Hypoalbuminemia has been observed consistently in patients and experimental animals with
chronic renal failure (CRF). A defect in
albumin synthesis, catabolism, or distribution has been invoked as the cause, but there is no agreement as to which, if any, of these disorders results from the uremic state. We studied
albumin homeostasis in 7/8-nephrectomized rats with CRF.
Serum albumin concentration was lower in CRF (29.6 +/- 4.59 mg/ml) than in
sham-operated control rats (36.3 +/- 4.3 mg/ml).
Albumin synthesis, determined directly by measuring incorporation of 14CO2 into
arginine in
albumin, was increased in CRF rats as was total
albumin clearance, measured using 125I-albumin disappearance. Rats with CRF were albuminuric.
Albumin synthesis was increased by the amount necessary to replace urinary losses, but net
albumin catabolism was the same as in control animals.
Albuminuria was prevented by addition of excess
tryptophan to the diet. Total
albumin clearance and
albumin synthesis were the same in these
tryptophan-fed CRF animals as in CRF
sham-operated animals, but these CRF rats were still hypoalbuminemic (33.6 +/- 5.27 vs. 36.3 +/- 4.3 mg/ml). Rats with CRF were plasma volume expanded. Institution of a
low-sodium diet at the time of partial
nephrectomy prevented plasma volume expansion and
albuminuria as well.
Serum albumin concentration,
albumin distribution, pool sizes, and total
albumin clearance remained the same as in CRF
sham-operated animals.
Hypoalbuminemia in CRF rats is due to two factors. Plasma volume expansion with pool dilution contributes 40% of the decrease and external
albumin losses resulting from
albuminuria contribute the other 60%.
Albumin synthesis, catabolism, and distribution are intact.