Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the effect of high-dose cisplatin (40 mg/m2 daily for 5 days), 51Cr-EDTA clearance was used as a measure of glomerular filtration rate (GFR). 51Cr-EDTA clearance decreased significantly from 109 +/- 3 ml/min * 1.73 m2 to 68 +/- 3 ml/min * 1.73 m2 after three cycles of cisplatin and remained at this decreased level during the observation period (24 months). To determine the reliability of creatinine as a measure of GFR, we compared the simultaneous clearance of creatinine to that of 51Cr-EDTA. A good correlation between 51Cr-EDTA clearance and creatinine clearance was observed before and 3 months after termination of treatment, but no correlation was found during treatment. S-creatinine decreased significantly during treatment, probably due to muscle wasting. We conclude that s-creatinine and creatinine clearance are unsuitable measures of glomerular function during high-dose cisplatin treatment. All patients developed proteinuria during treatment. The changes in clearance ratios of beta-2-microglobulin/albumin and IgG/albumin show that the proteinuria observed during cisplatin infusion is predominantly of tubular origin, whereas the proteinuria between the treatment periods is mainly of glomerular origin.
Cancer Chemother Pharmacol 1988
PMID:Effects of cisplatin on different measures of glomerular function in the human kidney with special emphasis on high-dose. 328 Jan 53

Idiopathic membranous nephropathy has been reported rarely to develop in genetic association with certain HLA antigens. This paper describes two male siblings presenting with nephrotic syndrome with histologically proven membranous nephropathy. The younger brother maintained a normal renal function with slight proteinuria during the 3 years of follow-up, but the older one experienced a rapid decline in renal function and had to be put on maintenance hemodialysis. No clinical evidence of contributory underlying disease such as malignancy or systemic lupus erythematosus could be found. HLA typing was carried out in the two patients and in members of their family. Several HLA antigens were found to be shared by the two patients. However, the HLA antigens which have been reported to be associated with idiopathic membranous nephropathy were not found in either of them.
 ...
PMID:Idiopathic membranous nephropathy in two brothers. 329 23

A toxicology study of cis-diamminedichloroplatinum (II) (CDDP), aqua(1,1-bis-(aminomethyl)cyclohexane)sulfatoplatinum(II) (TNO-6), diammine(1,1-cyclobutanedicarboxylato)platinum(II) (CBDCA), cis-dichloro-trans-dihydroxo-cis-bis(isopropylamine)platinum-(IV) (CHIP) and ethylenediaminemalonatoplatinum(II) (JM-40) was carried out in dogs. The main purpose of the study was to compare the results with those obtained earlier in mice and rats and with the toxicology data in humans. Each platinum compound was tested in three dogs. Each dog received three intravenous bolus injections at intervals of 3 weeks. The compounds were administered in dosages of 1.2, 1.0, 12, 10 (or 6) and 10 mg/kg, respectively. Toxic death occurred for two dogs (both on day 54) from haematotoxicity (10 mg/kg CHIP) and renal toxicity (TNO-6), respectively. Serum urea nitrogen and creatinine concentrations were variable after TNO-6 and remained within normal values after treatment with the other compounds. Severe proteinuria was observed in all three dogs treated with TNO-6. Values returned to normal within 16 days. JM-40 did not cause significant proteinuria. CDDP, CBDCA and CHIP caused short-lasting and slight proteinuria. CHIP caused a severe reduction in the number of leukocytes and platelets, while the other drugs caused acceptable reductions. Except after the high dose CHIP regimen, haematotoxicity was of a transient nature. Vomiting in order of severity occurred after TNO-6, CHIP, CDDP and JM-40, while CBDCA did not cause any vomiting. The dogs were sacrificed 6 weeks after the last drug dose. Organs were fixed for histopathology to complete and support clinical-toxicological parameters. On the basis of the results from the single-dose study in dogs and those obtained earlier in mice and rats it can be concluded that the gain from the use of the dog as a prognosticator for organ toxicity in man was disappointing and limited to the prediction of vomiting.
Eur J Cancer Clin Oncol 1987 Aug
PMID:Preclinical toxicology of platinum analogues in dogs. 330 82

