Major amounts of water and electrolytes are reabsorbed in the proximal tubule and 97-98% of filtered Na+ (about 20 Eq/day) is so reabsorbed in an obligatory manner. The remaining 2-3% of Na+ in tubule fluid (about 500 mEq/day) is reabsorbed in a controlled manner in the distal tubules and collecting ducts under the influence of aldosterone. Under conditions of maximum aldosterone stimulation, only about 10-25 mEq of sodium is excreted per day. The maximum amount of sodium excreted in the absence of aldosterone stimulated reabsorption is about 500 mEq/day. Sodium retention occurs if intake exceeds this amount.
Excess Na+ accumulates in extracellular fluid and consequent hyperos-molality is sensed by the hypothalamus stimulating thirst and ADH elaboration by the pituitary. Increased water intake and renal retention occurs until osmolality is within normal limits. The consequence of sodium excess is therefore not frank hypernatremia but hypervolemia and hypertension. Serum urea increases from coreabsortion with ADH stimulated water reabsorption. The hypertension inhibits renin release by the kidneys and, thereby, aldosterone elaboration by the adrenal cortex is diminished. Decreased renal H+ and K+ secretion result from decreased Na+ reabsorption with consequent hyperkalemia and acidosis. Urine pH is not as low as would be expected considering the acidemia. Hypertension and hyperkalemia are more characteristic of sodium retention than is hypernatremia.
L. Insufficient Sodium Intake
Prolonged dietary deficiency of salt (less than about 25 mEq/day Na+), or prolonged heavy sweating with insufficient replacement of salt, results in sodium deficit. The tendency to hypoosmolality is sensed by the hypothalamus with consequent inhibition of thirst and of pituitary ADH elaboration. Even with adequate water intake, diminished water reabsorption results in hypovolemia. The consequence of sodium deficit is therefor hypovolemia rather than hyponatremia. The kidneys release renin in response to decreased perfusion pressure and the consequent increase in angiotensin-II causes decreased renal blood flow and increased adrenal cortical elaboration of aldosterone so that Na+ reabsorption is maximized. GFR decreases in proportion to decreased renal blood flow and serum concentrations of urea and creatinine increase correspondingly. The serum urea/creatinine ratio is normal to low. Increased cosecretion of H+ and K+ from increased sodium reabsorption causes alkalosis and hypokalemia. Urine is acidic despite alkalemia.
M. Primary Hyperaldosteronism (Conn's disease):
A small fraction of adrenal cortical tumors are functional and some of these elaborate aldosterone autonomously. The consequent increase in Na+ reabsorption and associated increase in secretion of H+ and K+ causes alkalosis and hypokalemia. Urine is acidic despite alkalemia. The tendency to hypernatremia and hyperosmolality is counteracted by increased pituitary elaboration of ADH and consequent increased water reabsorption causing hypervolemia and hypertension. Urea is reabsorbed along with water and the serum urea concentration is increased. There is no corresponding increase in serum creatinine concentration, since GFR is not reduced, so that the serum urea/creatinine ratio is increased.
N. Adrenal Cortical Insufficiency:
Decreased aldosterone elaboration results in diminished Na+ reabsorption and consequently diminished H+ and K+ secretion causing acidosis and hyperkalemia. The tendency to hyponatremia and hypoosmolality inhibits thirst and pituitary elaboration of ADH. Hyponatremia and hypoosmolality are thereby prevented but at the expense of the development of hypovolemia. Decreased renal perfusion pressure results in increased renin release and increased formation of angiotensin-II and consequent decreased renal blood flow. Aldosterone secretion from residual functional adrenal cortical tissue is already maximum, but deficient so that there is no further increase from angiotensin stimulation. Decreased GFR, from decreased renal blood flow, results in a corresponding increase of serum urea and creatinine concentrations with a normal serum urea/creatinine ratio.
Fasting serum glucose concentration is low or low-normal, as well, because of decreased glucocorticoid elaboration.
