Volume homeostasis in the fasting rate and 24-hr sodium balance are maintained in chronic renal insufficiency as a result of adaptations in the residual nephrons. This study evaluates the limitations to these adaptations and the dynamics of sodium excretion (UNaV) after an acute challenge with 100 mEq of sodium chloride in normal dogs (GFR 50 ml/min) and in dogs with one remnant kidney and moderate chronic renal insufficiency (GFR 15 ml/min). When food was administered with the sodium challenge, no or minimal changes in serum protein and hematocrit values occurred, and the natriuretic responses were small and equivalent in normal and remnant dogs. On the other hand, when the sodium challenge was given without food, the natriuretic response was large in normal dogs and markedly blunted in remnant. Within 5 hr of the sodium challenge, the various groups of normal dogs excreted 40 to 63% of the sodium load, but the remnant animals eliminated only 12 to 22% (P less than 0.001). The blunted natriuresis in remnant dogs was associated with a prolonged hemodilution of circulating proteins, indicating a longer lasting expansion of the intravascular volume. The blunted response was independent of sodium diet, of the administration route (p.o. vs. i.v.) or strength (isotonic vs. hypertonic) of the sodium load, and appears to result from an inability of the remnant kidney to rapidly excrete a sodium load. Thus, administration of sodium to dogs with chronic renal insufficiency leads to prolonged sodium retention, prolonged extracellular fluid (ECF) volume expansion, and requires a prolonged excretory cycle to restore 24-hr balance.