Follow-up survival and health information were obtained, after a median of 27.5 years, from 132 patients who had been seen originally as children with nephrotic syndrome between 1951 and 1967. Ninety seven patients were alive. Recurring edema or proteinuria, or both, persisted in 15 percent of those still alive. Eight of 11 parous women reported relapses during pregnancy. There was no apparent increase in malignancies, atopic diseases, clinical defects in cell-mediated immunity, or cardiovascular diseases. Twenty two patients (17%) died of renal causes between 3 months and 8 years after the onset of nephrotic syndrome. Steroid resistance was the presenting feature universally predictive of a poor outcome; nine of the 11 such patients died and the other two are now receiving hemodialysis. Hematuria was present initially in 41 percent of the patients who died of renal causes, compared with 14 percent of those still alive. Hypertension was noted on the first examination in 22 percent of those who died of renal causes, compared with 10 percent of those alive.
 ...
PMID:Long-term prognosis for children with nephrotic syndrome. 333 30

Trichosporonosis due to Trichosporon beigelii or T. capitatum is an infrequent but potentially fatal invasive fungal infection in cancer patients. We studied epidemiologic, clinical, pathologic, and microbiologic features of this infection during a 7-year period at the University of Maryland Cancer Center. Fifteen patients with involvement by Trichosporon were identified: 5 were infected, 5 were possibly infected, and 5 were colonized but not infected by Trichosporon. Four of the infected patients had trichosporonemia and/or positive skin biopsy cultures as the first evidence of infection. The fifth infected patient had positive marrow and skin biopsy cultures. Serial surveillance cultures of infected patients showed preceding Trichosporon colonization in only 1 of 5 cases. Pulmonary infiltrates in 3 infected patients correlated at postmortem examination with Trichosporon pneumonia. Renal dysfunction marked by proteinuria, hematuria, red blood cell casts and azotemia correlated with widespread glomerular infiltration with the fungus. The five infected patients died of their infection, whereas the 2 possibly infected patients who died succumbed to their underlying illness. Trichosporonemia may have been averted in possibly infected patients because of a shorter median duration of profound (less than 100/microliter) neutropenia (5 days) when compared to that of infected patients (20 days). No environmental source of Trichosporon was found in environmental surveillance cultures of food, air, or inanimate surfaces. In vitro studies of three pathogenic strains showed resistance to 5-fluorocytosine but susceptibility to amphotericin B, ketoconazole, and miconazole. Norfloxacin augmented the in-vitro antifungal activity of amphotericin B. Trichosporon must be considered an opportunistic pathogen that can cause serious infections among patients with cancer.
 ...
PMID:Trichosporonosis in patients with neoplastic disease. 352 14

The health effects of human exposure to cadmium are discussed with emphases on intake, absorption, body burden, and excretion; osteomalacia in Japan; hypertension; and proteinuria, emphysema, osteomalacia, and cancer in workers. Elevated blood pressure has not been observed as a result of excessive exposures to cadmium in Japan or the workplace. Renal tubular dysfunction and consequent proteinuria is generally accepted as the main effect following long-term, low-level exposure to cadmium. Studies of workers show that proteinuria may develop after the first year of exposure or many years after the last exposure. Proteinuria and deterioration of renal function may continue even after cessation of exposure. The immediate health significance of low-level proteinuria is still under debate. However, there is evidence that long-term renal tubular dysfunction may lead to abnormalities of calcium metabolism and osteomalacia. The few autopsy and cross-sectional studies of workers do not permit conclusions to be drawn regarding the relationship between cadmium exposure and emphysema. Retrospective and historical-prospective studies are needed to settle this important question. No conclusive evidence has been published regarding cadmium-induced cancer in humans. However, there is sufficient evidence to regard cadmium as a suspect renal and prostate carcinogen. Because of equivocal results and the absence of dose-response relationships, the studies reviewed should be used with caution in making regulatory decisions and low-dose risk assessments.
 ...
PMID:Human health effects of exposure to cadmium. 352 15

