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The urinary excretion of N-acetyl-beta-glucosaminidase (NAG) and beta 2-microglobulin (beta 2M) was studied in 43 patients with various forms of renal parenchymal disease. Patients with membranous nephropathy, membranoproliferative glomerulonephritis, focal segmental glomerulosclerosis, obstructive pyelonephritis, nephrosclerosis, and minimal change nephropathy generally had urinary NAG and beta 2M levels more than 3 SDs above those seen in normal subjects. Patients with progressive renal disease averaged higher NAG and beta 2M urinary levels than those with the same renal lesion and stable function. Since elevated urinary levels of NAG and beta 2M suggest renal tubular injury or dysfunction, our observations suggest tubulointerstitial involvement in a wide variety of renal diseases.

The thiobarbituric acid (TBA) assay was applied to uremic blood. Significant TBA-reactive material was found in patients with chronic renal failure compared to normal controls. The presence of TBA-reactive material correlated with the degree of renal failure, and was removed by hemodialysis. The reactive material is not 2-deoxyribose or sialic acid. In addition, the presence of TBA-reactive material in uremic blood is not abolished by prior aspirin ingestion, suggesting it is not related to active prostaglandin synthesis. The possible origin of the TBA-reactive material in uremic blood is discussed.

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