Urinary α1-microglobulin (α1-m) and β2-microglobulin (β2-m) can be used as early indicators of renal tubular dysfunction. However, low levels of lead exposure cause an increase in urinary α1-m, but not in urinary β2-m. In order to clarify the level of tubular dysfunction in early lead nephropathy, fractional clearances of α1-m (FC-α1-m) and β2-m (FC-β2-m), i.e., the ratios of these clearances to the creatinine clearance, were measured in 99 male lead workers. Blood urea nitrogen, serum creatinine, uric acid, and urinary creatinine and N-acetyl-β-D-glucosaminidase activity were also measured to di-agnose the presence of other renal dysfunction.
The median of FC-α1-m was 0.13% in the control group. The FC-α1-m increased in lead workers with blood lead (B-Pb) levels above 20 μg/dl. The correlation of FC-α1-m with urinary α1-m was highly significant, but there was no correlation with serum α1-m. The median of FC-β2-m was 0.065% in the control group. There was a correlation of FC-β2-m with FC-α1-m, but there was no correlation with B-Pb, or with serum β2-m. These results suggest the following: There was a very low excretion rate of α1-m and β2-m in both the control group and the lead exposed groups. The excretion rate of α1-m was higher than that of β2-m. There seemed to be slight a dysfunction of tubular reabsorption in the lead workers, and the elevation of α1-m excretion reflected the dysfunction more sensitively than the elevation of β2-m excretion in lead poisoning.