A GSK-3 inhibitor Capture

652, P Quisinostat mouse suggesting that hypothyroidism alters renal function, both the glomerular filtration rate [14] and the tubular function [15]. Recent publications illustrate the growing interest in the association between thyroid and renal functions [16, 17]. The increase in serum creatinine levels observed in hypothyroidism is relevant in clinical practice since it may mislead physicians in handling the care of the patients with thyroid dysfunction. As stressed by Kreisman and Hennessey ankyrin GSK3 inhibitor [14], frankly abnormal serum creatinine levels may occur in some cases of hypothyroidism and not taking into consideration the association of thyroid metabolism and glomerular filtration rate may lead to unnecessary and costly investigations. On the other hand, in patients presenting mild renal failure without evident cause and a clinical record of hypothyroidism (as the ones that motivated our interest in thyroid metabolism), it may be helpful to determine thyroid metabolism and eventually to adapt the hormone therapy. Although not envisaged or proposed in internal medicine textbooks, the correction of the thyroid dysfunction will certainly be followed by an improvement of renal function. This has been documented by several isolated case reports in the literature, in childhood [18], or in adult patients with mild [19] or even with advanced renal failure [20]. This is also supported by a study using radiomarkers, which showed reversible reductions in glomerular filtration rates in hypothyroid patients [21]. Interestingly, Karanikas et al. [21] also showed that changes in measured GFR levels were consistent with changes in serum creatinine. In contrast, plasma cystatin C levels appear to be increased in hyperthyroidism and decreased in hypothyroidism rendering the use of cystatin C-based estimations of GFR inappropriate in these clinical situations [22].