Conversely, hyperthyroidism increases beta-adrenergic receptors in kidney cortex, and synthesis and secretion of renin by juxtaglomerular cells, which enhance angiotensin-converting enzyme activity, and the activation of RAS and the decrease in the resistance of afferent glomerular arterioles lead to an increase in the glomerular hydrostatic pressure and GFR (25). This evidence concerns the gene ACE and hyperthyroidism.