What is hypervolemia?
Hypervolemia is due to an excess of total body sodium and water, which leads to expansion of the ECF compartment. Hypervolemia is therefore synonymous with ECF volume overload. Hypervolemia is typically due to kidney retention of sodium and water. This kidney retention may be primary or secondary. Primary kidney sodium retention may be caused by kidney failure; in this setting the diseased kidneys may be unable to match sodium excretion with sodium intake. Drugs may also lead to primary kidney retention. The direct vasodilator minoxidil and the thiazolidinedioines commonly cause kidney sodium retention and edema. The dihydropyridine calcium channel blockers may cause edema; with these drugs, capillary leak plays an important role in the development of edema. Secondary kidney retention occurs when there is a reduction in effective arterial volume. The most common causes of reduced effective arterial volume are congestive heart failure (CHF) and cirrhosis. In these conditions, the reduction in sensed volume leads to enhanced kidney sympathetic nerve activity, enhanced activity of the renin-angiotensin-aldosterone system, and enhanced secretion of ADH. Avid kidney sodium and water reabsorption ensue. In the case of the nephrotic syndrome, both primary and secondary kidney sodium retention may contribute to varying degrees. The kidney disease itself may lead to primary sodium retention (overfill hypothesis). The low plasma oncotic pressure from hypoalbuminemia may lead to movement of fluid from the intravascular compartment to the interstitial compartment. The contraction of the intravascular volume leads to secondary kidney sodium retention (underfill hypothesis).
