A mononuclear cell component in experimental immunological glomerulonephritis.

TLDR

The study examined an accelerated form of nephrotoxic serum nephritis in rats. The experimental model involved preimmunizing rats with rabbit IgG five days before administering subnephrotoxic doses of rabbit anti‑rat kidney serum. The results showed that preimmunized rats developed early proteinuria with neutrophilic glomerular infiltration and later proteinuria associated with mononuclear cell infiltration and glomerular cell proliferation; these mononuclear cells, identified as monocytes/macrophages derived from extrarenal precursors, were essential for the sustained proteinuria, as their depletion by irradiation abolished the late proteinuria, indicating that mononuclear phagocytes contribute to glomerular dysfunction.

Abstract

An accelerated form of nephrotoxic serum nephritis in the rat was examined. The experimental model consisted of preimmunization of the rat with rabbit IgG 5 days before injection of subnephrotoxic doses of rabbit anti-rat kidney serum. The immunized rats developed proteinuria during the first 24 h, increasing by 48-96 h. The early 24-h proteinuria correlated with a neutrophilic infiltration of glomeruli and with deposition of rat Ig and C. The 48- to 96-h proteinuria was associated with a glomerular infiltration by mononuclear cells and proliferation of intrinsic glomerular cells. Many of the mononuclear cells were morphologically identical to monocytes and macrophages. [3H]thymidine labeling experiments indicated that the mononuclear cells originated from dividing precursors localized outside the kidney. Preimmunized rats given systemic irradiation (the kidney being protected by a shield) showed loss of the mononuclear cell infiltrate and absence of 48- to 96-h proteinuria. We conclude that mononuclear phagocytes can infiltrate the kidney in immunological glomerular disease and might contribute to the functional abnormalities.