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

Studies were undertaken to determine the long-term effects of the nephrotoxin, uranyl nitrate, on the function and structure of the rat kidney. Animals were injected with 10 mg/kg B.Wt. of uranyl nitrate and renal function studies were performed one, two, four and eight weeks after drug administration. Light microscopy and scanning and transmission electron microscopy were used to characterize the morphologic changes at each time interval. Glomerular filtration rate was significantly reduced (P less than 0.01) one week (0.18 +/- 0.06 ml/min/100 gm B.Wt.) and two weeks (0.54 +/- 0.09 ml/min/100 gm B.Wt.) after drug treatment compared to controls (1.01 +/- 0.4 ml/min/100 gm B.Wt.) and returned to normal values by four weeks. The fractional excretion of sodium was significantly increased (P less than 0.01) one week after uranyl nitrate treatment (2.45% +/- 0.82) compared to controls (0.29% +/- 0.11). No further differences in this parameter were noted after one week. At all time intervals studied the pars recta of the proximal tubule (S2 and S3 segments) was the most consistently damaged region of the nephron. Acute tubular necrosis and tubular regeneration of these segments were evident one and two weeks after drug administration. Many of the tubules were widely dilated and lined by low-lying squamous epithelial cells. By four weeks some of these pars recta segments could be classified as microcysts and this type of lesion persisted as long as eight weeks after treatment. Regeneration of most injured proximal tubules was complete by eight weeks. Atrophic proximal tubules, marked interstitial fibrosis and a mononuclear cell infiltration, consistent with a chronic type of injury, were noted at the later time intervals. These results suggest that uranyl nitrate induces a persistent injury to the kidneys of rats causing lesions as long as eight weeks after injection.
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PMID:The long-term effects of uranyl nitrate on the structure and function of the rat kidney. 619 Mar 5

Most antipyretic analgesics can cause acute nephrotoxic effects, including acute tubular necrosis, acute interstitial nephritis, glomerular toxicity, and functional changes, such as "salicyl edema," following large doses of sodium salicylate. Most functional changes are related to acute suppression of prostaglandin synthesis, "the acute prostaglandin-effect," and have been primarily noted with the use of indomethacin. The association between prolonged and excessive consumption of compound analgesics and the development of renal disease and renal failure, characterized by renal papillary necrosis, is now well established. Studies in several countries have shown that the incidence of analgesic nephropathy as an indication for dialysis and transplantation corresponds to the per capita consumption of phenacetin in compound analgesics. Analgesic nephropathy, which is part of a wider clinical syndrome, the analgesic syndrome, is uncommon following the use of single analgesics. Analgesic nephropathy and the analgesic syndrome are discussed in detail, including the development of uroepithelial tumors.
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PMID:Renal effects of antipyretic analgesics. 635 70

The experiments were made to determine whether alpha-adrenergic blockade would reverse the vascular spasm in kidney grafts exposed to a warm ischaemia time of 30 min and 24 hr cold storage. Total vascular resistance per unit kidney mass, hematocrit, urinary flow, plasma and urine concentrations of creatinine, [Na+] and [K+], blood gases, renal O2 consumption and acid-base balance were studied in 21 anaesthetized dogs before and after kidney transplantation and administration of the blocking agent. Seven dogs were used to evaluate the effects of warm and cold ischemic stress on graft circulation and function without blockade (group 1). In the remaining dogs the blockade was induced by infusion of phentolamine (100 micrograms/kg/min) over 20 min. Controlled normal level of blood pressure was maintained throughout the experiments by infusion of 10% dextran 40 in saline (group 2) or by blood transfusion (group 3). Despite of interruption of neural pathways phentolamine induced a marked decrease in graft vascular resistance ranging from 89.2% +/- 5.9 (group 2) to 78.5% +/- 6.7 (group 3) in relation to the difference between the resistances before and after transplantation. In contrast, the decrease in vascular resistance of untreated grafts amounted only to 10.7% +/- 7.8 within a recirculation period of 4 1/2 hours. The increased renal blood flow following the blockade was associated with a considerable rise in urine flow and urinary excretion of creatinine, [Na+] and [K+] and a significant decrease in their plasma levels. The reduced O2 utilization by the grafts and the metabolic acidosis remained unchanged. These results indicate that phentolamine caused an effective suppression of vasoconstriction in kidney grafts exposed to warm ischemia and cold storage reflecting the intensive sympathetic activity under these conditions. Although the recovery of ischemic damaged tubular cells in this way was not acutely effected, the pharmacological enhancement of the cortical and medullary blood supply in the early posttransplant period may be helpful for overcoming the acute tubular necrosis and for preventing the development of hypertension due to the augmented release of vasodepressive medullary hormones.
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PMID:[Hemodynamic effects of an alpha-adrenergic blockade following experimental kidney transplantation]. 637 12

A study was conducted in oliguric and acutely azotemic patients, measuring: (i) the fractional excretion of sodium (FENa) using creatinine clearance as a measure of glomerular filtration rate, and (ii) sodium clearance relative to urea clearance, designated as the sodium/urea clearance ratio (Na:urea CR). It was found that FENa discriminated between "tubular" and "non-tubular" disorders in 96% of patients. Further, Na:urea CR was as discriminating as FENa. Patients with Na:urea CR above 2.5% can be reliably diagnosed as having acute tubular necrosis or acute urinary tract obstruction; those with a value less than 2.5% will have acute glomerulonephritis or pre-renal azotemia. As urea and sodium measurements are so readily available, this test can now be applied in the assessment of the oliguric or acutely azotemic patient in any hospital practice.
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PMID:A simple aid to the differential diagnosis of oliguria. 658 51

