INCREASED INCIDENCE OF GLOMERULONEPHRITIS FOLLOWING SPLENORENAL SHUNTSURGERY IN NONCIRRHOTIC PORTAL FIBROSIS

In a prospective study of 200 non-cirrhotic portal fibrosis (NCPF) pat ients. 7% had mild proteinuria and their renal biopsies showed mild me sangial proliferative glomerulonephritis (mes-PGN). The remaining 93% biopsies were normal. However, following the insertion of a spleno-ren al shunt (SRS) for portal hypertension 32% of these patients developed nephrotic syndrome in five years. Renal histology revealed mesangioca pillary glomerulonephritis (MCGN) (18.5%) mes-PGN (9%), minimal change nephropathy (3%), and chronic sclerosing GN (1.5%). Immunofluorescenc e showed granular deposition of IgA and C3. IgA2 was predominant form of 1g in the glomerular deposits, indicating that IgA in the immune co mplexes was derived from the gastrointestinal tract. Electron microsco py revealed electron dense deposits in the mesungium. In contrast to t he NCPF patients who underwent a SRS for portal hypertension the 200 p atients in our study who underwent spleno-renal shunting because of ex tra hepatic portal obstruction did not have renal disease nor did they develop renal disease during the five-year post-operative follow-up. fifty percent of the glomerulonephritis (GN) in the NCPF group progres sed to renal failure in five years 46.6% continued to have proteinuria . Low serum complement, C3 (50%) and circulating immune complexes (14. 8%) were detected in the glomerulonephritis of GN following SRS in NCP F patients, but not in those with normal livers; (ii) the type of GN i s primarily IgA nephropathy; and (iii) the GN could be the result of d etective hepatic reticuloendothelial function in the NCPF group that i s worsened by the shunting procedure.