Evaluation of urinary decay accelerating factor and CD59 in renal damage

Abstract

Decay accelerating factor (DAF) and CD59 (protectin) are complement regulatory proteins that can be detected in soluble form in urine. We studied the relationship between renal disease and the mechanisms involved in the urinary excretion of complement regulatory proteins. Urine samples were obtained from 143 patients with renal disease and 61 individuals with normal renal function, who served as control subjects. As a model of limited tubular injury, we also studied the urine of 5 patients who were being treated with cisplatin for lung cancer; samples were collected before administration of the chemotherapeutic agents (day 0) and every morning during the observation period (15 days). Urinary DAF, CD59, and SC5b-9 (a complement component) were measured by enzyme-linked immunosorbent assay, using monoclonal antibodies. In the patients with renal disease, urinary DAF and CD59 levels were higher than in healthy control subjects (P<0.001). The correlations between urinary DAF and CD59 levels were significant in patients with renal disease and healthy individuals (P<0.001). Urinary SC5b-9 was not correlated with either urinary DAF or CD59 in patients with IgA nephropathy. In the patients with lung cancer, urinary DAF and CD59 were elevated after the administration of cisplatin. This was accompanied by an increase in the secretion of urinaryN-acetyl-β-d-glucosaminidase and β2-microglobulin, both of which are markers for tubular injury. These results suggest that elevated levels of urinary DAF and CD59 are related to renal disease, as well as to the limited tubular injury associated with cisplatin treatment.