Respiratory syncytial virus nephropathy in rats.

The pathogenesis of minimal change nephrotic syndrome (MCNS) remains unclear. Respiratory tract viruses could contribute to MCNS, and respiratory syncytial virus (RSV) is the most common one. In this study, we planned to investigate the effects of RSV on the proteinuria and glomerular structure of rats and to explore the role of RSV in the pathogenesis of MCNS. Rats were inoculated with 6 x 10(2), 10(4), and 10(6) PFU (plaque-forming units) RSV and killed on days 4, 8, 14, 28, and 60 postinoculation (RSV(4), RSV(8), RSV(14), RSV(28), and RSV(60)). The proteinuria and serum parameters were measured; renal histology was observed by light microscopy and electron microscopy; immune complex deposits were detected by immunofluorescence microscopy; and RSV RNA and RSV titer were determined by in situ hybridization and plaque assay, respectively. After inoculation, the proteinuria increased, especially in 6 x 10(6) PFU RSV(14),(28). The serum albumin of 6 x 10(6) PFU RSV(14),(28) and different-titer RSV(60) decreased. Slight hypercellularity in minority glomeruli and swelling in partial tubular epithelial cells were observed in RSV(4),(8), whereas a relief of the above changes and no abnormalities were detected in RSV(14) and RSV(28),(60), respectively, under a light microscope. Extensive foot process effacement was observed in 6 x 10(6) PFU RSV(14),(28),(60) under an electron microscope. No immune complex deposits were detected in the renal tissues. RSV RNA signal and RSV titer of renal tissues, depending on the dose of inoculum, reached their climax on day 8 postinoculation. Our study reports for the first time that RSV can lead to nephropathy in rats on days 14-60 postinoculation, especially in 6 x 10(6) PFU RSV-inoculated rats, which may be a new exploration of the pathogenesis of MCNS.