Lacking evidence for calcium-binding protein fetuin-A to be linked with chronic kidney disease-related pruritus (CKD-rP)

syndrome [1], necrotizing and crescenting glomerulonephritis [3,5], minimal lesion glomerulopathy [2], extracapillary glomerulonephritis with IgA deposits or active follicular necrosis against a background of glomerular sclerosis [4]. It is noteworthy that, as with this Crohn’s disease case, favourable outcomes have been reported in all other rheumatoid arthritis cases. After adalimumab discontinuation and glucocorticoid [4] and/or immunosuppressive therapy [3,5], renal function recovered within a few weeks. Of interest, in one case proteinuria relapsed after adalimumab rechallenge [2]. In this case, the relative contributions of adalimumab and of the underlying Crohn’s disease to the development of proteinuria cannot be exactly determined. However, it is questionable whether in this particular patient adalimumab induction scheme was the only factor able to induce proteinuria. We believe that the complete reversibility of proteinuria after adalimumab discontinuation points towards adalimumab as a triggering factor to a strongly predisposed for a renal dysfunction individual. As there have been some concerns regarding safety issues during administration of anti-TNF-α agents, it is of importance to understand the mechanism(s) of their interference in the normal kidney function. By this way, we may able to properly screen and possibly identify high-risk groups before initiation of anti-TNF-α therapies. For the moment, careful patient selection for biological agents as well as regular follow-up can promptly diagnose and completely reverse rare or unexpected episodes.