BUBREŽNE PROMJENE U BOLESNIKA S REUMATOIDNIM ARTRITISOM

Krešimir Galešić, Ingrid Prkačin, Miroslav Tišlja, Jadranka Morović Vergles

In rheumatoid arthritis (RA) kidney is commonly affected organ with clinical presentation characterised by proteinuria (often nephrotic range) and microhematuria followed by chronic renal failure. This condition is well recognized as a rheumatoid nephropathy (rheumatoid glomerulonephritis), which is mediated by an immunological infl ammation and by nephrotoxic effects of numerous drugs usually used in rheumatoid arthiritis treatment, such as NSAID, DMARD. In the patohistological examination various kinds of associated renal lesions could be seen. The most often are amyloidosis, glomerulonephritis, interstitial nephritis. In this study, we presented 15 patients, 10 women and 5 men, mean age of 60.2 with average rheumatoid arthritis duration of 19.4 years and signs of rheumatoid nephropathy. In all patients renal biopsy was performed with frequency of histopathological findings as follows: amyloidosis in 5 patients, IgA nephropathy in 3 patients, FSGS in 3 patients, mesangial proliferative glomerulonephritis in 3 patients, minimal change disease, pauci-immune glomerulonephritis and thin membrane disease in 1 patient. In all patients (except patient with thin membrane nephropathy) we started immunossuppresive therapy with glucocorticoids in combination with cyclophosphamide or cyclosporin or azatioprine. In conclusion, in all patients with rheumatoid arthritis, parameters of renal function should be monitored and in the case of patologic results, renal biopsy should be be performed. In the treatment of RA patients with related renal disorder, suspected causal drug should be removed from the treatment and specific immunosuppressive therapy initiated.

U bolesnika s reumatoidnim artritisom (RA) često je zahvaćen bubreg. Klinički se bubrežna bolest očituje proteinurijom (često nefrotskog ranga) i mikrohematurijom uz razvoj bubrežne insuficijencije. Bubrežnu bolest u bolesnika s RA nazivamo reumatoidnom nefropatijom a posljedica je imunološke upale u glomerulu i nefrotoksičnog učinka lijekova koji se uobičajeno primjenjuju u liječenju RA (NSAR i DMARD). Najčešće u bolesnika s RA patohistološki u tkivu bubrega nalazimo amiloidozu, potom glomerulonefritis i intersticijski nefritis. U radu prikazujemo 15 bolesnika, od toga 10 žena i 5 muškaraca prosječne dobi 60,2 godine, s prosječnim trajanjem RA od 19,4 godine i razvijenim znakovima reumatoidne nefropatije. Svim bolesnicima učinjena je biopsija bubrega, te je u petero bolesnika patohistološki utvrđena amiloidoza, u troje IgA nefropatija i FSGS, dok je mezangio proliferativni GN, bolest minimalnih promjena, pauci-imuni GN i bolest tankih membrana utvrđena u po jednog bolesnika. Svi bolesnici (osim bolesnice s bolesti tankih membrana) liječeni su glukokortikoidima u kombinaciji s ciklofosfamidom, ciklosporinom ili azatioprinom. Zaključno ističemo da je u svih bolesnika s RA potrebna i redovita kontrola bubrežne funkcije a u jasnim indikacijama kompletna nefrološka obrada uz biopsiju bubrega.