Publications by authors named "Eric G De Prez"
Exposure to aristolochic acid (AA) is associated with human nephropathy and urothelial cancer. The tumour suppressor TP53 is a critical gene in carcinogenesis and frequently mutated in AA-induced urothelial tumours. We investigated the impact of p53 on AAI-induced nephrotoxicity and DNA damage in vivo by treating Trp53(+/+), Trp53(+/-) and Trp53(-/-) mice with 3.
View Article and Find Full Text PDFEvaluation of diagnostic criteria for endemic nephropathy.
Pril (Makedon Akad Nauk Umet Odd Med Nauki)
March 2016
Article Synopsis
- The study aimed to evaluate existing and new diagnostic criteria for endemic nephropathy (EN), as no specific biomarker has been identified yet.
- Researchers compared clinical and laboratory data from a population in EN-affected villages using modified WHO criteria and applied ROC analysis to determine the predictive value of various variables.
- Findings highlighted that while certain urinary markers and kidney measurements could effectively distinguish EN patients, the cut-off values for alfa1-microglobulin needed adjustment, and family history significantly increased the risk of developing the disease.
Article Synopsis
- Experimental aristolochic acid nephropathy leads to early kidney damage in mice, mimicking chronic human kidney issues.
- Probenecid, when tested, blocks the harmful effects of aristolochic acid by preventing its entry into cells, reducing DNA damage, and maintaining cell health.
- Treatment with probenecid in mice significantly decreases kidney injury and DNA adducts compared to mice only exposed to aristolochic acid, indicating its protective role against acute kidney toxicity.
Background: Aristolochic acid (AA), the plant extract of Aristolochia species, is involved in the onset of progressive tubulointerstitial renal fibrosis in humans. Clinical and in vitro findings have previously suggested that the proximal tubule was the target of AA.
Methods: Using a rat model of AA nephropathy, the proximal tubular lesions induced by daily subcutaneous injections of AA for 35 or 5 days were characterized biochemically and histologically.
Background: Experimental aristolochic acid nephropathy (AAN), characterized by interstitial fibrosis, tubular atrophy, and chronic renal failure, was reported after 35-day injections of aristolochic acids (AA) to salt-depleted male Wistar rats. The link between renal fibrosis and the renin-angiotensin system (RAS) in this model remains unknown.
Methods: We investigated the impact of sodium diets (low and normal), of RAS inhibition with enalapril (ENA) alone, or combined with candesartan (CSN) for 35 days, and ENA + CSN for 65 days on AAN development.
Chinese-herb nephropathy (CHN) is a rapidly progressive renal fibrosis associated with the intake of a Chinese herb (Aristolochia fangchi) containing nephrotoxic and carcinogenic aristolochic acids (AA). This study attempted to reproduce the main features of human CHN (renal failure, tubular atrophy, and interstitial fibrosis) in a rat model similar to that of cyclosporin-induced nephropathy. Salt-depleted male Wistar rats received daily subcutaneous injections of either 1 mg/kg body wt AA (low-dose AA group), 10 mg/kg body wt AA (high-dose AA group), or vehicle (control group) for 35 d.
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