Immunoglobulin L-chain metabolism was studied in normal mice, mice with sodium maleate-induced renal tubular disease but normal glomerular filtration rate (GFR), and mice with both tubular disease and decreased GFR. The proteinuric rate of L-chain was increased twofold in mice with tubular disease alone though there was no alteration in the over-all rate at which L-chain disappeared from the circulation in these animals. This was in sharp contrast to findings in mice with tubular disease and a decreased glomerular filtration rate in which L-chain disappearance rates were markedly reduced. These findings demonstrate that in the normal state, L-chain and presumably other proteins of similar size pass through the glomerulus and are avidly taken up and catabolized by the convoluted tubular cells. In tubular proteinuric states this linked uptake-catabolic function fails, resulting in elevated urinary excretion but normal serum levels and turnover rates of these proteins. In uremic states with decreased glomerular filtration, less small protein is delivered into the tubular lumen and the processes of excretion and catabolism are reduced. This results in prolongation of the survival of small proteins and explains the elevated serum concentrations of these proteins observed in uremia.