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)

Aspects of the renal function were assessed in rats treated with the pentavalent antimonials Glucantime (Meglumine Antimoniate, Rhodia) or Pentostam (Sodium Stibogluconate, Wellcome). In dose of 30 mg of Sbv (Glucantime or Pentostam) by 100 mg of weight by day for 30 days, renal functional changes were observed consisting of disturbances in urine concentrating capacity. Such disturbances were expressed by significantly low values of urine osmolality as compared to the basal values previous to the drugs. The decrease in urine osmolality was associated to a significant increase in urinary flow and in negative free-water clearance. There was no alteration in osmolar clearance and in fractional excretion of sodium. These observations suggest an interference of the drugs in the action of the antidiuretic hormone. The disturbance in urine concentration was reversible after a seven days period without the drugs administration. No significant histopathological alterations were observed in the kidneys of the rats treated with the drugs. On the other hand, the rats treated with a high dose of Pentostam (200 mg/100 grams of weight/day) showed the functional and the histopathological alterations of the acute tubular necrosis.
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PMID:Pentavalent antimonial nephrotoxicity in the rat. 210 25

We investigated the relationship between urinary prostaglandin E2 (UPGE2), kallikrein (UKal), graft function and complications after renal transplantation in 11 patients. Grafts of 9 patients were from living-related donors (LRD), and other 2 patients were from a cadaveric donor (CAD). UPGE2 was measured by the radio immunoassay, and UKal was measured by the amidolytic method using Pro-Phe-Arg-MCA. The results were as follows. 1. In 5 of 6 patients from LRD without acute rejection episode (ARE), both UPGE2 and UKAL were within normal and/or slightly less than normal. UKal values of the other patient were high in his donor. 2. In 2 of 3 recipients from LRD who experienced ARE, UKal increased prior to ARE. UPGE2 also increased at the time of ARE, but it showed a periodic rise in the stable condition. 3. In 1 of 2 recipients from CAD, UKal exhibited a transient elevation at the time of acute tubular necrosis (ATN) and pyelonephritis while UPGE2 was low. In another recipient, UKal was almost within normal range at the time of ATN, and UPGE2 showed a periodic rise. 4. A significant correlation was seen between UKal, UPGE2 and UAld in the recipients from LRD without ARE (except 1 patient who showed high UKal values). However, the correlation was blurred inclusive of values in the patients who experienced ARE or other complications. There was no relationship between UKal, UPGE2, creatinine clearance, urine volume and urinary sodium. 5. Soybean trypsin inhibitor (STI) was used for the confirmation of specificity of the amidolytic method.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Urinary prostaglandin E2 and kallikrein-like activity excretion in renal transplant recipients]. 235 62

In 55 patients with either the oliguric and nonoliguric form of acute renal failure, some laboratory parameters for the analysis of prerenal and intrinsic types of acute renal failure were examined. The parameters were analyzed within 7 days of the clinically known beginning of the illness. The parameters were analyzed as follows: sodium in urine, creatinine urine/plasma ratio, urine osmolality, osmolality urine/plasma ratio, renal failure index, and fractional excretion of filtered sodium. Hemodialysis was performed in 29 of the 55 patients. The oliguric form of acute renal failure was present in 49 of the 55 patients. In relation to renal failure index, prerenal acute renal failure was present in 7 patients and intrinsic acute renal failure in 48. It appears that in patients with a clinical diagnosis of prerenal acute renal failure, the urinary parameters do not separate them from those with acute tubular necrosis. It also appears that in patients with laboratory diagnosis of prerenal acute renal failure (i.e., a RFT less than 1.0), the response to treatment is unpredictable and in fact may have a worse prognosis than in those with a RFI greater than 1.0 (5/7 deaths vs 10/48 deaths).
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PMID:The lack of clinical value of laboratory parameters in predicting outcome in acute renal failure. 248 85

