Its mechanisms include inhibition of thyroid-stimulating hormone (TSH)-sensitive adenylate cyclase, leading to hypothyroidism; reduced aquaporin-2 expression, contributing to nephrogenic diabetes insipidus; and disruptions in calcium homeostasis, resulting in hyperparathyroidism and hypercalcemia, by interfering with transmembrane signal transduction in calcium-sensing receptors (CaSR). Here, CASR is linked to nephrogenic diabetes insipidus.