Effects of hemodialysis and saline loading on body fluid compartments, plasma renin activity and blood pressure in patients on chronic hemodialysis.

The influence of one hemodialysis session and of subsequent loading by 1.5-2 liters N saline on blood pressure, PRA and body fluid compartments was assessed in seven patients with chronic renal failure on maintenance hemodialysis. Dialysis caused only slight decreases in plasma volume, ECV and in TEBS. Lying mean blood pressure by 5-10 mm Hg and PRA increased by 30%. Saline loading resulted in a significant increase in plasma volume by 0.4 liters and in blood pressure by 10-5 mm Hg, but in a decrease in PRA by 40%. The changes in mean blood pressure correlated positively with the changes in plasma volume, and negatively with the changes in PRA. It is concluded that the renin-angiotensin system in patients on chronic hemodialysis still functions as one of the adjustment mechanisms for the circulatory homeostasis, when challenged by volume loss or volume and sodium loading.

Relationships of the renin-angiotensin-aldosterone system and sodium balance to blood pressure regulation in chronic renal failure of polycystic kidney disease.

In 5 patients with polycystic kidney disease and creatinine clearances ranging from 4 to 40 ml/min, relationships between changes in blood pressure, sodium balance, body fluid compartments, plasma renin activity (PRA), urinary aldosterone excretion, and plasma aldosterone concentrations were studied during periods of low, medium, and high sodium intake. Total body water (TBW), total exchangeable body sodium (TEBS), and extracellular volume (ECV) were measured by isotope dilution techniques, plasma volume with Evan's blue dye, and PRA and aldosterone by radioimmunoassay. Low sodium intake reduced kidney function, blood pressure, and serum sodium, while PRA reached its highest levels. Subsequent increases in sodium intake improved kidney function and increased blood pressure. Plasma volume increased slightly and ECV markedly, while PRA dropped to 15 percent of the value noted after the low sodium intake. TBW and TEBS showed inconsistent changes. Aldosterone changes correlated closely with PRA. Blood pressure showed a negative correlation with PRA, but a positive one with body weight and cumulative sodium balance, and with plasma and extracellular volumes.it is suggested that whereas renin and aldosterone are involved in the maintenance of circulatory homeostasis during sodium loss, sodium retention causes an increase in blood pressure by concomitant changes in body fluids.