These results strongly suggest that the strategy of 'volume control', also when applied with conventional dialysis times, normalizes BP and increases survival of dialysis patients. Cardiomegaly, as evidenced on the chest X-ray despite normal BP, had a strong negative influence on survival. The large majority of the patients had low-normal BP after long periods of treatment and showed the lowest mortality, favouring the view that target BP should be lower than advised by most authors.

The results of this uncontrolled retrospective study suggest that good long-term BP control and a decrease of LVM can be achieved by continuous efforts to control hypervolaemia. The decrease in volume may be even more important than pressure reduction to achieve this goal.

Estimations of proximal tubule sodium reabsorption with the FELi method come closer to direct measurements than any other indirect method. There is little doubt that most lithium reabsorption takes place in the proximal tubules, very likely in proportion to the reabsorption of sodium and water. It is also likely that changes in proximal tubule sodium reabsorption due to changes in volume status are paralleled by changes in proximal tubule lithium reabsorption, at least in the superficial nephrons. Nonetheless, changes in FELi probably do not purely reflect changes in proximal reabsorption, since lithium is also handled beyond the proximal tubules. Acknowledged problems are lithium reabsorption in Henle's loop and in the late distal and collecting tubules. The latter occurs in the rat and the dog, but not or much less in men. Sodium restriction enhances this lithium transport considerably. It is as yet uncertain whether other conditions, such as increased vasopressin activity or lowering of renal perfusion pressure, also influence this transport. Amiloride appears to prevent this reabsorption of lithium. Therefore, this drug can be used in lithium clearance studies whenever unwanted "distal" lithium reabsorption is expected. Lithium reabsorption in Henle's loop forms a greater problem as it cannot be prevented by any drug without influencing proximal tubule reabsorption. It is estimated that about 7% of the filtered lithium (one-tenth of total lithium reabsorption) is normally taken up here, preferentially in deep nephrons. In view of studies with furosemide, this reabsorption probably varies with sodium intake, but the proportion of this variation to that of proximal tubule lithium reabsorption is obscure. This remains an uncertain factor in any circumstance where the lithium clearance method is used. In some conditions the change in FELi may be so large relative to the expected changes in proximal reabsorption, that use of FELi as marker of end-proximal solute delivery seems unjustified. Disproportionately large suppression is likely during mineralo-corticoid-induced volume expansion, and stimulation during prostaglandin synthesis inhibition and vasopressin. Based on observations in these conditions the potential range of lithium reabsorption in the loop of Henle would be 0 to 15% of filtered load. In this review attention was paid mainly to the validity of lithium clearance as a pure "proximal marker". Many of our interpretations suffer from incomplete certainty with respect to the renal effects of tested maneuvers, a problem which is acknowledged.(ABSTRACT TRUNCATED AT 400 WORDS)

The disagreement in the literature concerning the role of aldosterone in the maintenance of potassium homeostasis in chronic renal disease might be partially explained by differences in plasma renin activity (PRA) among individual patients. Therefore, a study was done in 28 selected patients with varying degrees of renal insufficiency whose serum potassium and PRA concentrations were within the normal range. The results indicate that at comparable serum potassium and PRA concentrations, plasma aldosterone is in most instances elevated when creatinine clearance is lower than 50% of normal.

SUMMARY Twenty-three patients with different degrees of renal insufficiency were studied after equilibration on two levels of salt intake. Blood pressure was found to increase after increased salt intake. This blood pressure increase, when related to sodium excretion increase (salt sensttirity index), tended to be larger in patients with a greater loss of kidney function. In fact, the salt sensitivity of blood pressure rose exponentially with tbe decline of the kidney function, which resulted In a linear negative relationship between tbe log of salt sensitivity index and creatinine clearance (r -0.89, p < 0.0001). After increased salt intake, plasma renin activity (PRA) decreased, whereas body-fluid volumes Increased. Concotnitantly, the products of log PRA and extracellular-fluid volume or blood volume decreased (p < 0.005). Weak interrelations were found between increases of body fluid volumes and blood pressure (r -0.49, p < 0.05). When the patients were divided into two groups according to creatinine clearance, Group 2 (creatinlne clearance < 22 ml/mln, n • 13) showed a significantly greater increase of blood pressure for any given expansion of extracellular fluid volume than Group 1 (creatinine clearance > 32 ml/mln, n -9). Moreover, for any given increase in sodium excretion blood volume increased more in Group 2 than in Group 1 (p < 0.03), whereas the increase of extracellular fluid volume was similar in the two groups. Consequently, after increase of salt intake the plasma volume/interstitial fluid volume ratio (PV/IF) tended to decrease in Group 1 and to increase in Group 2. This difference In PV/IF ratio behavior was significant (p < 0.01). A significant interrelation was also found between the salt sensitivity index and change of PV/IF ratio (r =• 0.60, p < 0.01). It is concluded that, with decrease in functioning renal mass, the salt sensitivity of tbe blood pressure increases. This increase in salt sensitivity is accompanied by an increased intra/extravascular-fluld volume ratio after salt loading, which suggests a change of tissue-capillary filtration forces in patients with renal insufficiency.