Glomerular expression of lipocortin-1 in human glomerulonephritis

Lipocortin-1 (LC-1), a Ca++-dependent phospholipid binding protein, is believed to be involved in anti-inflammatory actions of glucocorticoids. To prove the hypothesis that steroid-resistant glomerulonephritis would show increased expression of LC-1, we evaluated the expression of LC-1 in various types of glomerulonephritis. Frozen samples of seven normal kidneys and 30 kidney biopsy tissues were stained with indirect immunofluorescent method. In the normal tissues, minimal change disease (n = 9), lupus nephritis (n = 5) and IgA nephropathy (n = 6), glomeruli did not stain for LC-1. Positive reactions for LC-1 were observed along the peripheral capillary walls in all five patients with membranous nephropathy without hepatitis B surface antigen (HBsAg). In the patients with membranous nephropathy (MN) who also had chronic liver disease and HBsAg (n = 3), only weak reactions for LC-1 were found along the capillary walls and mesangial area in 1 patient. Patients with membranoproliferative glomerulonephritis (n = 2) showed positive reactions for LC-1 along the capillary walls. Fourteen patients with minimal change disease or lupus nephritis were treated with prednisolone. Ten patients showed substantial reduction of proteinuria, but four patients did not; however, staining for LC-1 was not negative in the kidney tissues of both steroid-responsive and steroid-resistant patients. These findings suggest that LC-1 does not mediate the action of glucocorticoids in human glomerulonephritis.