The effect of secondary HPT on PMN function, as assessed by CL, was studied in two groups of patients. Group 1 comprised seven patients with no clinical evidence of secondary HPT and mildly elevated levels of serum iPTH (mean 2.7 +/-0.9 microleq/ml), and group 2 had six patients with clinical and radiological evidence of secondary HPT and higher ( p < 0.001) levels of iPTH (mean 26 +/- 7 microleq/ml). PMNs from group 2 patients demonstrated 68% +/- 9 augmented CL in the presence of autologous serum. Cross-incubation studies showed that sera from group 2 patients induced augmented CL in normal PMNs. In contrast, PMNs from group 2 patients showed reduced CL in the presence of normal serum. The augmenting effect of group 2 sera did not correlate with the level of calcium, phosphorus, creatinine, or BUN in serum. After successful subtotal parathyroidectomy, evident by the decrease of serum iPTH levels, both the CL of group 2 PMNs and the ability of group 2 sera to induce augmented CL in normal PMNs decreased (p < 0.025). These results suggest that secondary HPT is directly or indirectly responsible for the altered leukocyte function in some patients with uremia, particularly those with marked elevation of iPTH.