In order to determine the relationships between allograft function and the recipient's plasma concentrations of atrial natriuretic factor (ANF), plasma ANF was measured by radioimmunoassay for 14 days after cadaveric renal transplantation in 9 patients aged 19-64 years. All received immunosuppression with prednisolone, azathioprine, and cyclosporine. No patient was in heart failure. During the study period, six grafts functioned, and three were nonfunctioning--two due to rejection and one to acute tubular necrosis. Plasma ANF concentration at the time of transplantation was 48 +/- 16 pmol/L (mean +/- SEM) range 15-145 pmol/L. In the six patients with functioning grafts, ANF declined in parallel with the fall in serum creatinine (658 +/- 35 to 210 +/- 34 mumol/L). In the three with nonfunctioning grafts, serum creatinine and plasma ANF concentration both increased. There was overall a significant linear relation between serum creatinine and plasma ANF (r = 0.527, P less than 0.001). The changes in plasma ANF after renal transplantation bore no relationship to changes in body weight or blood pressure. However, plasma ANF concentration was related to allograft fractional sodium excretion (r = 0.687, p less than 0.001). We conclude that elevated plasma ANF concentrations in end-stage renal disease are restored to normal by successful renal transplantation, implying that renal function is a determinant of plasma ANF concentration. Circulating plasma ANF may also have a direct effect on allograft sodium excretion.
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PMID:Plasma atrial natriuretic factor and graft function in renal transplant recipients. 253 Jun 66

The effects of intramuscular glycerol on ischemic acute renal failure was investigated in dogs. Anesthetized dogs received a bilateral 120-min renal artery obstruction (RAO) alone, RAO plus 5 ml/kg of 50% glycerol or RAO plus 5 ml/kg of 75% glycerol. Control groups received the glycerol injection, but not RAO. Renal histopathology was minimal in dogs receiving glycerol alone. In RAO dogs, those receiving 50% glycerol showed diffuse acute tubular necrosis (ATN), while those receiving 75% glycerol had severe ATN with extreme mortality. Changes in serum creatinine, creatinine clearance, and fractional excretion of sodium were consistent with the histopathologic changes. We conclude that myoglobinuria, of a degree insufficient to cause renal failure itself, can interact with renal ischemia to significantly exacerbate the renal damage produced.
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PMID:Myoglobinuria exacerbates ischemic renal damage in the dog. 279 46

During a one-year period, drug-associated acute renal failure (ARF) was prospectively recorded in 398 patients, registered in 58 french nephrology Units. Drugs involved were primarily antibiotics, mainly aminoglycosides, glafenine, non-steroidal antiinflammatory drugs and contrast media. Hypersensitivity reactions were reported in 69 patients. Renal biopsy, performed in 81 instances, showed acute tubular necrosis in 42 and acute interstitial nephritis in 20 patients. Hypotension, sodium depletion and/or cardiac failure were predisposing factors in 198 cases. Fifty patients died, 251 recovered fully or regained previous renal function, and in 93 permanent renal damage remained. Advanced age, oliguria, severe ARF, and preexisting cardiac, hepatic or renal insufficiency were poor prognostic factors. Prevention of drug-associated ARF should be directed to high-risk patients, particularly those receiving aminoglycosides and contrast media.
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PMID:[Acute renal failure associated with drugs or iodinated contrast media. Results of a cooperative multicentric study by the Nephrology Society]. 287 11

Splenectomy (SPLX) prevents ischemic acute tubular necrosis (ATN) and peritubular capillary (PTC) congestion. This study attempts to reverse the protective effect of splenectomy in the ischemic model of ATN by increasing hematocrit before inducing ATN. Sham-SPLX, SPLX, and SPLX dogs given packed red cells to elevate hematocrit by 30% (SPLX-high hematocrit) received bilateral renal artery obstruction (RAO) for 120 minutes. Renal function was tested for 6 days post-RAO. Hematocrit in the SPLX-high hematocrit group was greater (p less than .05) than the SPLX-RAO group but did not differ from the non-SPLX group. All groups had different (p less than .05) serum creatinine levels for 48 hours post-RAO, and untreated animals differed from all the others at 144 hours. Serum creatinine was highest in untreated, lowest in SPLX-high hematocrit, and intermediate in noninfused SPLX animals. The same pattern was observed in blood urea nitrogen, creatinine clearance and renal histopathology. Fractional excretion of sodium in the SPLX groups was six times that in the intact animals (p less than .05), irrespective of hematocrit level. We conclude that increased hematocrit is protective in ischemic ATN, and does not promote PTC congestion or ATN in the SPLX animal. In addition, the protective effect of splenectomy may be mediated, in part, by mechanism(s) that alter sodium transport or osmolar excretion.
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PMID:Increased hematocrit mitigates ischemic renal damage in the splenectomized dog. 292 39

