Imidazole-salicylate is a non-steroidal anti-inflammatory drug with limited inhibitory effects on prostaglandin synthesis. The renal effects of this drug were investigated by a double-blind cross-over study in 10 patients with cirrhosis and ascites. Two therapeutic doses of imidazole-salicylate (750 mg each) were given at midnight and 08:00 h and 80 mg of furosemide were injected intravenously at 09:00 h. The same procedure was followed on another day but a placebo replaced imidazole-salicylate. Renal function (creatinine clearance, free water and electrolyte excretions) and urinary excretion of prostaglandin E, 6-keto-prostaglandin F1 alpha and thromboxane B2 were evaluated for 8 h after the first dose of the drug and for 2 h after furosemide injection. Platelet thromboxane production was also determined 9 h after the first administration of drug or placebo. Imidazole-salicylate did not affect renal function or inhibit kidney prostanoid production either under basal conditions or after the stimulating effect of furosemide. On the contrary, imidazole-salicylate significantly inhibited platelet thromboxane production (45.8 +/- 9 vs. 69.4 +/- 7.5 ng/ml, P < 0.05). These results suggest that imidazole-salicylate is an anti-inflammatory drug that can be given to patients with decompensated cirrhosis without risk of inhibiting kidney prostaglandin synthesis or the renal response to furosemide.
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http://dx.doi.org/10.1016/s0168-8278(05)80583-5 | DOI Listing |
PLoS One
January 2025
Department of Rheumatology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, P.R. China.
Introduction: Lupus nephritis (LN) is one of the most frequent and serious organic manifestations of systemic lupus erythematosus (SLE). Autophagy, a new form of programmed cell death, has been implicated in a variety of renal diseases, but the relationship between autophagy and LN remains unelucidated.
Methods: We analyzed differentially expressed genes (DEGs) in kidney tissues from 14 LN patients and 7 normal controls using the GSE112943 dataset.
PLoS One
January 2025
Department of Pulmonary Diseases, Uludag University Faculty of Medicine, Bursa, Turkey.
Background: End-stage renal disease (ESRD) patients frequently experience protein-energy wasting (PEW), which increases their morbidity and mortality rates.
Objective: This study explores the effects of nutritional status and pulmonary function on the short- and long-term mortality of ESRD patients undergoing hemodialysis.
Materials And Methods: 67 consecutive ESRD patients on maintenance hemodialysis were included in the study.
Angiotensin II (Ang II) is the most active peptide hormone produced by the renin-angiotensin system (RAS). Genetic deletion of genes that ultimately restrict Ang II formation has been shown to result in marked anemia in mice. In this study, adult mice with a genetic deletion of the RAS precursor protein angiotensinogen (Agt-KO) were used.
View Article and Find Full Text PDFAnnu Rev Med
January 2025
Division of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, USA; email:
Hepatorenal syndrome-acute kidney injury (HRS-AKI) occurs in the setting of advanced chronic liver disease, portal hypertension, and ascites. HRS-AKI is found in ∼20% of patients presenting to the hospital with AKI, but it may coexist with other causes of AKI and/or with preexisting chronic kidney disease, thereby making the diagnosis challenging. Novel biomarkers such as urinary neutrophil gelatinase-associated lipocalin may be useful.
View Article and Find Full Text PDFDiscov Oncol
January 2025
Department of Gastroenterology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, 710068, China.
Background: Clear cell renal cell carcinoma (ccRCC) is the most common subtype of kidney cancer with a high metastatic rate and high mortality rate. The molecular mechanism of ccRCC development, however, needs further study. Aurora kinase B (AURKB) functions as an important oncogene in various tumors; therefore, in the present study, we aimed to explore the mechanism by which AURKB affects ccRCC development.
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