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)

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

Magnesium is an essential cation, involved in many enzymatic reactions, as a cofactor to adenosine triphosphatases. It is critical in energy-requiring metabolic processes, as well as protein synthesis and anaerobic phosphorylation. Serum Mg concentration is maintained within a narrow range by the kidney and small intestine since under conditions of Mg deprivation both organs increase their fractional absorption of Mg. If Mg depletion continues, the bone store contributes by exchanging part of its content with extracellular fluid (ECF). The serum Mg can be normal in the presence of intracellular Mg depletion, and the occurrence of a low level usually indicates significant Mg deficiency. Hypomagnesemia is frequently encountered in hospitalized patients and is seen most often in patients admitted to intensive care units. The detection of Mg deficiency can be increased by measuring Mg concentration in the urine or using the parenteral Mg load test. Hypomagnesemia may arise from various disorders of the gastrointestinal tract, conditions affecting Mg renal handling, or cellular redistribution of Mg. The gastrointestinal causes include the following: protein-calorie malnutrition, the intravenous administration of Mg-free fluids and total parenteral nutrition, chronic watery diarrhea and steatorrhea, short bowel syndrome, bowel fistula, continuous nasogastric suctioning, and, rarely, primary familial Mg malabsorption. The renal causes include Bartter's and Gitelman's syndrome, post obstructive diuresis, post acute tubular necrosis, renal transplantation, and interstitial nephropathy. Many therapeutic agents cause renal Mg wasting and subsequent deficiency. These include loop and thiazide diuretics, aminoglycosides, cisplatin, pentamidine, and foscarnet. Magnesium deficiency is seen frequently in alcoholics and diabetic patients, in whom a combination of factors contributes to its pathogenesis. Hypomagnesemia is known to produce a wide variety of clinical presentations, including neuromuscular irritability, cardiac arrhythmias, and increased sensitivity to digoxin. Refractory hypokalemia and hypocalcemia can be caused by concomitant hypomagnesemia and can be corrected with Mg therapy. The dose and route of administration of Mg in the treatment of hypomagnesemia is dictated by the clinical presentation, the degree of Mg deficiency, and the renal function.
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PMID:Magnesium deficiency: pathophysiologic and clinical overview. 777 97

A 42-year-old female was admitted to a hospital, because of acute hepatitis A. Laboratory data were GOT 8210mU/ml. GPT 4650mU/ml, LDH 11860mU/ml, total bilirubin 4.7mg/dl, BUN 19.5mg/dl and creatinine 1.9mg/dl. Urinalysis showed proteinuria 3+ and occult blood 1+. Soon after admission, she suffered from anuric acute renal failure and was transferred to our hospital for hemodialysis. Her urine-volume was under 20 ml per day. Urinalysis showed proteinuria 4+, occult blood 1+ and casts. Laboratory data showed BUN 58.2mg/dl and creatinine 8.5mg/dl. She was treated by hemodialysis for 35 days, before recovering from renal failure. However, her renal function did not recover perfectly and her 24-hour creatinine clearance remained at 50ml/min after 6 months. Renal biopsy was performed on the 17th day after admission. Examination by light microscopy revealed the findings of acute tubular necrosis and examination by immunofluorescence antibody method was negative. Urinalysis of 8 patients with acute hepatitis A showed that all patients had proteinuria at the onset. Patients with acute hepatitis A have symptoms of appetite-loss, nausea, vomiting and/or diarrhea. These symptoms cause hypovolemia, and hepatic dysfunction causes discontrol of vasoactive hormones, which gives rise to disturbance of renal circulation. Subsequently, acute tubular necrosis and acute renal failure occur.
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PMID:[A case of acute hepatitis A associated with acute renal failure from the onset]. 823 Aug 22

Gallbladder toxin of the grass carp (Ctenopharyngodon idella) is a less well-known cause of acute renal failure. Three cases are reported and the diagnosis is primarily clinical. All our patients presented initially with gastrointestinal upset including nausea, vomiting, diarrhea, and abdominal fullness. These symptoms usually occurred with 10 min to 18 h after the ingestion the raw gallbladder of the grass carp. All our cases developed acute renal failure and in two of them toxic hepatitises were noted. An acute tubular necrosis was demonstrated on renal biopsy in one of our patients. The treatment is mainly supportive and two of them received hemodialysis. All three cases recovered, with normal renal and liver functions 2-4 weeks after the incident. A review of the cases previously reported in the English literature is presented.
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PMID:Acute renal failure due to ingestion of the gallbladder of grass carp: report of 3 cases with review of literature. 829 Jul 11

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.
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PMID:[Acute renal failure as a complication of cholera]. 868 55

Hemolytic uremic syndrome (HUS) in childhood is recognized as the most frequent cause of acute renal failure and is greatly associated with verotoxin-producing E. coli (VTEC) infection. Most of the prodromal feature in HUS associated with VTEC infection is hemorrhagic colitis (HC). HC progresses to HUS in several days. So it is important to detect whether the patient with bloody diarrhea is associated with VTEC infection or not. From 1992 to 1996 we analyzed clinical findings of 80 HUS and 29 HC patients. High level of beta 2-microglobulin (BMG) and N-acetyl-D-beta-glucosaminidase (NAG) in the urine were observed in the early stage of the disease. We went on to examine verotoxin (VT2)-binding in mouse (ICR) renal sections by enzyme immunoassay. Specific binding of VT2 to tubules was seen in mouse kidney, and intravenous injection of VT2 to mice caused acute tubular necrosis in 15 h whereas glomeruli were intact. These data suggest that the primary target cell of VT2 was tubules in the kidney of the HUS patients with VTEC infection.
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PMID:[Primary tubular impairment by verocytotoxin in hemolytic uremic syndrome]. 908 88

