hyperthyroidism, but the cystatin C values in hyperthy- roidism

roidism are 46% higher than those in hypothyroidism. Existing literature suggests that it is creatinine that is providing the correct assessment of GFR changes (17 ), but because definitive work formally assessing GFR in thyroid disease (using a “gold standard” marker) has yet to be performed, this cannot be stated categorically. Until now, one of the most appealing aspects of using cystatin C as a marker of GFR has been the apparent lack of influence of medical conditions on its clinical utility, with the only debate being whether cystatin C concentrations are influenced by some metastatic malignancies or after renal transplantation (18, 19). A likely explanation for our findings here is that hyperthyroidism is associated with a reversible increase in cystatin C production that is in excess of the expected increase in GFR, whereas in hypothyroidism, cystatin C production is reduced to a greater extent than is the GFR. The reasons for these changes in production remain speculative, but if similar to the cause suggested for 2-microglobulin, then it would seem that it is simply through a metabolic-rate-mediated mechanism (14 ). In summary, this study has shown a clinically significant discrepancy between GFR assessed by serum creatinine and that found using cystatin C in untreated thyroid disease. This raises doubts as to the reliability of cystatin C measurement in these common conditions, but it also suggests that further work needs to be performed to confirm which marker is giving the true reflection of GFR. This work was supported by funding from the Hull and York Diabetes and Endocrinology Endowment funds.