Abstract
We are happy to answer to the concerns raised by Malhotra et al. (1). First, we would like to note that diligence was made to retrieve and look at all references in the literature relating to the topic of renal metastasis in thyroid cancer. We acknowledge that it is plausible that more cases could have been reported in the worldwide medical literature; however, at the time of writing and review of our article, to the best of our knowledge, very few cases of renal metastases from thyroid cancer were reported. Our PubMed/National Library of Medicine search produced only 10 case reports. Notably, we tried to include only histologically proven cases of renal metastasis. In reviewing the case recently published by Malhotra et al. (2), we note that there is no histological proof for a renal metastatic lesion.
Our contention that thyroid cancer renal metastases are uncommon and require multimodality imaging and aggressive treatment remains valid. Our article brings histopathologic evidence for the thyroid Hurthle cell origin of the renal metastatic lesion, and this does not apply to the article of Malhotra et al. that reports on a patient with advanced, multisystem metastatic thyroid cancer, with widespread skeletal, pulmonary, mediastinal, hepatic, and adrenal involvement. The authors state that the metastatic sites were iodine-avid on 131-I scintigraphy, with the exception of the renal lesions (1.5 = 0.7 cm lesion in the right kidney, and a tiny 0.7 cm lesion in the left kidney) that were seen on computed tomography (CT) only. These lesions could be incidental and not related to the thyroid cancer.
The authors state that a focus of fluorodeoxyglucose (FDG) uptake was seen in the superior pole of the right kidney on postdiuretic spot view on positron emission tomography (PET), and they present this as evidence that the lesion seen on CT represented a renal metastasis; however, in the absence of cross-sectional anatomic imaging correlation with PET-CT, this activity may represent retained urinary FDG activity in an upper pole calyx. Evidence that the small renal lesions seen on CT scan represent thyroid cancer metastases is not compelling: although all the other metastatic sites displayed focal 131-I uptake, the renal lesions remained non-observed on both diagnostic and post-therapy 131-I scintigraphy. Histological evidence of the nature of the renal lesions was not presented.
We agree with Malhotra et al. that in patients with thyroid cancer regular surveillance is crucial. Their patient lived for two decades without thyroid hormone replacement due to functional thyroid cancer metastases producing thyroxine; the case is illustrative of the importance of long-term levo-thyroxine suppression for disease containment, limiting further progression and improving survival.