The serum level and urinary excretion of beta2-microglobulin in health and renal disease

Abstract

In healthy subjects with normal renal function beta2-microglobulin (beta2m) is constantly produced in the body. It is eliminated almost exclusively by the kidneys, predominantly by glomerular filtration but possibly also by some direct uptake from the blood. After glomerular filtration more than 99,9% of excreted protein is reabsorbed in the kidney tubules where it is catabolized. The main factor, influencing on the serum level of beta2m is the GFR. Determination of S-beta2m appears to be more effective than analysis of S-creatinine for the detection of a slightly reduced GFR. A relatively high S-beta2m, in comparison with the GFR, may be seen in e.g. malignant proliferative disorders and SLE. This indicates an increased production of the protein. An entirely free passage over the glomerular membranes is not likely for beta2m in healthy subjects but the sieving coefficient might approach 1,0 in renal disease. The increased glomerular elimination of the protein could then possibly be counterbalanced by an increased synthesis, which should explain the pronounced relationship at a log/log scale between S-beta2m and the GFR. An increased excretion of beta2m in the urine is a sensitive indicator of proximal tubular dysfunction in many clinical conditions. In marked renal insufficiency there is, however, an obligatory 100-1 000-fold increase of the normal excretion, not related to the kind of renal disorder. In studies of the protein precautions are necessary to avoid degradation of the protein, in urine with a low pH.