Hypertension and Chronic Renal Failure

147

102

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.

Section: Discussionmentioning

confidence: 99%

Salt sensitivity of blood pressure in chronic renal failure. Evidence for renal control of body fluid distribution in man.

Koomans¹,

Roos²,

Boer³

et al. 1982

147

102

“…1 Contrarily, in humans with advanced renal failure, hypertension frequently occurs even during a normal sodium intake. 2 •' Since the classical report of Ambard and Beaujard 4 in 1904, it has been known that increases in sodium intake in patients with diminished renal function are accompanied by increases in arterial pressure. Indeed, in a previous study we found that, within a group of patients with varying degrees of renal failure, the salt sensitivity of the blood pressure increased with decreasing renal function.…”

mentioning

confidence: 99%

Sodium balance in renal failure. A comparison of patients with normal subjects under extremes of sodium intake.

Koomans¹,

Roos²,

Mees³

et al. 1985

SUMMARY To gain insight into the factors involved in the maintenance of sodium balance in patients with chronic renal failure, we studied 10 patients with a creatinine clearance of 11.5 ± 4.0 ml/min after equilibrium on 20 and 120 mEq of sodium per day. The measurements included blood pressure, plasma volume, blood volume, extracellular fluid volume, plasma renin activity, plasma aldosterone, and plasma norepinephrine. For comparison, eight normal volunteers were studied after equilibration on 20, 200, and 1128 mEq of sodium per day. The latter intake was chosen to match the high sodium intake per residual renal function in the patients. In the patients, equilibrium after raised sodium intake was accompanied by a marked increase in blood pressure and blood volume, a moderate fall in plasma renin activity and levels of aldosterone and norepinephrine, and only little expansion of the interstitial space. The 24-hour creatinine clearance rose by 21.2 ± 7.2%. Fractional sodium excretion (x 100%) was 5.3 ± 0.8% during the 120 mEq sodium diet. In the normal volunteers, increasing the sodium intake from 20 to 1128 mEq/day evoked no consistent change in blood pressure but caused a comparable rise in blood volume, considerable suppression of plasma renin activity, aldosterone, and norepinephrine, and a much larger increase in interstitial volume. Their creatinine clearance had risen by 22.4 ± 6.5%, and their fractional sodium excretion during the 1128 mEq sodium intake was 3.9 ± 0.2%. These results suggest that in normal subjects the maintenance of sodium balance over a wide range of sodium intake is particularly dependent on variations of neurohumoral influences on the kidney, while in patients with renal failure relatively large variations in arterial pressure are necessary as well. The marked difference in amount and distribution of the retained volume may be explained by a vasoconstrictive reaction to sodium loading in the patient group. (Hypertension 7: 714-721, 1985) KEY WORDS volume sodium loading renin • aldosterone hypertension • norepinephrine blood volume extracellular fluid

“…- 67 Most such patients also have very high levels of plasma renin activity and plasma renin concentration. The two groups (high renin and high substrate) may not, in fact probably do not, completely coincide.…”

mentioning

confidence: 99%

The role of renin substrate in hypertension.

Gordon¹

1983

1 reported that intravascular injections of antiserum to renin substrate cause a prompt fall of blood pressure in rats. This suggests that renin substrate may play a role in maintenance of normal blood pressure. Numerous other studies have indicated a possible relation between elevated renin substrate and elevated blood pressure. A review of the literature concerning the relation of plasma renin substrate concentration and the level of blood pressure reveals a frequent positive correlation between these two entities. The results of my review are presented here according to the following outline: