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)

The retrospective review of 115 case-histories of patients with acute renal failure (ARF) seen over the last two years showed that etiologies were distributed as follows: acute tubular necrosis in 65% of cases, urinary tract obstruction in 16%, acute glomerulonephritis in 3,5%, acute interstitial nephritis (AIN) in 8% and acute microvascular nephropathy in 3,5%. The diagnostic value of renal biopsy in ARF is discussed. In spite of recent advances in the treatment of ARF, the mortality rate remains as high as 48%. This is mainly due to current etiologic circumstances, to the age of the patients and to the complications of ARF, with infectious complications being the most serious. Urea nitrogen accumulation is not a poor prognosis factor. Furosemide in high doses does not alter the prognosis but reduces the total number of dialysis indications (81% in 1970, 60% in 1980), the number of dialysis sessions per patient (1 only in 62% of patients), and the duration of the ARF episode (mean duration: 10,7 days).
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PMID:[Current aspects of acute renal failure]. 629 41

Sodium diethyldithiocarbamate (DDTC) administered following cis-diamminedichloroplatinum(II) (DDP) has been reported to attenuate structural renal damage and elevation of blood urea nitrogen in rats. Since DDP damages primarily proximal tubular epithelium in this species, we compared proximal tubular function, glomerular function, and histology in male Sprague-Dawley rats treated with DDP followed by either DDTC or 0.9% NaCl solution (NS) rescue. Male Sprague-Dawley rats received a single i.p. injection of DDP (7.5 mg/kg)-mannitol (75 mg/kg)-NaCl (67.5 mg/kg). Forty-five min later, rats were given i.p. injections of either DDTC (750 mg/kg) dissolved in 0.5 ml of NS (DDP + DDTC group; ten rats) or 0.5 ml NS (DDP + NS group; nine rats); additional rats received either DDTC only (DDTC group; six rats) or no treatment (untreated control group; six rats). All groups were sacrificed 5 days later by ether anesthesia and exsanguination. Compared to the untreated control group, the DDTC group had slightly lower mean blood urea nitrogen at sacrifice [12.5 +/- 0.5 (S.E.) versus 15.4 +/- 0.8 mg/dl; p less than 0.025 by unpaired Student's t test]; there was no difference in serum creatinine. The DDP + DDTC group had no diarrhea and no presacrifice deaths in contrast to diarrhea and three presacrifice deaths in the DDP + NS group. Blood urea nitrogen was also lower in the DDP + DDTC group at sacrifice (187 +/- 30 versus 383 +/- 39 mg/dl; p less than 0.005). However, weight loss and serum creatinine were not different. Structural acute tubular necrosis was marked in both DDP groups but was less severe in the DDP + DDTC group than in the DDP + NS group. Proximal tubular function was indexed by the uptake of the organic base N-[14C]methyl nicotinamide (NMN) and the organic acid p-aminohippurate in renal cortical slices incubated 90 min in Cross and Taggart medium. NMN uptake (expressed as slice to medium ratio) was slightly lower in the DDTC group than in untreated controls (4.1 +/- 0.2 versus 5.0 +/- 0.2; p less than 0.025). Marked depression of p-aminohippurate and NMN uptake occurred in both DDP + DDTC and DDP + NS groups. There was no difference in NMN uptake, but depression of p-aminohippurate uptake was slightly less severe in the DDP + DDTC group (5.3 +/- 0.7 versus 3.1 +/- 0.3; p less than 0.005). We conclude that DDTC rescue attenuates structural DDP injury in this animal model. DDP-mediated proximal tubular dysfunction was only marginally attenuated by DDTC; glomerular filtration rate, as indexed by serum creatinine, was not protected. DDTC attenuation of DDP toxicity may be mediated in part via reducing volume depletion due to DDP-associated diarrhea.
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PMID:cis-diamminedichloroplatinum(II) nephrotoxicity: tubular function after rescue with sodium diethyldithiocarbamate in rats. 630 93

Immunological events in the acute, recovery and convalescent stages of typhoid fever were correlated with the occurrence of renal disease in 24 consecutively selected patients. Serum complement levels (C3) were significantly reduced in patients with renal disease during the acute state (p less than 0.01) and increased to normal levels in the recovery phase. IgG and IgM immunoglobulin levels were significantly lower than control values in all three stages (p less than 0.05). While IgA levels were elevated to above control levels in patients with and without renal disease in all three stages, IgA levels were lower in patients with renal disease compared to those without renal involvement in the acute stage (p less than 0.025). The percentage of T cells was increased significantly in all three stages (p less than 0.01). Seven patients showed renal abnormalities. All of them had glomerular disease demonstrated by proteinuria of 1.0 g or greater per 24 h, associated with significant haematuria. Almost all of these patients were glucose-six-phosphate-dehydrogenase (G.6.P.D.) deficient. Serum blood urea nitrogen was elevated in five of these patients who were G.6.P.D. deficient, and two of them developed classical acute tubular necrosis. It appears that renal involvement in typhoid fever commonly occurs as transient glomerular or tubular disease in G.6.P.D. deficient individuals. Glomerular disease is associated with a decrease in serum complement (C3) level in acute stage.
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PMID:Immunological and clinical aspects of kidney disease in endemic typhoid fever in Iran. 660 45