Renal failure in cancer patients is a common problem in oncology; this complication is frequently multifactorial in origin. Several antineoplastic agents are potentially nephrotoxic; previous renal impairment as well as combinations with other nephrotoxic drugs may increase the risk of nephrotoxicity during administration of chemotherapy. Methotrexate-related renal damage most frequently occurs with high-dose therapy and can be avoided by forced alkaline diuresis and administration of folinic acid. Renal dysfunction secondary to semustine (CH3-CCNU) is clearly related to cumulative doses in excess to 1,200 mg/m2; the onset may be delayed and renal failure progress despite drug discontinuation. Streptozotocin is also nephrotoxic and may cause proteinuria and renal tubular acidosis; progressive renal failure can be predicted by a close monitoring of proteinuria and prevented by drug discontinuance. Mitomycin-associated renal failure frequently presents with signs of microangiopathic hemolytic anemia; renal failure is usually delayed but occasionally, it may be rapidly progressive despite drug discontinuance. Cisplatin nephrotoxicity is clearly dose-related and used to be considered dose limiting. Renal insufficiency can be prevented by hydration and forced diuresis; in addition, hyperhydration with mannitol-induced saline diuresis may allow administration of high doses and thus circumvent the dose-limiting effect of cisplatin-induced renal toxicity. Cisplatin-induced renal magnesium wasting occurs frequently and should be supplemented. Other approaches to reduce cisplatin nephrotoxicity are currently under investigation and are discussed.
 ...
PMID:Nephrotoxicity induced by cancer chemotherapy with special emphasis on cisplatin toxicity. 353 60

A 65-year-old woman was found to have the nephrotic syndrome eight months before the onset of a new left neck mass. Biopsy specimen of the mass showed metastatic adenocarcinoma, which was subsequently found to be from an ovarian primary. Operation and triple chemotherapy has markedly diminished the degree of proteinuria. Although uncommon, ovarian carcinoma must be considered in the differential diagnosis of cancer-related nephrotic syndrome.
 ...
PMID:Ovarian cancer associated with the nephrotic syndrome. 362 17

The syndrome of intrahepatic inferior vena cava obstruction has neither been commonly recognized nor adequately described. Symptoms include the abrupt onset of ascites, hepatomegaly, and fluid retention below the diaphragm with edema of the lower extremity. Proteinuria can be associated with these symptoms. When this syndrome has been caused by malignant hepatic enlargement, it has not been well characterized in the literature, and its treatment has been ignored. We have diagnosed the inferior vena cava syndrome due to metastatic liver involvement in 34 patients before death. Thirty-three of these patients were treated using a combination of strip radiotherapy to the hepatic vena cava, with or without hepatic arterial infusion of chemotherapy. Fifty-six percent of the patients completed a full course of radiotherapy, with an 83 percent response rate. A dose of 3,000 to 4,500 rads was found to be safe and provided excellent palliation of ascites and edema. Tumors known to be radiosensitive had the best responses and side effects were few and mild in nature. Recognition and treatment of this condition will assume greater importance as survival is prolonged in more patients with advanced malignancy.
 ...
PMID:Diagnosis and treatment of the inferior vena cava syndrome in advanced malignant disease. 372 21

Beta-interferon serine (IFN-beta ser) is a genetically altered recombinant IFN with a specific activity of 2 X 10(8) IU/mg protein. We undertook a Phase I trial of this agent in 18 patients with metastatic renal cell carcinoma. IFN-beta ser was given by a 4-h intravenous infusion twice weekly (Monday and Thursday). Three patients were placed on escalating dose levels. Doses were also escalated in each patient if no unacceptable toxicity was detected on the previous treatment. The maximum initial tolerated dose was less than or equal to 150 million units/m2. However, development of patient tolerance allowed escalation beyond this dose and chronic therapy at this or higher doses in most patients. Toxicity was largely limited to the symptom complex of fever, malaise, mild hypotension, and anorexia. One patient developed reversible proteinuria (10 g/24 h) with no change in serum creatinine. Limited or no renal, hepatic, or hematological toxicity was observed. Six of 16 patients developed anti-IFN antibody levels. Fifteen patients received twice weekly treatments at near their maximum tolerated dose for greater than or equal to 4 weeks and were evaluable for response. Two patients developed a partial and one patient a minor response. We conclude that IFN-beta ser is a well tolerated IFN with minimal renal, hepatic, and bone marrow toxicity. It has apparent activity in metastatic renal cell carcinoma.
Cancer Res 1986 Oct
PMID:Phase I/II trial of human recombinant beta-interferon serine in patients with renal cell carcinoma. 375 86


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>