Cold-induced diuresis: pathophysiological mechanisms and clinical significance

Introduction: Cold-induced diuresis is a characteristic increase in urine output during acute cold exposure and the early stages of hypothermia. The phenomenon is clinically relevant because increased urine production may coexist with progressively reduced renal blood flow and glomerular filtration rate and may contribute to hypovolemia and electrolyte disturbances.Aim: To summarize current evidence regarding the renal, hemodynamic, and hormonal mechanisms of cold-induced diuresis and to evaluate their clinical significance.Materials and Methods: A narrative review of experimental and clinical publications addressing cold exposure, renal hemodynamics, arginine vasopressin, aquaporin-2, and fluid and electrolyte homeostasis was performed. Major experimental models, human studies, contemporary reviews, and clinical guidelines for the management of hypothermia were analyzed.Results: Peripheral vasoconstriction causes redistribution of blood volume toward the central circulation and modifies baroreceptor and neurohormonal signaling. Suppression of arginine vasopressin secretion contributes substantially to acute cold-induced diuresis but does not fully explain the phenomenon. Experimental evidence also supports reduced renal responsiveness to vasopressin, downregulation of V2 receptors and aquaporin-2, impairment of the renal medullary osmotic gradient, and reduced tubular reabsorptive capacity. Increased sodium excretion is a consistent component of the response, whereas evidence regarding the role of atrial natriuretic peptide remains inconsistent. As hypothermia progresses, renal vascular resistance increases and both renal blood flow and glomerular filtration rate decrease. Clinical studies of controlled temperature management demonstrate that increased urine output is most evident during the induction phase of cooling and does not necessarily indicate preserved renal perfusion.Conclusion: Cold-induced diuresis is a multifactorial renal response resulting from the interaction of hemodynamic, hormonal, and tubular mechanisms. Increased urine output should not be interpreted as evidence of adequate renal perfusion or preserved circulating volume. Recognition of this phenomenon is important for appropriate assessment of intravascular volume, renal function, and electrolyte balance during cooling and subsequent rewarming.