Triiodothyronine attenuates the progression of renal injury in a rat model of chronic kidney disease

This study was designed to investigate whether and how triiodothyronine (T-3) affects renal function in an experimental model of chronic kidney disease. Twenty-four female rats were divided into the following groups: sham-operated control group (n = 8), 5/6 nephrectomized group (Nx, n = 8), and 5/6 nephrectomized group treated with T-3 for 2 weeks (T-3-Nx, n = 8). T-3 administration significantly decreased serum levels of urea, creatinine, tumour necrosis factor alpha, and interleukin-6 compared with serum levels in the Nx group. The levels of malondialdehyde, transforming growth factor beta, fibronectin, and collagen IV, as well as the expression of inducible nitric oxide synthase, nuclear factor kappa B, poly(ADP-ribose) polymerase, caspase-3, and Bax were all significantly decreased, though not normalized, in the remnant kidney of rats in the T-3-Nx group compared with Nx rats. Glutathione, heme oxygenase-1 levels, as well as endothelial nitric oxide synthase expression were increased in the remnant kidney of the T-3-Nx group. Histological studies revealed focal necrosis of renal tubules associated with inflammatory cell infiltration and fibrosis in the Nx group. These changes were alleviated in T-3-Nx rats. This study showed that T-3 administration attenuated the clinical and histological signs of renal injury in 5/6 nephrectomized rats by mitigating renal oxidative stress, inflammation, apoptosis, and fibrosis.