Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Merbarone, NSC 336628, is an investigational anticancer drug with activity against experimental animal tumors including melanoma. This paper presents results of a Phase II clinical study of merbarone in patients with biopsy proven stage IV malignant melanoma without prior chemotherapy and with no evidence of CNS involvement. Thirty-five patients with median age 58 (range 27-81), with performance status 0-2 were treated with merbarone 1000 mg/m2/day for five days by intravenous continuous infusion repeated every 3 weeks. All patients (21 males and 14 females) were evaluable for toxicity. Two patients were not evaluable for response having been removed from protocol treatment due to toxicity and received other treatment during the first course of chemotherapy. Among the evaluable patients there was one complete response in a supraclavicular lymph node lasting four months and one partial liver response lasting three months. The remaining thirty-one patients were non-responders. Of these one had a stable disease lasting 21 months. The overall objective response rate was 6% (2/35) with a 95% confidence interval of 1%-19%. Twenty-six of the 35 patients have died. The estimated median survival of the entire group was 9 months with a 95% confidence interval six to eleven months. Renal toxicity was dose-limiting and manifested as increasing serum creatinine (54% of patients), proteinuria (51%) and hematuria (9%). One patient experienced grade 4 creatinine increase, proteinuria and acute renal failure. Other toxicities included nausea (71%), vomiting (51%0, malaise (23%), weakness (20%), alopecia (17%), diarrhea (17), anorexia (14%) transaminase (SGOT, SGPT) increase (14%), constipation (14%), alkaline phosphatase or 5'nucleotidase increase (9%), and fever (9%). Hematologic toxicity (granulocytopenia, leukopenia, and anemia) was generally mild and infrequent (29%, only one patient had grade 4 granulocytopenia). Overall 9 patients (26%) had at least one grade 3 toxicity. We conclude that merbarone at this dose and schedule has detectable but minimal activity in the treatment of metastatic malignant melanoma and given the significant renal toxicity this schedule does not merit further evaluation in this disease.
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PMID:Evaluation of merbarone (NSC 336628) in disseminated malignant melanoma. A Southwest Oncology Group study. 861 77

The aim of our study was to analyze the clinical course and outcome of acute renal failure (ARF) in patients with hemorrhagic fever with renal syndrome (HFRS). From 1983 to 1995, we treated 33 patients (27 males, 6 females) aged from 16 to 71 years. Half of patients were connected with work at a farm or in a forest. The disease was confirmed serologically with indirect immunofluorescence test (IFT) and enzyme-linked immunosorbent assay (ELISA). In 18 patients percutaneous kidney needle biopsies were analyzed. In 85% of the cases, the disease broke out from June to October. The most frequently expressed clinical signs and symptoms were fever, nausea/vomiting, headache, backache, abdominal pain, myalgia, diarrhea, conjunctival injection, and hemorrhages. Four patients had concomitant pancreatitis. In 25 patients, oliguria was present, and transient hemodialysis treatment was needed in 19 patients. Infection with Hantaan virus was established in 20 patients and with Puumala virus in 13 patients. At renal biopsy, acute interstitial nephritis accompanied with hemorrhages and necrosis was found, and at a later biopsy there were also signs of interstitial fibrosis. All patients were cured, but renal function was not completely recovered in some. We conclude that ARF is a serious complication in patients with HFRS. Although not lethal in our group of patients, many of them showed severe signs and symptoms of illness. Transient hemodialysis was necessary in two-thirds of the patients. Some degree of functional defects and morphological changes might persist.
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PMID:Acute renal failure due to hemorrhagic fever with renal syndrome. 887 90

