Gene expression of vasopressin receptor type 2 and aquaporin 2 in acute renal failure versus chronic renal failure in rats

Urinary concentration decreases in response to a reduction of functioning renal mass. Although a variety of factors have been implicated, the pathogenesis of impaired urinary concentration ability in acute renal failure [ARF] and in chronic renal failure [CRF] especially the cellular and molecular defects, were poorly understood. Our study therefore aimed to present a possible explanation for the pathogenesis of impaired urinary concentration and the molecular defect in kidney tissue of experimental ARF and CRF rat models and aimed to find and compare any molecular defect difference between ARF and CRF. Thirty albino adult male rats were used in our study and the animals were divided into three groups. Group I: Sham-operated controls [n=10]. Group II: Renal ischemia-reperfusion injury group [n=10] in which the renal artery and vein were bilaterally exposed and occluded for 30min with vascular clamps to produce renal ischemia-induced acute renal failure [ARF], the clamps were removed to allow kidney reperfusion then the animal sacrified after 24H. Group III: Chronic renal failure group [n=10], this group of animals underwent right total nephrectomy and removal of 2/3 of the left kidney and the experimental protocol lasted about one month then the animals were sacrified. Blood, urine and kidney tissue samples were collected from the three groups to measure serum urea and creatinine and 24 hour-urinary albumin for evaluation of kidney function and to measure aquaporin 2 water channel and vasopressin-receptor type 2 [V[2]] gene expressions in kidney tissue. Kidney function tests as regards serum urea, serum creatinine and 24 hour-urinary albumin in group II and group III showed a significant [p<0.05] increase in comparison to control group [group I]. Ischemic-reperfusion rats [group II] showed the highest of these parameters indicating that, they had the worst kidney function. A significant [p<0.05] decrease in vasopressin-receptor type 2 [V[2]] mRNA expression in kidney tissue was shown in group II [ARF] and group III in comparison to the control rats [group I] with the highest reduction in group II. A similar result was found as regards Aquaporin 2 water channel mRNA expression with a significant [p<0.05] reduction in group II and group III in comparison to group I, and the highest reduction was seen in group II among the three studied groups. In both ischemia-reperfusion rats and CRF rats, the ischemic and nephrectomy insults were associated with decreased mRNA expression of the aquaporin 2 and vasopressin-receptors type 2 [V[2]] in the kidney tissue, coinciding with the impairment of kidney function. This may contribute to the impairment in urinary concentration in the post-ischemic period and the urinary concentration defect associated with CRF

Serum zinc concentration in Egyptian patients with chronic hepatitis C

The prevalence of HCV infection varies throughout the world, with the highest number of infections reported in Egypt. Zinc has been closely related to the pathogenesis of chronic hepatitis C. Zinc deficiency causes reduction in glutathione [GSH] which has been implicated in various cellular events. Zinc may play an important role as a negative regulator in HCV replication; zinc supplementation increases the therapeutic response of Interferon [IFN]. To detect serum zinc concentration in adult patients with chronic [compensated] hepatitis C prior to treatment with IFN, and correlate the levels with the degree of inflammation and stage of fibrosis. This study was conducted on 40 adult patients chronically infected with HCV as well as 10 healthy subjects serving as a control group. Participants were subjected to complete clinical and laboratory assessment, quantitative analysis of HCV RNA by PCR technique and abdominal ultrasonography, in addition to estimation of serum Zinc by Graphite Furnace Atomic Absorption Spectrometer. A significant negative correlation was found between the level of zinc and liver fibrosis. The mean value of zinc in patients was 39.5ug/dl, while in the control it was 75ug/dl [normal range: 70-80ug/dl]. There was a non significant negative correlation between serum zinc and serum AST, ALT, disease activity and level of viraemia. Our study suggested the possible important protective role of zinc in patients with chronic hepatitis C, as serum zinc levels showed negative significant correlation with the stage of liver fibrosis