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

Patients with lupus nephritis and severe renal failure progress to end-stage renal disease despite aggressive therapy to suppress immunologic function. Within this group is a small subset presenting with rapid progression of renal failure and requiring dialytic support. We reviewed the clinicopathologic data of four such patients who were able to terminate dialysis after acute renal failure due to lupus nephritis. Three of these patients have remained independent of dialysis up to 4 years, and one patient returned to dialysis 1 month following discontinuation. Although glomerular pathology was variable in the four patients, a lesion common to all at presentation was acute tubular necrosis. It is suggested that tubular necrosis may cause reversible renal failure when part of the nephropathy of disseminated lupus treated with corticosteroids.
 ...
PMID:Histopathologic evaluation of lupus patients with transient renal failure. 381 70

Combined hepatocellular injury and renal tubular necrosis developed in five alcoholic patients who were receiving acetaminophen therapeutically. Two patients were taking doses prescribed by a physician. The hepatitis was characterized by extremely high serum transaminase values that were maximal on admission. Two patients died, and autopsy disclosed hepatic centrizonal necrosis and acute renal tubular necrosis. The three who survived had clinical features typical of acute tubular necrosis. All five had measurable concentrations of acetaminophen in plasma, although measurements were requested on admission only in two patients. When an alcoholic presents with combined hepatic and renal insufficiency, acetaminophen should be considered as a possible inciting agent. This diagnosis should be considered when serum transaminase levels are markedly elevated and when renal failure is due to acute tubular necrosis.
 ...
PMID:Combined hepatic and renal injury in alcoholics during therapeutic use of acetaminophen. 406 53

A growing list of drugs, metals, and chemicals has been implicated as the cause of functional and structural damage specifically to the proximal tubular epithelium. Renal biopsies were obtained from three patients who had developed nephrotoxic agent-related acute renal failure. Two of the patients had received gentamicin and viomycin; the third patient had heavy exposure to chromium. All three biopsies showed acute tubular necrosis (ATN) on light microscopy. Electron microscopy revealed that the proximal tubular cells and, to a lesser degree, the distal tubular cells, contained abundant, variably sized myeloid bodies. In our previous experimental study of viomycin-induced ATN in rats, similar ultrastructural findings of a gradual increase in the number of myeloid bodies in the proximal tubular cells were also observed. The constant presence of myeloid bodies in the tubular epithelial cells following drug-induced tubular necrosis suggests that they may represent lysosomal isolation of drug-bound cytoplasmic structures, as a cellular mechanism to degrade toxic substances and, therefore, may serve as an ultrastructural marker of cellular drug uptake and drug disposition.
 ...
PMID:Myeloid bodies in drug-induced acute tubular necrosis. 629 92

Nephrotoxicity of sodium arsenate was evaluated in dogs to determine the pathophysiologic basis for renal lesions caused by this heavy metal. Examination of biopsy specimens indicated that the low dose of the As salt (0.73 mg/kg of body weight) produced histologic changes consisting of mild degeneration and vacuolation of renal tubular epithelium. Vacuolation involved mainly the ascending thick portion of the nephron. Clinical pathologic changes were not demonstrable at this dosage level according to glomerular filtration rate (creatinine clearance), fractional reabsorption of sodium, potassium, and chloride; plasma osmolar and free water clearance; and urinalysis. The medium dose (7.33 mg/kg) resulted in alterations determined by urinalysis, but did not markedly affect other clinical pathologic measurements. Histopathologic changes were equal to or greater than those seen with the low dose. Tubular necrosis was observed in the cortical portion of the nephron and the ascending thick limb. The high dose (14.66 mg/kg) consistently produced marked changes in all parameters evaluated. Clinical pathologic alterations were compatible with acute tubular necrosis involving all segments of the nephron. Histologically, moderate glomerular sclerosis and severe tubular necrosis were observed. During recovery from the high dose of As, a gradual compensatory healing process was observed that was evident in all clinical pathologic parameters and was confirmed from sequential renal biopsy specimens.
 ...
PMID:Nephrotoxicity of sodium arsenate in dogs. 668 17