One of the controversies in the nutritional therapy of patients with renal failure is the respective role of either the essential amino acids alone or both essential and nonessential amino acids in the treatment of these patients. During a period when essential amino acids were unavailable, a large number of patients with acute renal failure was treated with a modified solution consisting of both essential and nonessential amino acids. The solution consisted of 3.8 grams of nitrogen in 46 per cent dextrose in units of 750 milliliters. A mean of 2,322 +/- 151 calories was administered to this group of patients. Over-all, the survival rate was 9 per cent as opposed to 75 per cent in the previous group treated with essential amino acids only and hypertonic dextrose, 40 per cent, in the group of historical controls treated with hypertonic dextrose. The groups are not strictly comparable because the group treated with both essential and nonessential amino acids may not have been strictly comparable, particularly with a slightly longer duration of renal failure, higher initial blood urea nitrogen level and lower urine volume than either of the other two groups previously treated. While adequate stabilization, but not a decrease in the blood urea nitrogen level, may be achieved from the use of both essential and nonessential amino acids, the excessive mortality seen may be related to differential effects of essential amino acids in supporting host resistance, while nonessential amino acids do not. The results of this study suggest that, until the safety and efficacy of a mixture of essential and nonessential amino acids in renal failure can be demonstrated, essential amino acids remain the treatment of choice as the nutritional support of patients with acute tubular necrosis.
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PMID:Comparative study of parenteral nutrition in renal failure using essential and nonessential amino acid containing solutions. 677 42

We examined the protective effects of medical castration by means of gonadotropin-releasing hormone analogue (GnRHA) on the toxic effects of cisplatin in rats. Twelve days after a s.c. injection of a slowly-releasable form of leuprolide acetate (GnRHASR), rats were injected i.p. with cisplatin daily (3 mg/kg body weight (BW) for males and 4 mg/kg BW for females) for four days and sacrificed 24 h after the last injection. The doses caused acute tubular necrosis and gastrointestinal (GI) symptoms, i.e., diarrhea and fluid retention and bleeding in GI tract. GnRHASR pretreatment reduced serum urea nitrogen (SUN) and serum creatinine (SCre) increase and the incidence of GI symptoms. Histological analysis showed that rats pretreated with GnRHASR had noticeably less kidney damage. GnRHA thus demonstrated its ability to protect the kidneys and GI tract against cisplatin toxicity in both male and female rats. This finding suggests a potential clinical application of GnRHA in antineoplastic chemotherapy.
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PMID:Leuprolide acetate prevents toxic effects of cisplatin on the kidneys and gastrointestinal tract. 767 May 59

Haemorrhagic fever with renal syndrome (HFRS) is an acute disease caused by Hantavirus and clinically characterised by abrupt onset of fever, various haemorrhagic manifestations and transient renal and hepatic dysfunction. We retrospectively reviewed 63 cases of HFRS in children from 13 different hospitals in Korea who presented over a 15-year period. The age of the patients ranged from 7 to 15 years, with a male to female ratio of 8 to 1. Fifty-four (86%) patients were 10 years or older. On admission, 24 (38%) were in the febrile phase and 35 (56%) were in the oliguric phase. Fever (100%) abdominal pain (91%), headache (76%) and vomiting (73%) were the most common symptoms. Backache, subconjunctival haemorrhage and hypertension were also noted in about one-third of patients. Hypotension was documented in only 7 (11%) patients. Leucocytosis (> 10,000/mm3) and thrombocytopenia (< 150,000/mm3) were noted in more than two-thirds of patients. Elevated blood urea nitrogen and serum creatinine was observed in 94% by the 7th (median) day of illness. Elevated aspartate aminotransferase and/or alanine aminotransferase were found in more than two-thirds of patients. Renal biopsy was performed in 12 patients and revealed various stages of acute tubular necrosis with occasional interstitial cell infiltration and oedema. Only 2 showed evidence of interstitial haemorrhage. Eleven patients required 1-3 days of dialysis and the remaining patients required only conservative management. Three (5%) patients died of shock, respiratory failure and pulmonary haemorrhage. All other patients recovered without sequelae. Although childhood cases were much less common than adults, clinical and laboratory findings were in general similar between children and adults.
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PMID:Haemorrhagic fever with renal syndrome in Korean children. Korean Society of Pediatric Nephrology. 781 97

