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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 kidney is one of the organs susceptible to heavy metal intoxication. The total body burden and "saturation" level in renal tissue are important limiting factors to the onset of renal injuries. Acute or chronic exposure to many of heavy metals can induce renal tubulointerstitial injuries, including acute tubular necrosis, chronic tubulointerstitial nephritis, Fanconi syndrome, renal tubular acidosis, and renal tubular dysfunction without morphological changes. Chronic cadmium intoxication can cause irreversible Fanconi syndrome with chronic tubulointerstitial nephritis. Both urinary low-molecular weight protein excretion and urinary cadmium excretion (greater than 200-400 ppm) are the most reliable earlier markers of tubulointerstitial injury in chronic cadmium intoxication. The role of metallothionein is central to an understanding of cadmium-induced nephropathy. Acute lead intoxication in children can cause reversible Fanconi syndrome. Hypertension, hyperuricemia, and elevated serum creatinine, without Fanconi syndrome, are clinical manifestations of chronic lead exposure in adults. Nuclear inclusion body in proximal tubular cell is characteristic. Chronic exposure to inorganic germanium can cause chronic renal failure without urinary abnormalities, due to tubular degeneration and interstitial fibrosis, mainly in the thick ascending limb of Henle and distal tubulus.
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PMID:[Tubulointerstitial injuries in heavy metal intoxications]. 756 49

Acute renal failure in Legionnaires' disease is rare, but the mortality rate is high [1-3]. Although the actual pathogenesis is not clear, the renal pathology discloses either acute tubulointerstitial nephritis or acute tubular necrosis in most cases [3]. We report two cases of Legionnaires' disease complicated by acute renal failure. One patient was completely healthy before, and the other had underlying gouty arthritis and diabetes mellitus. Their renal function was normal before these episodes. The diagnosis of Legionella infection was proved by the indirect fluorescent antibody test on paired sera. After erythromycin treatment, both patients survived. One patient required long-term maintenance hemodialysis, and the other recovered to only mild azotemia after a follow-up period of 5 months. Including our cases, only 55 patients have been reported to have Legionella-induced acute renal failure. This is a rare and serious complication of Legionnaires' disease. Early recognition and treatment is mandatory.
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PMID:Legionnaires' disease with acute renal failure: report of two cases. 761 43

A 9-year-old castrated male domestic shorthair cat with dysuria, anorexia, vomiting, and lethargy was admitted to the veterinary teaching hospital. A large, firm mass was palpable in the ventral cervical region. Hypercalcemia, azotemia, and nonregenerative anemia were evident on serum biochemical analysis and CBC, and multiple uroliths were detected by abdominal radiography. At necropsy, light microscopy of the ventral cervical mass revealed a parathyroid adenocarcinoma. Light microscopy of sections of the kidneys revealed multifocal, chronic, lymphocytic/plasmacytic, tubulointerstitial nephritis, as well as moderate multifocal acute tubular necrosis. On quantitative analysis, the uroliths were composed of calcium oxalate. Determination of serum calcium concentration is indicated in cats with calcium oxalate urolithiasis to aid in detection of primary hyperparathyroidism.
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PMID:Calcium oxalate urolithiasis in a cat with a functional parathyroid adenocarcinoma. 775 34

To clarify the acute and subchronic inhalation toxicity of tetraethoxysilane [TEOS, Si(OC2H5)4], groups of ten male ICR mice (SPF grade) were exposed to 1000 ppm TEOS for 1,2,4 or 8 h (acute inhalation study), or to 200 ppm of TEOS for 6 h/day, 5 days/week, for 2 or 4 weeks (subchronic inhalation study). The numbers of mice that died during 2 weeks of observation were 0, 1, 1 and 6 in the 1-, 2-, 4- and 8-h inhalation experiments and zero in the subchronic inhalation study. In the acute inhalation study, body weight decreased after TEOS exposure and did not reach the level of control mice during 2 weeks of observation except in the 1-h inhalation study. In the subchronic exposure study, weight gain was suppressed during the exposure period. Body weight in mice exposed for 2 weeks reached the level of non-exposed mice during the 2-week observation period, but did not do so in mice exposed for 4 weeks. Acute tubular necrosis (ATN) and acute splenic atrophy (ASA) were observed in all dead mice in the acute inhalation study, and tubulointerstitial nephritis (TIN) was frequently found in the surviving mice in both the acute and subchronic studies. However, blood biochemical examinations revealed no evidence of renal dysfunction. The olfactory epithelium was necrotic in all dead mice. In the subchronic inhalation study, infiltration of polymorphonuclear neutrophils in the nasal mucosa was observed in all mice killed 1 day after exposure. These results indicate that the LCL0 for 1-h exposure to TEOS and LC50 for 4-h exposure are greater than 1000 ppm, and that the kidney and nasal mucosa are the target organs for TEOS inhalation.
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PMID:Acute and subchronic inhalation toxicity of tetraethoxysilane (TEOS) in mice. 808 37

