DIPSOGENIC FACTORS OPERATING IN CHRONIC UREMICS ON MAINTENANCE HEMODIALYSIS

Thirst and hyperdipsia of anuric chronic uremics on maintenance hemodi alysis and the possible dipsogenic factors were studied. Exaggerated t hirst was present in 213 (86%) of the 247 studied patients. It usually started 4-6 h after the end of the dialysis session, persisted during the whole interdialytic period and often disappeared during the subse quent dialysis. Hyperdipsia, as indicated by the high body weight gain (> 4%) in the interdialytic periods, was present in 33.6% of patients . The highest rate of increase of body weight occurred in the first ho urs following the end of dialysis sessions. Hypernatremia, potassium d epletion, increasing plasma urea levels and elevated plasma angiotensi n II levels were considered as the possible dipsogenic factors of a no npsychic nature. Sodium is certainly of paramount importance for its o bliged extracellular position, and when sodium intake is elevated, hyp ernatremia is very likely the cause of exaggerated thirst and weight g ain in patients on hemodialysis. Potassium depletion may cause thirst in animals, but this condition is extremely rare in patients on mainte nance hemodialysis, who often accumulate it. In these patients it is, therefore, unlikely that potassium depletion is a dipsogenic factor. I ncreasing serum urea levels exert an evident dipsogenic effect in anep hric rats and urea, when infused into normal volunteers, stimulates th irst. The extracellular urea levels in the interdialytic period are ce rtainly higher than the intracellular ones, as a consequence of its co ntinuous accumulation, and this creates an osmotic gradient with a dip sogenic effect. When this gradient is reversed, following hemodialysis (which removes first the extracellular urea), the dipsogenic effect d isappears. The hypothesis of a dipsogenic effect of urea operating in the interdialytic period in anuric patients on hemodialysis is therefo re formulated. Angiotensin II is regarded as dipsogenic in patients on maintenance hemodialysis because of its high plasma concentrations. T he following evidence is, however, against this contention: the ACE in hibitors do not prevent hyperdipsia, the body weight changes due to hy perdipsia are not correlated with the plasma levels of angiotensin II, and, finally, thirst is often absent in the hours of maximum angioten sin II plasma levels. In conclusion, hypernatremia (frequently) and in creasing plasma urea levels (regularly) appear to be the dipsogenic fa ctors operating in patients on maintenance hemodialysis. The role of a ngiotensin II is doubtful and that of potassium depletion quite unlike ly. Psychogenic factors may play an important role, however, in some p atients.