Studies on Experimental Proteinuria I

Abstract

Experimental proteinuria was induced in-10 rats receiving equal amounts of a renal antiserum prepared according to Smadel and Farr. The course of the disease was followed for 43 days, after which time the animals were killed. The following results were obtained:

1. Seven of the animals developed a severe proteinuria which reached its maximum during the first 3 days after the injection and then slowly decreased but did not reach the normal level by the end of the experiment. One animal reached the normal level of proteinuria in a week, the other two animals did not develop any marked proteinuria at all. The proteinuria showed parallelism to water output in forced oliguria and polyuria. Oliguria occurred 6 times in all in three of the animals. At the end of the experiment all of the animals showed an intact diuresis regulating power.

2. The electrophoresis at the end of the observation time indicated rather small changes in serum proteins: a small decrease of albumin in most cases and a distinct increase of a-globulin in three cases. The electro-phoretic examination of urine showed that during the early phase of the disease 70 to 80 per cent of excreated protein is albumin, the rest being divided equally among the three globulins. As a general feature the relative albumin values have a tendency to diminish with the protein excretion, whereas the relative amount of γ-globulin increases. In three cases a small but distinct component was seen, which moved faster than the albumin. During the later course of the disease this component disappeared.

3. The total urine protein hexosamine values showed a decrease in all cases during the first two weeks, after which they remained at a nearly constant level (1.1 to 1.5 g per 100 g of protein). There seemed to be no correlation between hexosamine levels and the α- and β-globulins in the urine.

4. The histopathological investigations at the end of the experiment showed a slightly changed glomerular structure in all of the animals. No tubular alterations were seen.

Problems connected with the mechanism of proteinuria in the Masugi type of experimental renal disease are discussed.