TITLE:
Cyclosporine-Associated Nephrotoxicity
AUTHORS:
Maria Delia Colombo, Renata Perego, Gilberto Bellia
KEYWORDS:
Cyclosporine; Nephrotoxicity; Immunosuppression; Transplant; Creatinine
JOURNAL NAME:
Open Journal of Nephrology,
Vol.3 No.3,
September
10,
2013
ABSTRACT: Cyclosporine (CsA) has revolutionized transplant
medicine and is currently one of the most important immunosuppressive
agents for a wide range of organ transplantations and of autoimmune and
inflammatory diseases, such as rheumatoid arthritis, uveitis, psoriasis, and atopic
dermatitis. Renal impairment represents the main limitation to CsA long-term
continuous therapy. However, it has been shown that nephrotoxicity is
associated with longer treatment duration, larger cumulative doses and higher
daily dose of CsA. With low dose regimens (-20 years
after kidney transplantation. Intermittent therapy may offer a good therapeutic
strategy to limit long-term renal dysfunction, given the fact that renal
structural changes are dose- and time-dependent. The best predictor of
permanent renal damage is a persistent increase in serum creatinine level one
month after treatment withdrawal. In patients with autoimmune diseases, the
percentage increase in serum creatinine above baseline value during CsA therapy
has been shown to predict CsA-induced nephropathy. Before CsA therapy
initiation, patients should undergo a thorough baseline evaluation including
laboratory assessments, in particular electrolytes, serum creatinine, and urea
levels. Furthermore, patients should be evaluated for factors that might
increase the risk of nephrotoxicity, such as obesity, older age, hypertension,
concomitant use of nephrotoxic drugs, and pre-existing renal conditions.
In the present paper, CsA-induced nephropathy will be reviewed in terms of
pathophysiology, pathologic and clinical findings, and strategies for
prevention and management.