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.
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PMID:[Acute renal failure as a complication of cholera]. 868 55

Tenascin, a large oligomeric glycoprotein, is a recent addition to a list of increasing extracellular matrix proteins. Previous studies have documented the strong expression of tenascin in embryonic kidney and in both normal and abnormal mature glomeruli implicating an important role of this extracellular matrix protein in nephrogenesis and glomerular scarring. Whether tenascin plays any role in interstitial fibrosis, a common final pathway of tubulointerstitial nephritis, is no known; on the other hand, a detailed knowledge of the structural components of interstitial fibrosis is essential for further studies on other fundamental aspects of this biologically and clinically important process. In this study, the expression of tenascin in the renal interstitium was immunohistochemically evaluated in 208 renal specimens during normal kidney (23 cases), acute tubular necrosis (8), acute tubulointerstitial nephritis (8), chronic primary tubulointerstitial nephritis (30), tubulointerstitial nephritis secondary to glomerular diseases of mild (46) and severe (55) degree, ischemic damage (24), and rejection (14). It was found that in normal kidney tenascin expression was limited to the medullary interstitium. In kidney with tubulointerstitial nephritis, tenascin was ubiquitously and constantly expressed in any areas with tubulointerstitial damage regardless of diagnosis, etiology, the cortical vs. medullary location of the lesions, stage of the fibrogenetic process, density of fibroblasts, or severity of interstitial inflammation in the affected areas. Indeed, strong tenascin expression was seen in areas where there was only interstitial edema or inflammation as judged by routine light microscopic preparations. In summary, this study systematically documents tenascin as a novel extracellular matrix protein selectively expressed in the medullary interstitium in normal kidney, and ubiquitously present in areas with interstitial fibrosis.
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PMID:Tenascin is an ubiquitous extracellular matrix protein of human renal interstitium in normal and pathologic conditions. 873 Apr 25

A descriptive cross-sectional study was conducted on the prevalence and histologic characteristics of renal lesions found in the autopsies of 85 patients with HIV infection: also, a retrospective analysis of clinico-biological characteristics in 56 of these patients in order to establish the factors associated with the histological findings. A total of 85 autopsies were made from 1985 to 1993; 50 autopsies (58.8%) showed renal changes: 23 (27%) infections, 13 (15.2%) acute tubular necrosis (ATN), 6 (7%) tumors, 5 (5.8%) intersticial nephritis (IN), 5 (5.8%) nephrocalcinosis (NC), 10 (11.7%) others. In an additional study: group IIc (n = 37, study group with nephropathy) had a higher incidence in the hepatitis B surface marker (HBsAg) than in group Ic (n = 19, control group, without nephropathy) (0 vs 10, p < 0.05). The presence of disseminated mycobacteriosis in the autopsy was significantly higher in the group with nephropathy than in the group without nephropathy (11 vs 1, p < 0.05). No consistent data were observed between the clinical diagnosis of nephropathy and autopsic findings. In summary, a high incidence of nephropathy was found in the autopsies of HIV infected patients, although it was not previously suspected. Renal lesions in autopsies of HIV infected patients had a tubular-intersticial predominance over glomerular lesions. The use of potentially nephrotoxic drugs, the presence of HBsAG, and some opportunist infections apparently influenced on the development of renal lesions among these patients.
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PMID:[Spectrum of the renal pathology in HIV infection: description of 85 autopsies and clinico-pathologic correlation]. 896 17

