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

Acute tubular necrosis is not an uncommon phenomenon, but it rarely results from environmental factors. We describe a patient in whom acute renal failure developed 2 times after overexposure to aliphatic hydrocarbons and discuss some potential pathophysiological mechanisms. This association has rarely been reported in the literature. Considering the wide availability of aliphatic hydrocarbons in diesel fuel and solvents, associated renal toxicity is probably underrecognized. We stress the importance of identifying environmental and professional factors as causes of acute tubular necrosis.
Arch Intern Med 1998 Sep 14
PMID:Acute exposure to aliphatic hydrocarbons: an unusual cause of acute tubular necrosis. 973 13

Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension and heart failure. However, acute renal failure (ARF) may occur in patients who are taking these drugs in situations associated with decreased glomerular filtration pressure, such as dehydration caused by acute diarrhea or diuretic therapy. Sixty-four patients who were admitted to the intensive care unit for ARF associated with ACE inhibitor therapy were followed for more than 5 years. In this historical retrospective study, we documented that 45 patients were treated for hypertension (group I) and 19 were treated for heart failure (group II). Their mean age was 71.2+/-11.6 years. Patients with ARF presented with overt dehydration in 91% and 84% of the cases in groups I and II, respectively. Hypovolemia was caused by diuretics or gastrointestinal fluid loss. Bilateral artery-renal stenosis or stenosis in a solitary kidney was documented in 22% and 10% of patients in groups I and II, respectively. The probability of survival was 91% and 49% at 1 year and 64% and 18% at 5 years, for groups I and II, respectively. Acute renal failure required hemodialysis in seven patients, but none of them became dialysis dependent. In the subgroup of patients with preexisting chronic renal failure, all the patients except for one who belonged to group II died within 2 years. In both groups, after resolution of ARF, plasma creatinine concentration returned to baseline level and the course of renal function was not significantly worsened. In conclusion, ARF associated with ACE inhibitors is likely to occur in many patients without renal artery stenosis after unexpected dehydration, especially in older patients with congestive heart failure. In both groups of patients, in the absence of preexisting chronic uremia, recovery of renal function occurred without sequelae, even after an episode of acute tubular necrosis requiring dialysis.
Am J Hypertens 1998 Sep
PMID:Long-term follow-up of acute renal failure caused by angiotensin converting enzyme inhibitors. 1056 Jul 94

Long-term therapy with lithium may be associated with a broad spectrum of functional and structural side-effects in the kidney. Among these features, nephrogenic diabetes insipidus is the most frequent and it can be expected to occur in 20-70% of the patients. Diabetes insipidus is the result of a lithium induced resistance of collecting ducts to antidiuretic hormone. Additional functional disturbances are represented by renal tubular acidosis and consequences of hypercalcemia. Structural alterations of the kidney have a rare occurrence. In the literature, there are accounts of chronic tubulo-interstitial nephritis, acute tubular necrosis and few cases of glomerulopathies. Our report of a patient with chronic interstital nephritis is supplemented by a brief discussion of the diverse picture of the nephrotoxicity of lithium.
Ther Umsch 1998 Sep
PMID:[Impaired kidney function in lithium therapy]. 978 72

