Changes in body fluid homeostasis during acute hypoxaemia suggest a crucial role of renal function in acclimatization processes. Hypoxaemia stimulates sympathetic nervous activity, and also the cardiovascular system is affected with increases in heart rate and cardiac output. In most subjects, a hypoxic ventilatory response produces hypocapnia and respiratory alkalosis. Acute hypoxaemia depresses aldosterone secretion secondary to a direct effect on adrenal cells. Also plasma renin is decreased in resting hypoxaemic conditions, but the mechanism remains unknown. These hormonal changes may have the advantage of opposing excessive sodium and water retention, which characterizes acute mountain sickness. Short-term isocapnic or hypocapnic hypoxaemia in spontaneously breathing humans causes moderate if any increases in renal blood flow and only minor changes in GFR. In contrast, renal blood flow and GFR decreases during hypercapnic hypoxaemia. Renal clearance studies in humans after 24-48 hours in altitude hypoxia (4,350 m) demonstrate that glomerular and tubular function is only slightly changed in spite of marked depression of the renin-aldosterone system and increased plasma levels of norepinephrine. However, renal vascular tone may increase most probably secondary to the increased adrenosympathetic activity. In the first hours, acute hypoxaemia may induce an increased excretion of sodium and water. Previous studies suggest that the natriuretic response is caused by decreased reabsorption of sodium and bicarbonate in the proximal tubules secondary to the associated hyperventilation and hypocapnia. After 6 hours, sodium and water excretion is normalized or even depressed, dependent on the severity of acute mountain sickness. In view of the prompt increase in sodium and water excretion found during short-term hypoxaemia, the absence of such a response to more prolonged hypoxaemia suggests an adaptive time-dependent course of renal functional changes in hypoxaemia. Taken together, previous studies suggest that effects of acute hypoxaemia on renal haemodynamics are minor compared with effects on cerebral and coronary circulation. This might be the result of an appropriate resetting of autoregulatory mechanisms that would maintain the role of the kidney as a major sense organ to hypoxaemia and, subsequently, as a mediator of plasma volume regulation and erythropoietin synthesis.