Investigation of the Oxidative Stress and DIO1 Expression in CRF Patients Accompanied With and Without Euthyroid Sick Syndrome

Abstract

Background/Aims: Chronic renal failure (CRF) is often accompanied by increased oxidative stress and euthyroid sick syndrome (ESS). The cause of ESS is unknown, and it is unknown whether there exists a link between oxidant stress and ESS in CRF patients. Therefore, we aim to investigate oxidative stress and type 1 deiodinase (DIO1) expression, which plays the key role in the ESS in CRF patients. Methods: In-patients with CRF were divided into the two group: Group 1 is ESS patients consisting of 60 patients with low free triiodothyronine (FT3) and Group 2 consisting of 60 patients with normal FT3. Group 3 consisted of 60 healthy volunteers recruited as controls. The baseline clinical parameters of patients were evaluated with standard routine methods in a clinical laboratory. Serum levels of 8-isoprostane and DIO1 were measured by enzyme-linked immunosorbent assay (ELISA). Multiple regression analysis was used to analyze the relationship between oxidative stress, DIO1 and FT3. Results: The concentrations of serum 8-Isoprostane in Group 1 and Group 2 were substantially higher than that of Group 3 (p< 0.05), however there was no significant difference between Group 1 and Group 2 (p=0.516). The serum DIO1 level was higher in Group 2 than in Group 1 and Group 3 (p< 0.001). Multivariate linear regression analysis revealed that the DIO1 concentration and FT3 level were not associated with the concentration of serum 8-Isoprostane. Conclusions: CRF patients showed elevated oxidative stress. The CRF patients without ESS showed higher expression of DIO1 than patients with ESS and the control group. The concentration of serum 8-Isoprostane was not correlated with FT3 and DIO1 levels.

Glomerular Transcriptome Profiles in Focal Glomerulosclerosis: New Genes and Pathways for Steroid Resistance

“…Some investigators reported that the concentration of DIO1 in CRF patients without euthyroid sick syndrome (ESS) was higher than that in CRF patients with ESS and healthy subjects. This can help explain why CRF patients without ESS can maintain a normal level of FT3 is due to the increased serum DIO1 which can elevate serum FT3 production from T4 [24]. AK4, which is expressed mainly in tissues rich in mitochondria like the brain, heart, kidney and liver.…”