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.
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PMID:Nephrotoxicity of sodium arsenate in dogs. 668 17

The present prospective study was undertaken to evaluate the usefulness of urinary chloride concentration in determining the cause of an abrupt decline in renal function. 99 patients from diverse clinical settings with multiple causes of acute renal failure were evaluated. Urinary chloride concentrations of less than 20 mEq/l were observed in most cases of reversible prerenal azotemia (20 of 21 cases) and were observed in more frequently than urinary sodium concentration of less than 20 mEq/l (13 of 21 cases, p less than 0.01). Only prerenal azotemia accompanying diuretic use was associated with high urinary chloride concentrations (57 +/- 7 mEq/l). When prerenal azotemia occurred in the setting of metabolic alkalosis with bicarbonaturia, urinary chloride was low (4.0 +/- 1.0 mEq/l) while urinary sodium was high (65.0 +/- 19.0 mEq/l). In patients with oliguric and nonoliguric acute tubular necrosis, and in patients with acute exacerbations of chronic renal failure, mean urinary chloride concentration ranged from 40 to 67 mEq/l and mean fractional excretions of chloride ranged from 7.2 to 8.4%. Only 11% of patients with oliguric and nonoliguric acute tubular necrosis had urinary chloride concentrations of less than 20 mEq/l. Urinary chloride concentrations exhibited greater sensitivity and equivalent specificity as urinary sodium concentrations in differentiating patients with reversible prerenal azotemia from those with oliguric and nonoliguric acute tubular necrosis.
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PMID:Urinary chloride concentration in acute renal failure. 670 May 67

Sprague-Dawley rats given gentamicin from 10 to 70 mg/kg/day for 9 days showed a linear decrease in glomerular filtration rate with increasing dose, paralleled by histologic changes of acute tubular necrosis and cast formation only at the higher doses. Nephrotoxicity was correlated with the peak, rather than trough, serum gentamicin levels in this study, suggesting that it is the mean level of gentamicin over time that determines renal injury. The polyuria caused by gentamicin resulted mainly from a tubular concentrating defect rather than enhanced sodium or osmolal excretion and may be explained by the finding of a predominance of casts in the medullary thin limbs of the loops of Henle. No effect of gentamicin on the activity of cortical or medullary sodium-potassium adenosine triphosphatase was found to account for the modest sodium wasting. Concurrent administration of sodium cephalothin decreased the renal toxicity of gentamicin at high doses, an effect not explained by the added sodium or nonreabsorbable anion.
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PMID:Features of gentamicin nephrotoxicity and effect of concurrent cephalothin in the rat. 687 60

Two elderly women suffered an acute deterioration of renal function after treatment with cefoxitin sodium. One with stable chronic renal failure due to reflux nephropathy underwent a rapid deterioration of renal function which proved fatal. The other woman had rheumatoid arthritis and developed acute tubular necrosis after treatment with gentamicin and cefoxitin. All the data suggested that the antibiotic was responsible for the deterioration in renal function. The dose of cefoxitin should be reduced in patients with renal functional impairment. Cefoxitin should either be used with great caution or not prescribed in combination with aminoglycoside antibiotics.
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PMID:Cefoxitin-associated renal failure. 701 86

There are specific clinical settings in which each of the urine electrolytes may be diagnostically useful. The urine sodium alone is not efficient in differentiating prerenal azotemia from acute tubular necrosis, but if urine sodium is coupled with some measure of the renal concentrating ability, e.g., the urine:plasma creatinine ratio. discrimination between these two conditions is much improved. Usefulness of the urine sodium in other settings (evaluation of hyponatremia, prediction of acute rejection in renal transplant recipients, index of salt balance) is controversial. Urine potassium may be useful in the evaluation of hypokalemia of obscure etiology and, occasionally, in the form of the urinary Na/K ratio, as a guide to diuretic therapy. Urine chloride is assuming importance in the differential diagnosis of metabolic alkalosis, particularly when Bartter's syndrome is a consideration.
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PMID:Measurement of urine electrolytes: clinical significance and methods. 702 36

This report describes light and transmission electron microscopy (LM and EM, respectively) studies of kidneys from five cases of hepatorenal syndrome. The kidneys were removed and fixed for LM and EM between 30 and 120 min after death. All patients had progressive renal failure after admission to the hospital. All cases were jaundiced, had ascites, and exhibited features of hepatic encephalopathy. LM study revealed severe acute tubular lesions (ATL) or, more conventionally, acute tubular necrosis (ATN). EM study demonstrated necrosis of the proximal tubules characterized by swelling, disorganization of the cristae and appearance of dark bodies in the mitochondria, coalescence, fragmentation or displacement of the microvilli, loss of plasma membranes, rupture of the basement membranes, and separation of the cells from the basement membranes. Rupture of tubular basement membranes (tubulorrhexis) and mitochondrial dark bodies suggest an ATN due to ischemia or induced by vasoconstrictor substance(s). Glomerular lesions were infrequent (one in five) and therefore, do not seem to have contributed to renal failure. All cases terminally had extremely low urinary sodium (11 mEq/liter), high urinary potassium (50 mEq/liter), a remarkably low urinary sodium/potassium ratio (0.26, normal = 4.27), and a low urinary osmolality (less than 400 mOsm/kg). From this study we conclude that an ATN of variable severity may be associated with the hepatorenal syndrome. Since this ATN developed without preceding shock, sepsis, or hypotension it is possible that this ATN like that in ischemic acute renal failure may be due to reduced renal blood flow and intense cortical vasoconstriction which has been reported in hepatorenal syndrome. Finally, our data imply that low urinary sodium is consistent with this pathologic lesion in this clinical setting.
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PMID:Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study. 714 28


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