Here, we report a 35-year-old man with non-fulminant acute non A, non B, non C hepatitis which developed into acute renal failure. The patient was admitted to hospital with the chief complaints of general fatigue, nausea and a high-grade fever of 40 degrees C. Laboratory examination revealed severe liver dysfunction and renal insufficiency on admission: his serum glutamic oxaloacetic transaminase was 3.203 IU/ml, serum glutamic pyruvic transaminase was 3.825 IU/ml, lactic dehydrogenase was 2.840 IU/ml, blood urea nitrogen was 65 mg/dl, and creatinine was 7.6 mg/dl. Hemodialysis was conducted during the initial 19-day period after admission because anuria was manifested on admission. On the 36th day after onset, renal functions returned to normal and the patient was negative for IgM-HA antibody. HBs antigen, IgM-HBC antibody, HCV antibody, cytomegalovirus antibody, and Epstein-Barr virus antibody. However, liver biopsy for histological examination on the 44th day after onset revealed no specific findings except the healing stage of acute hepatitis. Renal biopsy on the 49th day showed the healing stage of acute tubular necrosis without any glomerular change. It has been infrequently reported that acute renal failure develops following a non-fulminant acute state without hepatitis A, B or C virus infection. It is necessary to take acute renal failure into account in the clinical course of non-fulminant non A, non B, non C hepatitis.
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PMID:[Acute renal failure in non-fulminant acute hepatitis without hepatitis A, B or C virus infection]. 951 78

A 47-year-old man presented with acute renal failure following oxalate ingestion. Nausea and hematoemesis appeared four hours after attempted suicide and acute oliguric renal failure ensued the following day. The patient underwent four sessions of hemodialysis and then reverted to normal state. Histopathologic examination of renal biopsy specimen revealed the degeneration of the renal tubular epithelial cells associated with intracellular calcium oxalate crystal deposition. Most of the renal tubules were patent despite the intraluminar crystal deposition. These findings suggest that dysfunction of the renal tubular epithelial cell plays a more important role than tubular obstruction in developing acute renal failure.
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PMID:Acute renal failure due to oxalate ingestion. 980 77

Acute interstitial nephritis with severe acute renal failure is reported following tetracycline treatment in a 22-year-old male medical student. Acute renal failure developed within 48 h of a single repeated tetracycline dose and presented 2 days after taking the drug when there was oliguria, nausea, vomiting and bilateral loin pain without rash and fever. The serum creatinine concentration was 8.6 mg/dl and blood urea nitrogen 84 mg/dl. Examination of the urinary sediment revealed 15-20 RBCs per high-power field, and occasional granular and hyaline casts. Percutaneous renal biopsy performed immediately after admission revealed acute interstitial nephritis with immune complexes along the tubular basement membrane and intact glomeruli and was consistent with type 2 interstitial nephritis. Within 4 days of commencement of steroid treatment and hemodialysis, the urine output started to increase with improvement in serum creatinine and BUN levels and after 2 weeks of therapy hemodialysis was discontinued. He remains well 1 year following his illness with complete normalization of his renal function. Although a number of renal side effects of tetracycline antibiotics have been reported, acute interstitial nephritis is rarely caused by tetracycline treatment having been reported just twice following systemic use of minocycline.
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PMID:Tetracycline-induced acute interstitial nephritis as a cause of acute renal failure. 988 23

We report the case of a 21-year-old man who had been developing acute renal failure with Methicillin-resistant Staphylococcus aureus (MRSA) colitis and sepsis. He was admitted for consciousness disturbance, nausea, vomiting, and diarrhea. Oliguria was also observed and his serum creatinine level was elevated to 10 mg/dl. Urinary protein was positive and an abundance of hyaline cast were seen in urinary sedimentation. Diarrhea and pyrexia were prolonged and serum C-reactive proteins were elevated, but lymphocyte and leukocyte counts temporarily decreased from the 3rd to the 6th hospital day and remained low until normalizing after the 14th day. His clinical symptoms improved with hemodialysis (HD) and effective antibiotic therapies. An MRSA strain producing toxic shock syndrome toxin-1 (TSST-1), a super antigen which specifically stimulates human V beta 2-positive T cells, was separated from his feces and blood. To ascertain the cause of his renal dysfunction, a renal biopsy was performed on the 8th day. His renal histology revealed acute interstitial nephritis with severe inflammatory cell infiltration around the medullary areas without glomerular changes. Most of the infiltrated cells were small monocytes, and lymphoid cells were rich in the interstitium. With immunohistochemical staining, over 70% of T-cells were V beta 2-positive. TSST-1-producing MRSA was detected in his blood specimen. Furthermore, V beta 2-positive T cells were accumulated in the renal intersititium, and transient lymphocytopenia was observed. These data suggested the following possible pathogenesis for interstitial nephritis: TSST-1 acts as a super antigen in the renal interstitium where major histocompatibility complex (MHC) is class-2-positive, thereby resulting in interstitial nephritis with T cell migration.
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PMID:[A case of interstitial nephritis induced by a super antigen produced by methicillin-resistant Staphylococcus aureus (MRSA) presenting as acute renal failure]. 1036 25