Acquired insensitivity to the nephrotoxic effects of gentamicin develops in Fischer 344 rats after 10 to 14 days' treatment after development of histologic acute tubular necrosis in a setting of extensive histologic regeneration. To determine the relative importance of aminoglycoside exposure, necrosis, and regeneration in the induction of insensitivity, we examined the effect on gentamicin toxicity of prior non-aminoglycoside-mediated tubular necrosis, antecedent nonnecrotizing aminoglycoside exposure, and unilateral Nx-induced renal tubular hyperplasia. Pretreatment with potassium dichromate, which causes tubular necrosis in the same part of the renal cortex as gentamicin, reduced gentamicin-mediated elevation of Scr but had little effect on gentamicin-related tubular dysfunction or structural damage. Pretreatment with netilmicin, which does not cause tubular necrosis, increased the sensitivity of the kidney to gentamicin; toxicity occurred earlier and was more severe. Antecedent unilateral Nx had no demonstrable effect on susceptibility to gentamicin-associated dysfunction, but histologic renal tubular epithelial regeneration and recovery from dysfunction occurred earlier, These results suggest that necrosis and/or regeneration is the major prerequisite for development of gentamicin insensitivity and that the onset of insensitivity is temporally related to the appearance of necrosis and regeneration. However, non-aminoglycoside-mediated necrosis and regeneration fail to fully-re-create insensitivity, suggesting that exposure to gentamicin is also necessary.
 ...
PMID:Gentamicin nephrotoxicity. II. Definition of conditions necessary to induce acquired insensitivity. 711 52

2 patients with systemic lupus erythematosus and mild renal functional impairment were treated with ibuprofen, one of the phenylproprionic nonsteroidal anti-inflammatory drugs. Within days after the onset of therapy, both developed renal insufficiency manifested by elevated serum creatinine levels, increased proteinuria, and active urinary sediments; 1 patient was oliguric. Renal biopsies disclosed mesangial proliferative lupus glomerulonephritis and acute tubular necrosis, the latter more pronounced in the oliguric patient. Renal failure resolved following discontinuation of ibuprofen and supportive therapy. It is postulated that altered blood flow, mediated through the well-known prostaglandin synthetase inhibitory effects of ibuprofen, resulted in tubular necrosis. This undesirable complication of ibuprofen therapy may be enhanced in patients with underlying renal disease, and may be a factor governing the limitation of its usage.
 ...
PMID:Ibuprofen-induced acute renal failure with acute tubular necrosis. 718 Sep 1

The mortality rate of acute renal failure is still high, about 50%. About 10% of the survivors have chronic renal failure, sometimes requiring dialysis. The course of some of these cases can be improved by appropriate therapeutic measures, if they are undertaken early. Early identification of these lesions is therefore mandatory. The clinical diagnosis is often difficult: 1. rare atypical forms of acute tubular necrosis, with renal or extrarenal signs, may lead to renal biopsy; 2. vascular and glomerular disease are most often recognized clinically (sometimes misdiagnosed), but the histological type (and therefore the appropriate treatment) cannot be determined; 3. acute interstitial nephritis is rarely diagnosed clinically and the nature of the infiltrate remains unknown. In certain cases of acute renal failure, the contribution of early renal biopsy to the etiological diagnosis and to prognosis and therapy is obvious. In acute renal failure, renal biopsy should be considered early in a rather limited number of patients (about 20%), everytime the diagnosis of tubular necrosis is doubtful, especially in acute renal failure associated with persistent infection, in order to guide the therapy.
 ...
PMID:[Contribution of renal biopsy to the diagnosis and treatment of acute kidney failure]. 756 93

