CNIs may lead to this complication by inducing hyporeninism-hypoaldosteronism, decreasing mineralocorticoid receptor expression by downregulation, and mimicking pseudohypoaldosteronism type 2 by stimulating the activity of the thiazide-sensitive renal sodium chloride co-transporter in the distal convoluted tubule [34-37]. The gene discussed is NR3C2; the disease is pseudohypoaldosteronism type 2.