Effect of impaired hepatic and renal function on [ 131]bence jones protein catabolism in human subjects

Abstract

The role of the kidneys and the liver in the catabolism of Bence Jones protein was investigated by studying the kinetics of [ 131]Bence Jones protein in normal subjects and in patients with hepatic and renal insufficiency. Bence Jones protein was isolated from urine of a myeloma patient who had earlier suffered from polycythemia vera. After radioiodination, [ 131]Bence Jones protein was infused to recipients, and both the protein-bound 131I and free 131I were determined serially from serum and urine. The kinetic analysis was carried out with an analogy computer. Results showed that the Bence Jones protein half-time was normally only about 4 h. The rapid disappearance of the protein from the circulation was mainly due to extensive catabolism because only 3 to 4% of the total removal was caused by proteinuria. The half-time of Bence Jones protein was longer in patients with renal insufficiency, ranging from 8 to 32 h. 30 to 50% of the urinary radioactivity was present in protein-bound form, indicating that the endogenous catabolism of Bence Jones protein is markedly reduced in uremia. Furthermore, gel filtration of the urine of the uremic myeloma patient suggested that a part of the bound radioactivity was in peptide form. That the liver apparently plays a minor role in the catabolism of Bence Jones protein was shown by finding that the half-time of [ 131]Bence Jones protein was within normal range in two patients with moderate liver damage. One patient with severe liver insufficiency and with signs of renal tubular dysfunction had, however, a markedly reduced Bence Jones protein catabolism.