In contrast to trivalent chromium (Cr(III)) compounds, hexavalent chromium ((Cr(VI)) compounds are oxidizing agents capable of directly inducing tissue damage and possessing carcinogenic, mutagenic and teratogenic potency. After oral or dermal absorption of Cr(VI), the kidney is the main target organ for chromium accumulation, which might result in acute tubular necrosis in humans. In contrast, an acute toxic effect of Cr(VI) on the liver has not yet been described. Therefore, we used two established epithelial cell lines from the kidney (Opossum kidney cells) and the liver (Hep G2 cells) to design an in vitro-assay which is able to examine acute toxic effects of chromium compounds. Cells of both cell lines were treated with various concentrations of Cr(III) and Cr(VI) ranging from 0.01 micromol/l to 1 mmol/l for 24 h. Thereafter, cell morphology, organization of the intracellular cytoskeleton, number of viable cells and mean cell volume were examined. The results show that Cr(VI), but not Cr(III), has an acute cytotoxic effect and causes a dose-dependent loss in cell viability. The effective dose that caused 50% of cell death was 5 micromol/l for kidney epithelial cells and 50 micromol/l for liver epithelial cells. This means that kidney epithelial cells are 10 times more sensitive towards Cr(VI) treatment than liver epithelial cells and this might explain the known nephrotoxicity in vivo. The loss in cell viability was accompanied by a rounding and detachment of the cells and a marked reduction of intracellular F-actin-containing stress fibers. Microtubules and intermediate-sized filaments were observed to be unaffected. Only in the case of kidney epithelial cells, a dose-dependent cell volume increase was observed after Cr(VI) treatment at concentrations up to 50 micromol/l. At higher concentrations, the cell volume decreased due to the high number of cells undergoing lysis and the appearance of cellular fragments. Various chloride channel blockers with different specificities, molecular structures and inhibitory potentials were tested for their ability to prevent Cr(VI)-induced cell damage. None of the channel blockers was able to inhibit cell damage, suggesting that the uptake of Cr(VI) through the general anion transport system of the cell membrane might be only one facet of cellular uptake and toxification. The data presented here not only confirm the different organ-specific effects of Cr(III) and Cr(VI), but also provide a basis for future experiments on the understanding of acute toxicity of Cr(VI) compounds. Moreover, the results demonstrate that the designed in vitro-assay might be a useful tool to prove whether non-toxic Cr(III) can be oxidized to Cr(VI) under specific industrial conditions (for example, in the leather or chrome industry).
Int Arch Occup Environ Health 1998 Sep
PMID:Investigations on the nephrotoxicity and hepatotoxicity of trivalent and hexavalent chromium compounds. 982 79

Nontraumatic rhabdomyolysis is an important but under-recognized cause of acute renal failure. In alcoholics, rhabdomyolysis most frequently develop following muscle necrosis during alcohol-induced coma, but has also been described rarely in those without prolonged coma or seizures. We describe a patient who developed myoglobinuric acute renal failure requiring dialysis following binge drinking in the absence of convulsions or coma. The renal biopsy showed acute tubular necrosis with pigment casts.
Ren Fail 1999 Sep
PMID:Acute renal failure due to nontraumatic rhabdomyolysis following binge drinking. 1051

A retrospective review of 246 patients with established acute renal failure (ARF) needing dialysis from 1990-1994 is reported from Hospital Sultanah Aminah, Johor Bahru. Peritoneal dialysis was more commonly used than haemodialysis or haemofiltration. Patients on mechanical ventilation in Intensive Care Unit (ICU) who were hypercatabolic and fluid overloaded were treated with haemofiltration. Males outnumbered females by a ratio of 1.5:1. The majority were Malays (61.4%). Most patients were from the district of Johor Bahru, but 41.5% were from other districts in the Johor state. The mean age was 47.1 years (SD 18.2). The ARF was caused by acute tubular necrosis in 55.3%, post-renal obstruction in 22.8%, nephrotoxins in 5.7% and other causes in 16.2%. The proportions of patients referred from the medical, surgical and obstetric and gynaecology units were 50.8%, 45.5% and 3.7% respectively. The mortality rate was 48%. Patients with established ARF should be dialysed early as they tolerate uraemia poorly. Prevention is by prompt treatment of patients with sepsis, avoidance of hypovolaemia and nephrotoxic drugs.
Med J Malaysia 1997 Sep
PMID:Acute renal failure requiring dialysis--a 5 year series. 1096 94

Research during the last few years has uncovered the mechanisms responsible for acute renal failure. During the initiation phase of acute tubular necrosis sublethal injury, apoptosis or necrosis of the tubular epithelium, hemodynamic alterations, tubule obstruction and back leakage occur. Hypofiltration persists due to imbalance between endothelins and endothelium derived nitric oxide, medullary congestion and tubuloglomerular feedback. Recovery is characterised by tubular epithelium regeneration. A greater understanding of the pathogenesis of acute renal failure will allow better management of such cases.
J Assoc Physicians India 2000 Sep
PMID:Evolving trends in the etiopathogenesis of acute renal failure. 1119 92

