary intrarenal disease other than acute tubular necrosis. Thousand hundred and twenty two cases of ARF of diverse etiology were studied over a period of 16 years; July 1984 to Dec, 1999. Surgical ARF 231 (20.6%) were not included in the present study. Intrinsic renal diseases were responsible for ARF in 891 (79.4%) of cases. The most common intrinsic renal diseases 705 (79.4%) causing ARF were ischemic/toxic acute tubular necrosis, but not included in this study. Acute renal failure was related to acute glomerulonephritis (9.3%), acute interstitial nephritis (7%), and renal cortical necrosis in (4.6%) of cases. Therefore intrinsic renal diseases other than ATN were the causative factor for acute renal failure in 186 (20.8%) patients in our study. Crescentic (51.8%) and endocapillary proliferative glomerulonephritis (34.9%), were the main glomerular diseases responsible for ARF and 75.9% of GN was related to infectious etiology. Fifty three percent of acute interstitial nephritis was drug induced and in 25 (40%) patients it was related to an infectious etiology. Renal cortical necrosis due to HUS was observed in 16 (39%) children and majority (76.47%) of the cases had a diarrhoeal prodrome. Obstetrical complications were the main causes (61%) of cortical necrosis in adults with acute renal failure. Thus, intrinsic renal diseases other than ATN were responsible for ARF in 186 (20.8%) cases. Post-infectious glomerulonephritis, acute interstitial nephritis and renal cortical necrosis (complicating HUS in children and obstetrical complications in adult) are the main causes of acute renal failure in our study. Both acute GN and interstitial nephritis had excellent prognosis, however renal cortical necrosis was associated with a very high mortality.
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PMID:Acute renal failure due to intrinsic renal diseases: review of 1122 cases. 1273 29

The paradigm for recovery of the renal tubule from acute tubular necrosis is that surviving cells from the areas bordering the injury must migrate into the regions of tubular denudation and proliferate to re-establish the normal tubular epithelium. However, therapies aimed at stimulating these events have failed to alter the course of acute renal failure in human trials. In the present study, we demonstrate that Lin-Sca-1+ cells from the adult mouse bone marrow are mobilized into the circulation by transient renal ischemia and home specifically to injured regions of the renal tubule. There they differentiate into renal tubular epithelial cells and appear to constitute the majority of the cells present in the previously necrotic tubules. Loss of stem cells following bone marrow ablation results in a greater rise in blood urea nitrogen after renal ischemia, while stem cell infusion after bone marrow ablation reverses this effect. Thus, therapies aimed at enhancing the mobilization, propagation, and/or delivery of bone marrow stem cells to the kidney hold potential as entirely new approaches for the treatment of acute tubular necrosis.
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PMID:Bone marrow stem cells contribute to repair of the ischemically injured renal tubule. 1282 56

Dysfunction of a transplanted kidney may develop at any time in the post-transplant period. The aim of this study was to differentiate levels of early dysfunction of a transplanted kidney. The study included 45 examinees undergoing kidney transplantation. They were divided into four groups, in regard to length of hospitalization and post-transplant complications: group I (up to 15 days, complication-free); group II (up to 15 days, with complications); group III (up to 30 days); group IV (up to 60 days). The control group included patients undergoing abdominal surgery, without uropoetic system disorders. The following parameters were examined on a daily basis a month after transplantation on average: creatinine clearance, creatinine and urea. Statistical analysis of these parameters revealed the following levels of renal dysfunction: control group--circulatory tubular dysfunction without azotemia; group I--polyuric acute tubular necrosis; group II and group III--severe or moderately severe polyuric acute tubular necrosis and group IV--polyuric acute tubular necrosis.
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PMID:Tubulointerstitial dysfunction in early post-transplant period. 1289 73

We investigated clinical, biochemical, and histopathological parameters in FK506-treated cynomolgus monkeys. Eight monkeys given oral FK506, 1 (n = 4) or 10 (n = 4) mg/kg daily, survived the 90 days of treatment apparently in good health and without significant changes in biochemical and histopathological parameters, as did 2 control monkeys except one monkey on 10 mg/kg/day FK506 orally, who was found to have a malignant lymphoma. In contrast, monkeys given intramuscular FK506 1 mg/kg daily (n = 4) had to be sacrificed at day 20, 25, 32, and 47 because of severe illness. They showed abnormal biochemical parameters (increased serum urea and aspartate aminotransferase activity) and major histopathological changes in the kidney (mesangial cell proliferation and acute tubular necrosis), pancreas (depletion of beta cells), liver (steatosis), and heart (cardiomyopathy). Intramuscular administration of 1 mg/kg daily resulted in serum levels ranging from 10 to 15 ng/ml, while oral administration at a dose of 1 or 10 mg/kg daily resulted in equal or even higher serum levels (range 2-70 ng/ml). Thus, the height of the serum trough level of FK506 using the enzyme immunoassay is not related to the toxicity of FK506 in cynomolgus monkeys.
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PMID:Toxicology of FK506 in the cynomolgus monkey: a clinical, biochemical, and histopathological study. 1462 44

