Influence of the level of hydration on the renal response to a protein meal

Abstract

Recent studies have suggested that the renal effects of high protein intake could be mediated, at least in part, by vasopressin and/or an increase in the urinary concentrating activity. The present study investigated the influence of the level of hydration, and hence of the activity of the concentrating process, on the renal response to an acute oral protein load. Clearance studies were performed before (Control) and during three hours after a protein meal (1.5 g/kg body wt protein as cooked meat) in ten healthy volunteers. This study was performed twice at a two to three week interval under either constant low (LowH) or high (HighH) hydration. In spite of the marked difference in initial diuresis (3.1 +/- 0.3 in LowH vs. 13.9 +/- 0.7 ml/min in HighH) and urine osmolality (501 +/- 42 in LowH vs. 99 +/- 3 mOsm/kg H2O in HighH), a similar relative decrease in urine flow rate was observed following the meal in both conditions. TcH2O increased progressively by 70% in LowH whereas CH2O decreased by 40% in HighH. Plasma vasopressin showed a progressive increase with time in LowH (from 1.10 +/- 0.26 in control, to 1.98 +/- 0.35 pg/ml at the third hour after the PM, P < 0.05) but not in HighH (0.53 +/- 0.09 to 0.70 +/- 0.17 pg/ml). Glomerular filtration rate (inulin clearance) increased significantly on the second post-prandial hour under LowH but not under HighH. Excretions rates of Na, Cl, K, and urea increased after the meal, however, not to the same extent nor with the same time course in the two conditions. Significant positive correlations were observed between GFR and TcH2O, urine osmolality, or the ratio of urine-to-plasma urea concentrations in LowH. These results suggest that the protein-induced hyperfiltration is partially blunted by a high water intake, and hence is dependent, directly or indirectly, on the urine concentrating activity.

Vasopressin and Diabetes mellitus

“…We postulate that a chronic elevation in the plasma level of some AAs could play a role in the high vasopressin secretion of diabetes. This assumption is supported by the fact that the P VP rises significantly after a protein meal, a rise which is well correlated with that in plasma osmolality but cannot be accounted for by changes in plasma sodium or urea [27]. Because the plasma AA concentration increases by 2–3 mmol/l after a protein meal, AAs represent the most likely substances that can have increased plasma osmolality and triggered vasopressin synthesis after the meal.…”

Vasopressin contributes to hyperfiltration, albuminuria, and renal hypertrophy in diabetes mellitus: Study in vasopressin-deficient Brattleboro rats

“…Hyperfiltration occurring in the early phase of DM (38)(39)(40) is known to lead to a delayed progressive deterioration of renal function (1). Now, chronic elevation in plasma VP, or in its selective V2 agonist dDVP, has been shown to induce distinct glomerular hyperfiltration (11,12,(41)(42)(43), rise in albumin excretion (suggesting an alteration of the glomerular filter) (14), and renal hypertrophy (15). In rats with 5͞6 nephrectomy, a reduction in VP level, brought about by a chronic elevation in water intake, slowed down the progression of chronic renal failure (10).…”

Limits of adaptation to high dietary protein intakes

“…An increase in protein intake to levels, which have usually been associated with adverse metabolic effects either, requires very high levels of activity and total food consumption, or the use of protein rich supplements. Protein rich supplements often have a relatively low water content and any effects of the protein content on metabolism have to take into consideration the requirements for water for effective renal responses (Hadj-Aissa et al, 1992).…”