To clarify an association between end-stage renal disease and antibodies to hantavirus [1, 2], we examined serum samples from patients seen in a dialysis facility and an emergency department in New York City.

Serum samples were screened by enzyme-linked immunosorbent assay (ELISA) using previously described protocols [1]. To confirm the ELISA results, a Western blot analysis of tentatively positive samples was done. Samples with antibodies directed against nucleocapsid protein [3] were considered seropositive.

Of 546 samples screened by ELISA, 292 were controls obtained from the emergency department population and 254 were obtained from patients undergoing hemodialysis. Overall, 28 samples (5.13%) were positive by ELISA. Of these, 4 (1.37%) were from the emergency department population and 24 (9.45%) were from the dialysis population. This difference was statistically significant (odds ratio, 7.5 [95% CI, 2.4 to 25.9]; P < 0.001).

Western blot analysis could not confirm many ELISA-positive results. Of the 4 ELISA-seropositive samples obtained from the emergency department population, only 1 (0.34%) was confirmed; of the 24 ELISA-seropositive samples obtained from patients undergoing dialysis, only 5 (1.97%) were confirmed. The latter patients tended to be infected with hantavirus more often than did the former (odds ratio, 5.8 [CI, 0.7 to 277.3]; P = 0.07).

Our data corroborate the observation [1] that patients undergoing hemodialysis tend to have antibodies to hantavirus more frequently than do control patients. The seroprevalences in the control group and dialysis group were similar to those observed in Baltimore (0.34% and 0.25% compared with 1.97% and 2.80%, respectively). These results also indicate a need to interpret ELISA results with some caution because 22 of 28 ELISA-positive samples were negative according to Western blot analysis. This suggests that uremic serum samples have nonspecific reactions to ELISA reagents. It is unclear whether results of the serologic tests for hantavirus represent infection or cross-reactive autoantibodies to shared epitopes. This question may be resolved by prospective studies of patients with acute hemorrhagic fever with the renal syndrome, who may develop hypertensive renal disease [4]. As an alternative, the presence of viral antigen or nucleic acids in these patients would provide critical supporting evidence of ongoing viral infection.