We investigated the effects of tempol (4-hydroxy tempo), a membrane-permeable radical scavenger, on gentamicin-induced renal failure in rats. The rats were given gentamicin (100 mg/kg/day, i.p., once a day); and gentamicin (100 mg/kg/day, i.p.) and tempol (3.5, 7 or 14 mg/kg/day, i.p., once a day). At the end of 7 days, the gentamicin group produced the remarkable nephrotoxicity, characterized by a significantly decreased creatinine clearance and increased serum creatinine, blood urea nitrogen (BUN) and daily urine volume when compared with controls. In control the BUN value was 21.2 +/- 0.07 (mg/100 mL); in comparison, it was 96.9 +/- 6.03 in gentamicin group (P < 0.05). Renal histopathologic examination confirmed acute tubular necrosis in this group. In rats treated with gentamicin and tempol a partial improvement in biochemical and histologic parameters was observed. BUN values were 96.9 +/- 6.03 and 36.3 +/- 2.39 in gentamicin, and gentamicin plus tempol (14 mg/kg) treated groups, respectively (P < 0.05). These results suggest that the administration of tempol may have a protective effect on gentamicin-induced nephrotoxicity in rats.
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PMID:Effect of tempol (4-hydroxy tempo) on gentamicin-induced nephrotoxicity in rats. 1474 58

Aristolochic acids (AA), present in Aristolochia plants, are the toxin responsible for Chinese herbs nephropathy (CHN), a rapidly progressive tubulointerstitial nephritis (TIN). To clarify the mechanisms of the development of CHN, we tried to induce TIN in mice using AA. Three strains of inbred mice, BALB/c, C3H/He and C57BL/6, received 2.5 mg kg(-1) of AA or AA sodium salt (AANa) daily by intraperitoneal or oral administration, 5 days a week for 2 weeks. Serum and renal tissue were obtained at sacrifice. Twelve-hour urine samples were individually collected in a metabolic cage at one-week intervals. In the AA-injected groups, severe tubular injury, with the appearance of acute tubular necrosis, and rare cell infiltration into the interstitium, were seen in BALB/c mice. C3H/He mice also developed TIN with prominent cell infiltration into the interstitium and interstitial fibrosis. In C57BL/6 mice, only mild and focal tubulointerstitial changes were seen. Serum creatinine and blood urea nitrogen increased in BALB/c and C3H/He mice. Immunofluorescent study revealed no deposition of immune components in kidneys. In the AANa-treated groups, TIN was also seen in all groups, but even more severe tubulointerstitial changes were induced by intraperitoneal injection. Further examination using purified AAI, AAII, AAIVa and aristolactam I (ALI) revealed that AAI induced strong nephrotoxicity in mice, and that AAII resulted in mild nephrotoxicity. However, AAIVa and ALI caused no nephrotoxicity in this experimental system. There are strain differences in mice in their susceptibility to AA nephropathy. AAI exerted the strongest nephrotoxic effect in mice.
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PMID:Acute nephrotoxicity of aristolochic acids in mice. 1500 81

Acute renal failure is one of the systemic complications that can be found in bothropic accidents. In this study the effects on male Wistar rats induced by the venom of Bothrops neuwiedii diporus were evaluated. The histopathology revealed acute tubular necrosis, lesions firstly were observed 3 hours post inoculation of 700 microg of venom. Cortical kidney congestion and granulohialin degeneration of tubular epithelial cells were observed, these lesions achieved a maximum at 24 hours after inoculation. Tubular epithelial hidropic degeneration and dilatation of tubular lumen with hyalin casts were present inclusive up to 4 weeks after inoculation. Biochemical parameter values associated with kidney renal failure were increased 6 hours after venom inoculation (urea: 1.10+/-0.22 g/dl; creatinine: 19.60+/-1.51 mg/dl), but at the end of the first week they decreased till normal values. The urinary density was lower than normal value: 1.005+/-0.001 (p<0.001) and at the end of the first month they oscillated between 1.005 and 1.060 (p<0.001). Renal injury induced by B. neuwiedii diporus could be better appreciated by histopathology than by the routine laboratory assays.
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PMID:[Renal injury in rats poisoned by venom of Bothrops neuwiedii diporus from Argentina]. 1533 74

