In patients with primary glomerulonephritis associated with proteinuria, renal function is considered to be progressively impaired, accompanied by the progress of tubulointerstitial disorder. While, in cases with endstage renal failure, the ratio of oxidized plasma albumin is markedly increased. With these backgrounds, we studied the potentiality for the mechanism of the progress of tubulointerstitial disorder in primary glomerulonephritis, to participate in the redox state of albumin molecule. Enrolled cases were 60 outpatients with primary glomerulonephritis or chronic renal failure. The redox ratio of plasma albumin was measured by the HPLC method. At the same time, each concentration of urinary protein (u.Pr), urinary low molecular weight proteins (α₁-microglobulin: u.α₁-m, β₂-microglobulin: u.β₂-m), urinary transferrin (u.Tf), and urinary liver-type fatty acid binding protein (u.L-FABP), as well as urinary lysosomal activity (u.NAG) were measured. Further, serum albumin (s.alb) and L-FABP were also measured to study the relationships with other parameters.
The results of HPLC analysis of plasma albumin showed increase in the ratio of oxidized plasma albumin and decrease in that of reduced plasma albumin, both accompanied by decrease of eGFR. Negative correlation were found between concentrations of u.Pr, u.L-FABP, u.α₁-m, and u.β₂-m, as well as u.NAG and eGFR. And, it was recognized that the value of u.α₁-m, u.β₂-m, u.Tf, u.NAG and u.Pr were tend to high in patients with progressively impaired renal function. It was considered that tubulointerstitial disorder would progress, in cases with primary glomerulonephritis, through the hindrance of intercellular reductive environment by the load of oxidized plasma albumin to renal tubular epithelial cells. In addition, it was suggested that iron-bonding transferrin and fatty acid participated in oxidative damage to tubulointerstitium.

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