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

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

1-(2-Chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU) and chlorozotocin (CZ; 2-[3-(2-chloroethyl)-3-nitrosoureido]-D-glucopyranose) are structurally related anticancer agents which differ by virtue of the increased water solubility, and comparatively low carbamylating activity, of CZ relative to MeCCNU. In the present study, a single sc injection of either of these chloroethylnitrosoureas was nephrotoxic to male Fischer 344 rats. However, at equimolar doses, CZ was shown to be a much more potent nephrotoxicant. A lethal 40-mg/kg dose of CZ (127 microM) initially resulted in acute tubular necrosis of the proximal tubules of the cortex, followed later by a necrosis of papillary collecting ducts. In contrast, lethal doses of MeCCNU (100-180 mg/kg; 400-730 microM) produced only minimal proximal tubule injury. A 250-mg/kg (1 mM) dose of MeCCNU resulted in massive papillary necrosis within 7 days, with only limited necrosis to the proximal tubules. Sublethal doses of either drug, resulted in a similar, chronic, progressive nephropathy which was delayed in onset and was characterized by polyuria, enzymuria, a decrease in urine concentrating ability, and in renal slice organic ion accumulation. Alterations in less sensitive indicators of renal toxicity (i.e., proteinuria, glucosuria, and elevated blood urea nitrogen) were observed no earlier than 3 to 7 days after administration of only the highest tested doses of CZ (40 mg/kg) or MeCCNU (250 mg/kg). At sublethal doses, administration of either drug resulted in karyomegaly to the collecting ducts in the renal medulla within 2 to 4 weeks. These studies demonstrate that carbamylation-mediated reactions may not be necessary for nephrotoxicity to develop following administration of this class of antitumor agent.
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PMID:Comparative nephrotoxicity of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU) and chlorozotocin: functional-structural correlations in the Fischer 344 rat. 293 79

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

Naloxone HCl (Nx) improves cardiopulmonary performance, reverses cellular hypoxia, and stabilizes lysosomal membranes in shock states. However, no detailed study has yet explored its potential role in renal ischemia, which is inevitable in transplantation and surgical and nonsurgical conditions associated with hypotension and shock. This functional and microanatomical study was carried out on dogs subjected to renal warm ischemia with contralateral nephrectomy. Group I (control; N = 4) had bilateral renal dissection and right nephrectomy. Groups II-IV had their kidney pedicles cross-clamped for 60 min and then reperfused. Group II (N = 9) ischemic kidneys received no treatment. Group III (N = 6) kidneys were flushed with pure Nx HCl (2 mg/kg) during ischemia. Group IV (N = 6) dogs received one iv Nx bolus (2 mg/kg) before clamping and another dose before declamping. Biopsies for adenine nucleotides, histology, and ultrastructure were obtained before ischemia, before reflow, and 15 min and 7 days after reflow. Serum creatinine and blood urea nitrogen were measured daily. Ischemia induced significant renal dysfunction, which was reversed by systemic Nx. Nx offered a remarkable protection against postischemic structural damage. Seventy percent of Group II cortical sections showed grade 4 acute tubular necrosis (ATN), and severe residual damage after a week. Eighty-three percent of Group IV sections showed grade 1 ATN and no residual damage after a week. One week survival was 33% in Group II and 100% in Group IV. Nx can be useful in prevention of acute renal failure in clinical situations with arterial hypotension and shock.
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PMID:Naloxone in renal ischemia: a functional and microanatomical study. 358 32

Adult male Sprague-Dawley rats maintained on a low sodium diet were administered 100 mg of cyclosporine per kg b.wt. per day s.c. for 4 to 10 days. Serum urea nitrogen was significantly elevated by day 4 and continued to rise, whereas serum creatinine was not elevated above control until day 10. Morphologic examination of perfusion-fixed kidneys from cyclosporine-treated rats revealed focal areas of tubular atrophy and interstitial fibrosis in the outer cortex and a generalized increase in interstitial cells in the outer medulla. No areas of acute tubular necrosis were identified. The effect of this dose of cyclosporine on renal hemodynamics was examined in conscious restrained rats. Renal blood flow, measured by microsphere injection, was 70% of control after four daily doses and remained near this level after eight daily doses. The glomerular filtration rate, measured by iodothalamate clearance, was 70% of control after four doses but fell to 34% of control after eight doses. [3H]Thymidine incorporation into renal DNA was used as a sensitive index of renal cell proliferation after cyclosporine administration (100 mg/kg/day). [3H]Thymidine incorporation was increased over control 3-fold in the outer cortex, 7-fold in the inner cortex and 11-fold in the medullary-papillary regions of the kidney after eight daily doses of cyclosporine. Histoautoradiographic examination of renal sections revealed an increase in the number of labeled nuclei in all three regions of the kidney from rats treated with cyclosporine. Morphometric analysis demonstrated that the majority of proliferating cells were located in the interstitium and not in renal tubules.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in renal structure and function in a rat model of cyclosporine nephrotoxicity. 361 60

We reviewed our 10-year experience with neonatal hypertension. Fifty-three cases were identified, which represented 0.7% of all neonatal tertiary care admissions. Causes were identified in 23 (43%) neonates. These included acute tubular necrosis (n = 7), renal vascular abnormalities (n = 8), renal structural abnormalities (n = 4), interstitial nephritis (n = 2), and coarctation of the aorta (n = 2). No cause was identified in 30 (57%) infants. If the two neonates with coarctation are excluded, infants who had normal urinalyses, blood urea nitrogen (BUN), serum creatinine and plasma renin activity (PRA), had non-malignant hypertension that tended to be short-lived and always resolved spontaneously. In contrast, a cause of hypertension was found in 68% of those having an abnormal urinalysis, BUN, serum creatinine or PRA. There were two hypertensive deaths in this group. While the hypertension was usually more prolonged, it still generally resolved spontaneously by 1 year of age or following corrective surgery. Our experience indicates that diagnostic studies can be postponed if the urinalysis, BUN, serum creatinine and PRA are normal and if coarctation of the aorta has been excluded. If these preliminary studies are abnormal, however, a renal cause is likely and further studies are indicated.
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PMID:Hypertension in the first month of life. 379 27