To investigate the effect of gamma-aminobutyric acid (GABA) on acute renal failure, we used a rat model of acute tubular necrosis induced by glycerol. After deprivation of water for 6h, the rats received an injection of 50% glycerol into the muscle of the rear limb at 10 ml/kg body weight. GABA was then administered orally to the rats (100 or 500 mg/kg body weight/day) once every 12h for 3 days. The rats with acute renal failure showed arrested body weight gain and an increase of kidney weight, whereas oral administration of GABA attenuated the physiological changes induced by acute renal failure. However, GABA administration had no significant effect on increased urine volume. Oral administration of GABA at a dose of 100 or 500 mg/kg body weight/day for 3 days significantly improved the markedly elevated levels of blood urea nitrogen and creatinine and the reduced creatinine clearance related to progression of renal failure. Moreover, the rats with acute renal failure exhibited high levels of fractional excretion of sodium (FE(Na)) due to alteration of tubule function following injection of glycerol. However, administration of GABA lowered the FE(Na) levels dose-dependently. Furthermore, urine osmolarity was markedly reduced in control rats with acute renal failure as compared with normal rats, whereas it was significantly increased by administration of GABA at a dose of 500 mg/kg body weight/day. These results indicate that GABA has potential as a therapeutic agent against the renal damage involved in acute renal failure.
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PMID:Protective effect of gamma-aminobutyric acid against glycerol-induced acute renal failure in rats. 1550 Sep 37

To clarify the pathophysiological mechanism underlying acute renal injury caused by acute exposure to arsenic, we subcutaneously injected both BALB/c and C57BL/6 mice with sodium arsenite (NaAs; 13.5 mg/kg). BALB/c mice exhibited exaggerated elevation of serum blood urea nitrogen (BUN) and creatinine (CRE) levels, compared with C57BL/6 mice. Moreover, half of BALB/c mice died by 24 h, whereas all C57BL/6 mice survived. Histopathological examination on kidney revealed severe hemorrhages, acute tubular necrosis, neutrophil infiltration, cast formation, and disappearance of PAS-positive brush borders in BALB/c mice, later than 10 h. These pathological changes were remarkably attenuated in C57BL/6 mice, accompanied with lower intrarenal arsenic concentrations, compared with BALB/c mice. Among heavy metal inducible proteins including multidrug resistance-associated protein (MRP)-1, multidrug resistance gene (MDR)-1, metallothionein (MT)-1, and arsenite inducible, cysteine- and histidine-rich RNA-associated protein (AIRAP), intrarenal MDR-1, MT-1, and AIRAP gene expression was enhanced to a similar extent in both strains, whereas NaAs challenge augmented intrarenal MRP-1 mRNA and protein expression levels in C57BL/6 but not BALB/c mice. Moreover, the administration of a specific inhibitor of MRP-1, MK-571, significantly exaggerated acute renal injury in C57BL/6 mice. Thus, MRP-1 is crucially involved in arsenic efflux and eventually prevention of acute renal injury upon acute exposure to NaAs.
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PMID:MRP-1 expression levels determine strain-specific susceptibility to sodium arsenic-induced renal injury between C57BL/6 and BALB/c mice. 1569 64

The use of folk remedies is widespread throughout Africa. Acute renal failure (ARF) is one of the most severe, but under-recognized, complications of folk remedy use. This report aims to describe the clinical presentation, outcomes, and nature of renal injury in patients with folk-remedy-associated ARF. Clinical data were evaluated retrospectively in 78 patients with ARF associated with recent folk remedy use. ARF was defined as elevated serum urea and creatinine above the age-appropriate normal ranges, persistent oligoanuria, worsening renal function with time, or need for dialysis. Overall mortality in patients with ARF was 41%. Mortality was higher in adults (45.5%) than in infants (36.6%), in patients with both renal and liver dysfunction (62.5%) than in those with renal dysfunction alone (22.6%), and in HIV-positive (44.4%) versus HIV-negative (34.6%) patients. Vomiting (51.3%) and diarrhea (43.6%) were the most frequent presenting symptoms. Metabolic acidosis (80.8%) and volume depletion (62.8%) were the most frequent clinical findings. The definable causes of ARF were pre-renal (26.9%), acute tubular necrosis (ATN; 26.9%), hepatorenal syndrome (6.4%), urinary tract infection/sepsis (7.7%), and primary renal disorders (7.7%). Twenty-seven patients had concomitant medical conditions unlikely primarily related to folk remedy ingestion. In conclusion, ARF occurring after use of folk remedies in South Africa is associated with significant morbidity and mortality. The most common contributors to ARF in this setting are volume depletion and ATN. Significantly, although a proportion of patients have underlying systemic or renal conditions that may contribute to renal dysfunction, in the majority of patients, folk remedy use appears to be the most likely proximate cause. In view of the large numbers of Africans living abroad, more widespread awareness of this important clinical problem needs to be raised.
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PMID:Acute renal failure associated with the use of traditional folk remedies in South Africa. 1571 33


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