Povidone-iodine sclerosis has been suggested in the literature as a safe and effective treatment for post-renal transplant lymphoceles. No significant complications of this method have been described. We report on a kidney allograft recipient with recurrent lymphoceles treated with povidone-iodine instillations who developed acute renal failure secondary to iodine intoxication. Four days after the beginning of the povidone-iodine irrigations, metabolic acidosis was present, and renal function started to deteriorate. After a few days, despite the suspension of irrigations, the patient developed oliguria, and dialysis was needed. A renal biopsy was performed, and intense acute tubular necrosis was the only relevant finding. The lymphocele was corrected surgically, and the patient eventually recovered. As has been described in other settings, povidone-iodine instillation for the treatment of post-renal transplant lymphoceles may lead to iodine kidney toxicity and acute renal failure.
Am J Kidney Dis 2002 Sep
PMID:Nephrotoxic acute renal failure in a renal transplant patient with recurrent lymphocele treated with povidone-iodine irrigation. 1220 Aug 20

Transforming growth factor (TGF)-beta1 is important in fibrogenesis and has been involved in the pathogenesis of chronic allograft nephropathy (CAN). The angiotensinogen (AGT) gene encodes the only glycoprotein known to be a precursor of the vasopressor angiotensin II. Angiotensin II is also a growth factor and a profibrogenic cytokine. It mediates the induction of TGF-beta1. We studied the relationship among the intragraft expression of AGT, TGF-beta1, and CAN in stable renal transplant patients (RTP). We used a competitive quantitative reverse transcriptase-polymerase chain reaction (RT-PCR)-ELISA assay to identify intragraft amounts of AGT expression in RTP and correlated it with TGF-beta1 mRNA expression. We studied and performed kidney biopsies on 12 RTP with long-functioning grafts and 6 RTP in the immediate posttransplantation period (7 days) who had acute tubular necrosis as control. Histology was based on Banff working classification criteria. Total RNA was isolated from biopsy specimens. For RT-PCR-ELISA, we created heterologous RNA competitors that coamplified with the same primers as AGT and TGF-beta1. Six of 12 long RTP had proteinuria >1000 mg/24 hr and 6 had proteinuria <1000 mg/24 hr. The differences between Banff grades (P =0.03), AGT, and TGF-beta1 levels by RT-PCR-ELISA were statistically significant between both groups (106.2+/-60.7 vs. 34.1+/-11.9 pg/microg total RNA [P =0.01] and 5954+/-5612 vs. 436+/-517 transcripts/microg total RNA [P =0.01], respectively). The control group showed AGT levels of 25+/-12.2 pg/microg total RNA and TGF-beta1 levels of 228+/-111 transcripts/microg total RNA, significant only for the higher proteinuria group (P=0.01 and P=0.04, respectively). There was a correlation between AGT and TGF-beta1 in both groups (r=0.96, P=0.001). We showed a relationship between mRNA expression of AGT and TGF-beta1 in kidney transplant patients with different grades of CAN and proteinuria.
Transplantation 2002 Sep 15
PMID:Intragraft messenger RNA expression of angiotensinogen: relationship with transforming growth factor beta-1 and chronic allograft nephropathy in kidney transplant patients. 1235 92

A 15-year-old boy developed nephrotic syndrome and acute renal failure 4 years after allogenic bone marrow transplantation (BMT) for lymphoid crisis of chronic myelocytic leukemia. On admission, he presented with clinical features of chronic GVHD including transient exacerbation of cholestatic liver injury. Renal biopsy showed diffuse proliferative glomerulonephritis with cellular crescents. The patient was treated with methylprednisolone pulse therapy (1 g/day, for 3 days) followed by oral prednisolone. Renal function gradually improved but nephrotic state was persistent. A second renal biopsy showed improvement of acute tubular necrosis and endocapillary proliferation and transformation of crescents into a fibrous form. After tapering of oral prednisolone, cyclophosphamide was started, which resulted in a gradual improvement of proteinuria. Several cases of nephrotic syndrome occurring after BMT have already been reported, but most cases had membranous nephropathy. In our case, renal biopsy revealed diffuse proliferative glomerulonephritis with findings of active cellular immunity, and aggressive treatment resulted in attenuation of these findings. Moreover, chronic GVHD-related liver injury was noted at the time of this episode. Our findings suggest that chronic GVHD may be complicated with diffuse proliferative glomerulonephritis through unknown cellular immune mechanism.
Clin Nephrol 2002 Sep
PMID:Diffuse proliferative glomerulonephritis after bone marrow transplantation. 1235 94


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