Male Fischer 344 rats classified as young (2-4 months), middle-aged (12-14 months) and aged (22-25 months) received 300, 600 or 800 mg/kg acetaminophen (APAP) intraperitoneally and were sacrificed 24 hr later. Blood urea nitrogen (BUN) concentration and urinary glucose and osmolality were determined. In addition, kidneys were evaluated for histopathological changes. APAP did not affect osmolality or BUN concentrations and failed to produce lesions after any dose in young rats. Osmolality was decreased 40% and 50% in middle-aged and aged rats, respectively, after 800 mg/kg APAP. Glucosuria was prominent in aged rats after the 600 and 800 mg/kg doses were administered, while middle-aged rats showed little glucosuria after these doses. BUN concentrations were elevated 89% and 183% in middle-aged and aged rats, respectively, given 600 mg/kg APAP; after 800 mg/kg, BUN concentrations were elevated approximately four-fold in both age groups. Pathological evaluations showed a greater incidence of acute tubular necrosis (ATN) in aged kidneys compared to kidneys of middle-aged rats after 600 mg/kg, while the two older groups exhibited similar, more severe ATN after 800 mg/kg APAP. These data suggest an age-related increased susceptibility of male Fisher 344 rats to APAP nephrotoxicity.
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PMID:Age-related increased susceptibility of male Fischer 344 rats to acetaminophen nephrotoxicity. 379 97

The nephrotoxic potential of N-(3,5-dichlorophenyl)succinimide (NDPS) was examined, in male Fischer-344 rats. Rats were administered NDPS (0.1, 0.2, 0.4 or 1.0 mmol/kg intraperitoneally (i.p.) or sesame oil (2.5 ml/kg, i.p.), and renal function was monitored at 24 and 48 h. NDPS (0.1 mmol/kg) stimulated organic ion uptake at 48 h. NDPS (0.2 mmol/kg) produced diuresis but did not alter blood urea nitrogen (BUN), kidney weight or organic ion uptake by renal cortical slices at 48 h. High-dose NDPS (0.4 and 1.0 mmol/kg) administration produced diuresis, decreased accumulation of p-aminohippurate (PAH) and tetraethylammonium (TEA), increased BUN and kidney weight and caused acute tubular necrosis. At 24 h, NDPS (0.2 mmol/kg) decreased uptake of PAH and TEA and tended to increase BUN. These results are similar to previous reports of NDPS-induced nephrotoxicity in Sprague-Dawley rats and suggest that either rat model would be suitable for future studies on the mechanism(s) of NDPS-induced nephropathy.
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PMID:N-(3,5-Dichlorophenyl)succinimide nephrotoxicity in the Fischer-344 rat. 397 35

A total of 39 Holstein cattle were grazed in tracts of wild grassland on account of shortage in pasture grass. Twenty-nine cattle were affected and 26 of them died during a 21-day period. The main signs were depression, anorexia, ascites, and oliguria. There was elevated serum urea nitrogen and sugar and protein in the urine. Pathological examination revealed turbid swelling of the kidney, an increase in the amount of fluid in the body cavity, edema in the perirenal adipose tissue and hemorrhage in various visceral organs and tissues. Histologically, acute tubular necrosis in the kidney, hypoplasia of the erythroblast series in the bone marrow, atrophy and degeneration of the lymphatic tissue and focal necrosis of the liver were observed in many of the cattle. Among cows experimentally fed Narthecium asiaticum Maxim., Polygonum sachalinense Fr. Schum., and Vitis coignetiae Pulliat which were presumed to have been ingested in large amounts by grazing cattle in the field, the cows fed N. asiaticum revealed the clinical, biochemical and pathological changes similar to those noticed in naturally affected cattle. Cows fed P. sachalinense and V. coignetiae showed no distinct systemic symptoms except transient anorexia and hypothermia.
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PMID:Narthecium asiaticum Maxim. Poisoning of grazing cattle: observations on spontaneous and experimental cases. 398 97

The urine/plasma creatinine ratio (U/P Cr), the urine sodium concentration (UNa), and the diuretic response to mannitol infusion in 23 patients were reviewed in an attempt to differentiate functional renal failure (FRF) from acute tubular necrosis (ATN). FRF was diagnosed if the plasma urea nitrogen (PUN) or serum creatinine stabilized within 72 hours. When renal failure persisted longer, patients had ATN. Subjects dying within 72 hours were excluded. Ten patients had ATN and five survived. The minimum duration of renal failure among survivors was 10 days. None responded to mannitol. Of 13 patients with FRF, 11 survived. Seven of 12 who received mannitol responded with a diuresis. The mean UNa in the patients with ATN was 51.4 mEq./1. +/- 9.48 (SE). The mean U/P Cr was 11.2 +/- 1.12. In patients with FRF, the mean UNa was 14.0 mEq./1. +/- 4.2 and the mean U/P Cr was 42.5 +/- 11.5. A significant overlap was present between the two groups. When UNa was factored by the U/P Cr, the resultant ratio was significantly different for the two groups of patients (P < 0.01), and this proved to be a useful clinical index with which to distinguish FRF from established ATN.
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PMID:Diagnostic indices in acute renal failure. 601 69


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