IgA-AS A MARKER FOR THE DIAGNOSIS OF NEPHROPATHY IN PATIENTS WITH REACTIVE ARTHRITIS

Kidney injury during RA includes secondary renal amyloidosis, nephrotoxic effects of antirheumatic drugs and nephropathies as extra-articular manifestations (rheumatoid nephropathy). Amyloidosis affects survival, increases morbidity and is the main cause of end stage renal disease in patients with RA and nephropathy [1,4,9]. Amyloidosis is a group of diseases characterized by extracellular deposition of beta-sheet fibrils. In the systemic forms, the amyloid protein causes progressive organ dysfunction, which may lead to death of the patients [2,5,10]. Over 35 proteins capable of amyloid formation have been identified. Clinically evident kidney involvement most commonly occurs in AL (immunoglobulin light chain) or AA (previously referred to as secondary) amyloidosis but can also occur in other forms of amyloidosis [3,6,7,8]. The deposition of beta-2 microglobulin occurs in patients on prolonged maintenance dialysis; deposition in the kidney has been reported in autopsies but has no clinical significance. IgA nephropathy (IgAN) may be associated with reactive arthritis (RA). The course of RA-associated IgAN remains largely unknown due to the absence of large numbers of patients