Exercise-induced acute renal failure without rhabdomyolysis is not a rare condition. We experienced 6 cases (5 men and a woman) during last the 8 years. All cases complained of severe loin pain and nausea after mild to moderate exercises (for example, a track race in an athletic meeting). The elevation of serum and urinary myoglobin was undetected. In 4 of 5 patients with abdominal CT, renal patchy vasoconstriction (wedge-shaped low-density lesion) was observed. This was diagnosed as exercise-induced acute renal failure with loin pain (serum creatinine levels: 1.7-8.6 mg/dl). The renal function in 5 of the 6 cases normalized in about three weeks by fluid replacement therapy and hemodialysis support, which one patient received for 3 days. One patient required a long time for improvement of renal function and renal insufficiency persisted (serum creatinine 1.8 mg/dl). In 2 patients, the concentration of serum uric acid became very low after the recovery of renal function. These two patients were diagnosed as an isolated hyperuricosuric hypouricemia. More than half of the 6 patients had previously experienced the same episodes (loin pain and nausea) after exercise. Exercise-induced acute renal failure, probably due to renal patchy vasoconstriction, seems to be not a rare disease. The etiology of renal patchy vasoconstriction after exercises remains to be elucidated. The occurrence of acute renal failure must be taken into consideration when the youngster, especially with renal hypouricemia, complains of severe loin pain and nausea after exercise such as a track race.
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PMID:[Exercise-induced acute renal failure associated with renal vasoconstriction]. 1044 90

Out of 938 parasitologically confirmed patients with visceral leishmaniasis treated with amphotericin B (1 mg/kg bodyweight daily infused in 2 h for 20 days), 935 were cured clinically, 933 parasitologically and 931 ultimately (no relapse within 6 months). Two parasitologically 'not cured' and 4 relapsed patients were cured with 25 infusions, and 1 with double relapse with 30 infusions. The treatment was started only when serum haemoglobin reached 5 g/dL, serum electrolyte imbalance was corrected and sodium stibogluconate-induced myocardial damage stabilized after 10 days' rest. Bronchopneumonia, cardiac failure and acute renal failure caused the death of 1 patient each. Nightblindness, angular stomatitis, neuritis, and petechial haemorrhages improved with appropriate treatment; 2 patients were given blood transfusion for post-treatment anaemia. Nausea and anorexia, and changes in serum creatinine and potassium, became normal in 2 weeks. Immediate withdrawal of the drug and restart after 10 days cured 2 patients who developed acute renal failure. Infusion-related toxicities--shivering, rigor and fever--were minimized but not eliminated by prior administration of hydrocortisone. Tuberculosis and visceral leishmaniasis were treated concurrently. Four pregnant patients were successfully treated without harmful effects on mother and child. It was concluded that the dosage of amphotericin B used was an effective and well-tolerated regimen and achieved 99% cure. Toxicity could be minimized with some precautions. All unresponsive and relapsed patients responded to more amphotericin and no resistance to the drug was seen.
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PMID:Amphotericin B deoxycholate treatment of visceral leishmaniasis with newer modes of administration and precautions: a study of 938 cases. 1049 70


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