Fish gallbladders are consumed in rural areas of Asia as a traditional medicine to improve symptoms of arthritis, decreased visual acuity, and impotence. Consumption of large amounts of this traditional medicine can result in systemic toxicities; in particular, acute renal failure. We reviewed records of all admissions to Cho Ray Hospital (Ho Chi Minh City, Vietnam) between January 1995 and December 2000 after this ingestion. Clinical courses and outcomes were similar in 16 of 17 patients. Within hours, patients experienced profuse vomiting (n = 16) and diarrhea (n = 15). All developed acute renal failure, with a mean serum creatinine concentration of 14.7 +/- 3.9 mg/dL (1,299.5 +/- 344.8 micromol/L). Four patients administered intravenous fluid (IVF) developed extracellular fluid volume overload, as did 1 patient not administered IVF. Time to peak creatinine concentration was 8.6 +/- 3.0 days, which was accompanied by decreased urine volume (174.7 +/- 161.6 mL/24 h). Blood pressure remained normal, with a mean arterial pressure of 91 +/- 12 mm Hg. Twelve patients required renal replacement therapy. A mean of 1.9 +/- 1.1 hemodialysis sessions was performed per patient. Sixteen patients recovered renal function; 1 patient died of fulminant hepatic failure. Kidney biopsies showed features of acute tubular injury. Acute renal failure after fish gallbladder ingestion is characterized by a failure to respond to IVF, an 8.6-day interval to peak creatinine level, frequent need for dialysis therapy, and findings on renal biopsy consistent with acute tubular necrosis. Acute renal failure after fish gallbladder ingestion has an excellent prognosis. However, death from fulminant hepatic failure can occur.
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PMID:Ichthyotoxic ARF after fish gallbladder ingestion: a large case series from Vietnam. 1250 Feb 40

A 24-year-old woman with a history of penicillin allergy developed reversible acute renal failure after receiving cephalexin for 4 days. The patient experienced nausea, vomiting, diarrhea, pruritus, cough, and an elevated creatinine level of 2.2 mg/dl. The patient's creatinine level continued to rise, peaking at 5.3 mg/dl on hospital day 3. Nephrotoxic acute tubular necrosis was confirmed by electron microscopy. Within 1 month of discharge from the hospital, the patient's creatinine level decreased to 0.6 mg/dl. Although the renal injury most commonly associated with the cephalosporin class of antibiotics is allergic interstitial nephritis, currently available cephalosporins infrequently can cause direct tubular toxicity.
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PMID:Cephalexin-induced acute tubular necrosis. 1522 73

The use of folk remedies is widespread throughout Africa. Acute renal failure (ARF) is one of the most severe, but under-recognized, complications of folk remedy use. This report aims to describe the clinical presentation, outcomes, and nature of renal injury in patients with folk-remedy-associated ARF. Clinical data were evaluated retrospectively in 78 patients with ARF associated with recent folk remedy use. ARF was defined as elevated serum urea and creatinine above the age-appropriate normal ranges, persistent oligoanuria, worsening renal function with time, or need for dialysis. Overall mortality in patients with ARF was 41%. Mortality was higher in adults (45.5%) than in infants (36.6%), in patients with both renal and liver dysfunction (62.5%) than in those with renal dysfunction alone (22.6%), and in HIV-positive (44.4%) versus HIV-negative (34.6%) patients. Vomiting (51.3%) and diarrhea (43.6%) were the most frequent presenting symptoms. Metabolic acidosis (80.8%) and volume depletion (62.8%) were the most frequent clinical findings. The definable causes of ARF were pre-renal (26.9%), acute tubular necrosis (ATN; 26.9%), hepatorenal syndrome (6.4%), urinary tract infection/sepsis (7.7%), and primary renal disorders (7.7%). Twenty-seven patients had concomitant medical conditions unlikely primarily related to folk remedy ingestion. In conclusion, ARF occurring after use of folk remedies in South Africa is associated with significant morbidity and mortality. The most common contributors to ARF in this setting are volume depletion and ATN. Significantly, although a proportion of patients have underlying systemic or renal conditions that may contribute to renal dysfunction, in the majority of patients, folk remedy use appears to be the most likely proximate cause. In view of the large numbers of Africans living abroad, more widespread awareness of this important clinical problem needs to be raised.
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PMID:Acute renal failure associated with the use of traditional folk remedies in South Africa. 1571 33

This paper describes clinical, laboratory and pathological findings of sheep, which is intoxicated with castor bean. The source of intoxication was a miscellaneous garden waste. Forty-five animals showed clinical toxicosis and 17 died. The clinical signs included weakness, salivation, profuse watery diarrhoea, dehydration, mydriasis, teeth grinding, hypothermia and recumbency. The most significant haematological and biochemical findings were a high haematocrit, high concentration of serum BUN, creatinine and phosphorus and high activity of serum CK and AST. Pathology revealed severe gastroenteritis, cardiac haemorrhage and necrosis, hepatic necrosis and acute tubular necrosis in kidneys. Treatment included symptomatic and supportive care with fluid therapy and cathartic administration.
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PMID:Castor bean (Ricinus communis) toxicosis in a sheep flock. 1715 90


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