Twenty-six cases (4.8%) from a total of 540 patients with acute renal failure (ARF) of diverse aetiology had ARF in association with falciparum malaria. Their ages ranged from 15 to 85 years (mean 31.2). Urinary sediment abnormalities and proteinuria (less than 1 g/24 h) were observed in 15 (57.7%) cases. The probable underlying factors leading to ARF were: volume depletion 17 (65.3%), intravascular haemolysis 8 (30.8%), hyperparasitaemia 8 (30.8%), cholestatic jaundice 6 (23%), and hypotension 5 (19.2%). Dialysis therapy was required in 15 patients (57.7%) as they had severe renal failure, and the remaining 11 patients improved with supportive measures. All patients received antimalarial therapy. The clinical course of ARF was consistent with acute tubular necrosis in 20 patients. Six cases were subjected to percutaneous renal biopsy. One patient showed histological features of necrotizing glomerulonephritis along with acute tubulointerstitial nephritis. The biopsies in the other five patients showed features of acute tubular necrosis in three, and acute interstitial oedema with patchy tubular necrosis in two. The mortality rate was 30.8%. Thus falciparum malaria, which has been an important cause of ARF in certain highly endemic zones of India, is showing an increasing prevalence in other parts such as Eastern Uttar Pradesh due to an imbalance between the increasing population and inadequate sanitary facilities, which further worsen during floods.
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PMID:Acute renal failure in falciparum malaria--increasing prevalence in some areas of India--a need for awareness. 930 75

Hemorrhagic fever with renal syndrome is the most common clinical manifestation of hantavirus infection. The main target organ is the kidney, resulting in an interstitial hemorrhagic nephritis and sometimes acute tubular necrosis. The pathogenesis is still largely unknown, but several recent studies indicate an important role for immune mechanisms including increased expression of cytokines, for example, tumor necrosis factor. Immunohistochemical studies of kidney biopsies have revealed deposits of IgG, IgM, and C3, but deposits were significantly less numerous than in chronic immune complex disease. Since hantaviruses are not cytolytic, a direct detrimental effect of the infecting virus is less likely. The long-term prognosis of hemorrhagic fever with renal syndrome seems to be favorable, but there are reports that previous hantavirus infection is associated with an increased risk of hypertensive renal disease. Prospective longitudinal studies addressing this issue are underway.
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PMID:Pathogenetic and clinical aspects of the renal involvement in hemorrhagic fever with renal syndrome. 904 47

Nephropathy as the sequences of Hansen's disease before and after the introduction of chemotherapy was compared referring to the report by Hayashi in 1943 and the summary of the autopsy reports from 1978 to 1981 at National Hansen's disease hospital Zenseien. Unlike the high rates of tuberculosis as the cause of death before the introduction of chemotherapy (41.3%) those thereafter decreased to be negligible. On the other hand the comparison of the rates of nephropathy with the same way as that of tuberculosis was impossible since the description about nephropathy by Hayashi was not sufficient to characterize each nephropathy since he included arteriolitis, glomerulonephritis and interstitial nephritis together in the term of nephritis. Death rate due to nephritis among Hansen's disease patients according to Hayashi at that time was 21.2% which was twice as many comparing to that in the other cases. According to the report about the cases of Zenseien those reported to have glomerulonephritis was 37.3% though those were not necessarily listed as the cause of death. Also the nephropathy including fibrinoid angitis with occasional microaneurysmal dilatation of afferent arteries, glomerulitis, sclerosis and stricture of efferent arteries likewise ischemic acute tubular necrosis possibly as the result of these angiopathy seemed to be present. These vascular changes partially resemble to that of microscopic periarteritis nodosa but seems to be common in the smaller arteries. In conclusion, unlike the case of tuberculosis the rate of nephritis including glomerulitis, arteriolitis and interstitial nephritis as Hayashi used as his criteria does not seem to have decreased. Therefore, the critical analysis of the nephropathy especially of that relating to the arteriolitis should be done to obtain the knowledge to suppress its occurrence.
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PMID:[Hansen's disease and nephropathy as its sequence]. 930 Dec 9


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