genitourinary disorders
Polyuria
Pathophysiology of Polyuria
Water homeostasis is controlled by a complex balance of water intake (itself a matter of complex regulation), renal perfusion, glomerular filtration and tubular reabsorption of solutes, and reabsorption of water from the renal collecting ducts. When water intake increases, blood volume increases and blood osmolality decreases, decreasing release of antidiuretic hormone (ADH; also referred to asargininevasopressin) from the hypothalamic-pituitary system. Because ADH promotes water reabsorption in the renal collecting ducts, decreased levels of ADH increase urine volume, allowing blood osmolality to return to normal. 250 mg/dL [13.88 mmol/L]) exceed tubular reabsorption capacity, leading to high glucose levels in the renal tubules; water follows passively, resulting in Renal Glucosuria and increased urine volume. Glucose-induced osmotic diuresis in diabetes mellitus is further increased with use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) that lower plasma glucose levels by inhibiting renal glucose reabsorption and increasing renal glucose excretion. Therefore, polyuria results from any process that involves one or more of the following: Sustained increase in water intake (polydipsia) Decreased ADH secretion ( ArginineVasopressin Deficiency (Central Diabetes Insipidus) ) Decreased peripheral ADH sensitivity ( Nephrogenic Diabetes Insipidus ) Solute diuresis 