The physical properties and chemical composition of urine are highly variable and are determined in large measure by the quantity and the type of food consumed. The specific gravity is the ratio of the density to that of water, and it is dependent on the number and weight of solute particles and on the temperature of the sample. The weight of solute particles is constituted mainly of urea (73%), chloride (5.4%), sodium (5.1%), potassium (2.4%), phosphate (2.0%), uric acid (1.7%), and sulfate (1.3%). Nevertheless, urine osmolality depends only on the number of solute particles. The renal production of maximally concentrated urine and formation of dilute urine may be reduced to two basic elements: (1) generation and maintenance of a renal medullary solute concentration hypertonic to plasma and (2) a mechanism for osmotic equilibration between the inner medulla and the collecting duct fluid. The interaction of the renal medullary countercurrent system, circulating levels of antidiuretic hormone, and thirst regulates water metabolism. Renin, aldosterone, prostaglandins, and kinins also play a role. Clinical estimation of the concentrating and diluting capacity can be performed by relatively simple provocative tests. However, urinary specific gravity after taking no fluids for 12 h overnight should be 1.025 or more, so that the second urine in the morning is a useful sample for screening purposes. Many preservation procedures affect specific gravity measurements. The concentration of solids (or water) in urine can be measured by weighing, hydrometer, refractometry, surface tension, osmolality, a reagent strip, or oscillations of a capillary tube. These measurements are interrelated, not identical. Urinary density measurement is useful to assess the disorders of water balance and to discriminate between prerenal azotemia and acute tubular necrosis. The water balance regulates the serum sodium concentration, therefore disorders are revealed by hypo- and hypernatremia. The disturbances are due to renal and nonrenal diseases, mainly liver, cardiovascular, intestinal, endocrine, and iatrogenic. Fluid management is an important topic of intensive care medicine. Moreover, the usefulness of specific gravity measurement of urine lies in interpreting other findings of urinalysis, both chemical and microscopical.
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PMID:Relative density of urine: methods and clinical significance. 307 30

With PHP as an oxygen carrier, histologic studies in ET showed changes of renal tubular epithelial cells at 2 weeks post ET, with normal structure by 3-12 months post ET. The renal functional effects of PHP were evaluated by ET (30%, N = 3; 50%, N = 1; 80%, N = 3) in seven healthy mongrel dogs. Blood, urine, and renal biopsy specimens were taken pre ET and at 0, 1, and 2 days, 2, 4, and 6 weeks, and 3, and 6 months post ET. Data were compared to modified criteria of acute tubular necrosis. All dogs tolerated the procedure well and survived for 1 year. Urine output was normal with elevation during the first 2 days in the 50 and 80% ET, followed by stable output by 2 weeks, ranging from 12 to 60 ml/kg/day. Blood urea nitrogen (BUN) and serum creatinine (SCr) were normal. BUN/SCr was normal. The urine to plasma osmolality ratios were 2.6 to 8.3 (normal greater than 1), and fractional percent excretions of sodium (FES) were stable throughout. No existence of broad granular pigmented casts (BGPC) in urine sediment were noted. Renal histologic evaluation of vacuolization in the renal tubules were seen to be dose-dependent and transient, with normal histology by 3-6 months post ET. Dose-dependent vacuole formation observed in the early weeks post ET with PHP showed no renal functional changes. Based upon the modified criteria for acute tubular necrosis, no histologic abnormalities were noted.
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PMID:Renal effects of a pyridoxalated-hemoglobin-polyoxyethylene conjugate solution as a blood substitute in exchange transfusions. 319 21

The pathogenesis of acute renal failure (ARF) in such common conditions as acute tubular necrosis, acute interstitial nephritis, and primary graft anuria (ischemic transplant ARF) is poorly understood. Animal models may not exactly mimic the situation in man and thus human morphologic studies are of particular importance. Non-replacement of individual sloughed tubular cells and simplification of the brush border and basolateral infoldings of tubular cells are prominent morphologic changes which correlate with the presence of renal failure. It is possible that the initial injury inhibits cell membrane synthesis, thus interfering with proximal tubular sodium reabsorption with resulting activation of the renin angiotensin system and afferent arteriolar vasoconstriction. Tubular backleak, tubular obstruction by casts and debris, and decreased glomerular ultrafiltration coefficient may also play a role. Although poorly studied until now, the renal failure in primary graft anuria may have a completely different pathogenesis from that in acute tubular necrosis and acute interstitial nephritis. Cyclosporine nephrotoxicity is an important component of primary graft anuria, as seen in many transplant centers in the 1980's.
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PMID:Acute renal failure in man: pathogenesis in light of new morphological data. 330 Nov 19


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