Acute tubular necrosis induced by aminoglycoside antibiotics and various other nephrotoxins is followed by a regenerative process which leads to the restoration of damaged tubules. Several lines of evidence indicate that tubular regeneration is mediated by polypeptide growth factors such as epidermal growth factor (EGF). Previous studies devoted to cisplatin nephrotoxicity have shown that this agent causes tubular cystic degeneration possibly related to an impairment of renal tissue repair. Thus, we examined on a comparative basis the time course of the regenerative response subsequent to tubular damage induced by tobramycin or cisplatin, particular attention being paid to renal EGF and its receptor. Female Sprague-Dawley rats (160-180 g body weight) were treated during 4 consecutive days with daily doses of 200 mg/kg tobramycin i.p. (BID) or 2 mg/kg cisplatin (once a day). Sham-treated rats were given 0.9% NaCl i.p. following the same protocol. Groups of experimental animals (n = 5-10) were terminated at increasing time intervals (1, 4, 7, 14, 21, 60 days) after cessation of treatment. One hour prior to sacrifice, each individual received i.p. 200 mg/kg 5-bromo-2'-deoxyuridine (BrdU) for the immunohistochemical demonstration of cell proliferation. Blood was collected at the time of sacrifice in order to assess glomerular filtration rate by measuring serum creatinine and BUN levels. Kidneys were analyzed with respect to total EGF determined by RIA in renal tissue homogenates, and soluble EGF was assayed in extracts prepared by centrifugation. Renal tissue was processed for the immunohistochemical detection of S-phase cells, of EGF, of EGF receptors, and of the intermediate filament vimentin, the latter being used as a marker of epithelium dedifferentiation. In absence of nephrotoxic alterations, EGF was immunolocalized in distal tubules, whereas EGF receptor immunostaining was seen in proximal tubules cells. Vimentin immunostaining was confined to glomeruli and blood vessels. Tobramycin and cisplatin caused acute tubular necrosis in proximal convoluted tubules and proximal straight tubules, respectively. Tissue damage was accompanied by renal dysfunction reflected by an elevation of serum creatinine and BUN levels. Tubular necrosis was followed by a proliferative response indicative of tubular regeneration. Regenerative hyperplasia was associated with a reduction of total immunoreactive EGF due to a decrease of tissue-bound proEGF. Tubules undergoing regenerative repair were characterized by a disappearance of EGF receptors and the presence of immunoreactive vimentin. In tobramycin-treated rats, renal dysfunction lasted for 4-7 days and was fully reversible, as indicated by the return of serum markers to normal values.
 ...
PMID:Modification of immunoreactive EGF and EGF receptor after acute tubular necrosis induced by tobramycin or cisplatin. 785 15

To elucidate the role of apoptosis and cell desquamation in the repair phase of acute tubular necrosis, morphological findings after 60 min ischaemia were investigated in rats. A morphometric analysis of the cell proliferation and of the epithelial cellularity of reconstructing tubules was performed. The kinetics of apoptosis and cell desquamation were also examined. Ischaemia and reperfusion injury resulted in widespread necrosis of tubules at day 1. Subsequently, a regenerative epithelial hyperplasia took place in the early stage. The most marked increase in cellularity in the damaged tubules was on day 6, when the tubules became lined by hyperplastic epithelial cells with papillary clusters. The number of papillary clusters decrease up to day 8, and during this period many desquamated cells from the clusters were observed in the tubular lumen. In the later stage, hyperplastic epithelial cells were reduced to their original cellularity and during this period the number of apoptotic cells obviously increased, while the damaged tubules were reconstructed. We conclude that epithelial overproduction occurs in the early phase after tubular necrosis, and excess hyperplastic epithelial cells regress during the repair process by cell desquamation and apoptosis, both of which are essential for the recovery of the original tubular structure.
 ...
PMID:Apoptosis and cell desquamation in repair process of ischemic tubular necrosis. 824 76

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.
 ...
PMID:Acute renal failure in falciparum malaria--increasing prevalence in some areas of India--a need for awareness. 930 75


<< Previous 1 2 3 4 5 6 7 Next >>