1. Rats were studied 7 days and 17 days after the onset of renal failure which was induced by a surgical technique.

2. Plasma urea, creatinine (PCr) and potassium had increased after 7 days; plasma potassium increased much more after 17 days but PCr was slightly lower.

3. Renal failure caused resetting of erythropoietic control to a lower level of packed cell volume (PCV). After 7 days renal failure some rats had a low PCV, whereas others still had a normal PCV apparently due to slower erythrocyte destruction of pre-renal failure cells.

4. After 7 days renal failure, rats with a normal PCV had an increased erythrocyte membrane leak to potassium that resulted in a low erythrocyte potassium [K+]RBC. This was accompanied by an increase in active sodium pump units [increased ouabain sensitive sodium flux (Fo) and its rate constant (ko)] that caused erythrocyte sodium ([Na+]RBC) to fall. The increased active pump units retarded the fall in [K+]RBC and may have extended the life of the normal erythrocytes in the renal failure environment.

5. The PCV was below normal in all rats after 17 days renal failure. [K+]RBC was increased and since ko was normal there appeared to be compensation to produce erythrocytes with reduced membrane leak to potassium with longer standing renal failure.

6. PCr was only related to PCV after 17 days renal failure and not in the earlier phase of erythrocyte destruction. The changes in erythrocyte membrane permeability were very significantly related to PCV after 17 days.

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