We report two cases of acute renal failure induced by sciadopitysin, a type of flavonoid, and review related papers of flavonoid-induced acute nephropathy in the literature. A total of eight patients were studied. The purpose of this report is to alert physicians to consider this cause of acute renal failure with hemolysis, because flavonoids are widely used in the world. All patients initially presented with fever and gastrointestinal upset after the ingestion of a single large dose or long-term small doses. Symptoms that followed were cola-colored urine and jaundice. Elevation of blood nitrogen and serum creatinine lasted for 2 to 9 weeks. Hemolysis (100%), cholestatic hepatitis (50%), and disseminated intravascular coagulopathy (50%) were also noted in flavonoid-induced oliguric acute renal failure patients. All of these patients required hemodialysis and all but one who died completely recovered within 2 to 9 weeks. Renal biopsy was performed and showed acute interstitial nephritis with acute tubular necrosis. Moreover, we first demonstrated multiple polymorphous inclusion bodies within tubular epithelial cells in electron microscopic examinations. The definite pathogenetic mechanism of flavonoid-induced acute nephropathy needs further elucidation.
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PMID:Flavonoid-induced acute nephropathy. 812 47

Detachment of viable renal proximal tubular cells is seen in clinical and experimental acute tubular necrosis and may contribute to the acute renal dysfunction seen in acute tubular necrosis. Mechanisms of detachment of tubular cells are unknown but must involve changes in tubular cell adhesion. To begin to define mechanisms of altered cell adhesion, cultured human proximal tubular cells were made hypoxic by nitrogen gassing. Cells were monitored (blinded) for cell retraction and rounding over 90 minutes of N2. Hypoxia caused gradual alterations in cell shape, with 37.9% +/- 5.2% retracted-rounded cells by 90 minutes; control monolayers showed no significant change. Fluorescence confocal microscope imaging revealed that hypoxia caused displacement of actin filaments to basal margins of the retracted cells and produced a perinuclear aggregation of short filaments. Phalloidin (10(-6) mol/L), which stabilizes microfilaments and is able to penetrate these hypoxic cells, decreased the percentage of cells showing morphologic changes with hypoxia to < 5% by 90 minutes (p < 0.01). Viability, as assessed by Trypan blue dye exclusion, was well maintained (90% to 98% at 90 minutes) and did not correlate with shape changes. In separate experiments, cytochalasin (10(-6) mol/L)--which depolymerizes microfilaments--but not nocodazole--which disrupts microtubules--produced cell shape change in non-hypoxic monolayers. Disruption of microfilaments appears to play a role in loss of cell-to-cell and cell-to-substrate adhesion and loss of epithelial integrity in hypoxic injury to the renal tubule. These in vitro observations may be relevant to renal proximal tubular cell detachment in in vivo renal injury.
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PMID:Alterations in human proximal tubule cell attachment in response to hypoxia: role of microfilaments. 813 46

The toxicities of silicon tetraalkoxides, including tetramethoxysilane [Si(OCH3)4, TMOS], tetraethoxysilane [Si(OC2H5)4, TEOS], tetrapropoxysilane [Si(OC3H7)4, TPOS] and tetrabuthoxysilane [Si(OC4H9)4, TBOS], were investigated with intraperitoneal injection of 1,000 mg/kg of each compound. TMOS, as well as TEOS, caused acute tubular necrosis. Blood biochemical examination revealed elevation of blood urea nitrogen and creatinine in mice treated with TEOS, TPOS and TBOS, though TMOS treated mice died and therefore could not be examined. The severity of nephrotoxicity differs among these silicon tetraalkoxides. The spleens of mice treated with TMOS exhibited cytolysis in the white and red pulp, suggesting direct injury to the spleen. The kidney seems to be a common target organ of silicon tetraalkoxides.
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PMID:Toxicity of intraperitoneally administrated silicon tetraalkoxides in male ICR mice. 825 66

Prolonged intraoperative renal ischemia requires modalities to reduce the incidence of acute tubular necrosis, but there exists no definitive prophylactic regimen. We studied the effects of enalaprilat, an angiotensin-converting enzyme inhibitor, in an attempt to identify such a protective drug. Thirty-four mongrel dogs underwent 90 min of bilateral renal pedicle clamping. Group I was a control of 6 animals. Group II comprised 10 animals who received 12.5 g iv mannitol 15 min prior to clamping and 1 mg/kg iv furosemide immediately after clamp removal. Group III also comprised 10 animals who received enalaprilat 1 mg/kg iv enalaprilat each 15 min prior to clamp placement. Group IV consisted of 8 dogs, each of which received 12.5 g mannitol and 1 mg/kg iv enalaprilat 15 min prior to clamping and 1 mg/kg iv furosemide immediately upon removal of the clamps. Serum blood urea nitrogen (BUN) and creatinine levels were drawn preoperatively and at 12, 24, 48, and 72 hr postoperatively in each animal. The serum BUN levels in group III were significantly lower than those in group I at all times postoperatively (P < 0.05) and were not significantly different from those of group II at any time postoperatively. Similarly, the serum creatinine levels in group III were significantly lower than those of group I (P < 0.05) and were not significantly different from those in group II at any time postoperatively. Neither the serum BUN nor the serum creatinine levels in group IV were different from those of group I at any time postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effects of enalaprilat against postischemic renal failure. 838 87


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