When I was diagnosed and subjected to several CT scans, each one noted the existence of a renal cyst. I was told it was nothing to worry about although I did find the size worrying on the basis I didn’t think the average kidney could be so big to house a 55mm cyst! That was back in 2010 and they still mention that cyst today, but it no longer worries me. Like many cysts in the human body, these incidental findings on diagnosis are pretty common.
Simple renal cysts are very common, and the incidence increases with age. Approximately 25% of people who are 40 years or older and approximately 50% of people 50 years and older have simple kidney cysts. Simple renal cysts are known to double in size over 10 years. Solitary renal cysts are usually incidentally discovered and are typically asymptomatic. People with severe chronic kidney disease may often have multiple simple cysts. See Reference 4.
Complex cysts. As renal cysts become more complex, it becomes increasing difficult to make the distinction between benign and malignant causes, and the probability of malignancy increases. Complex renal cysts need to be differentiated based on imaging criteria to assess the risk of malignancy. Most hospitals work on the Bosniak classification of renal cysts based on CT findings. These have become the standard to ascertain which complex cysts have a high incidence of malignancy and require surgery or close follow-up imaging. The Bosniak classification is currently used by both radiologists and urologists to manage complex renal cysts. It was originally based on CT findings but has been expanded to MR imaging findings as well. Simple cysts fall into the Bosniak category 1 and do not require further workup or imaging (note but if you are under long-term surveillance as a NET patient, it will be checked).
How common is Neuroendocrine Cancer in the kidney?
According to my research, ultra rare. See Reference 4.
Abstract
Renal neuroendocrine tumors (RenNETs) are rare malignancies with largely unknown biology, hormone expression, and genetic abnormalities. This study aims to improve our understanding of the RenNETs with emphasis of functional, hormonal, and genetic features. Surgically resected RenNETs (N =13) were retrieved, and immunohistochemistry and next-generation sequencing (NGS) were performed in all cases. In addition, all published RenNETs were systematically reviewed. Our cohort (4 men and 9 women, mean age 42, mean tumor size 7.6 cm) included 2 patients with Cushing syndrome (CS). WHO grade (23% G1, 54% G2, and 23% G3) and tumor progression did not correlate. CS-associated RenNETs (CS-RenNETs) showed a solid and eosinophilic histology and stained for ACTH, while the remaining non-functioning tumors had a trabecular pattern and expressed variably hormones somatostatin (91%), pancreatic polypeptide (63%), glucagon (54%), and serotonin (18%). The transcription factors ISL1 and SATB2 were expressed in all non-functioning, but not in CS-RenNETs. NGS revealed no pathogenic alterations or gene fusions. In the literature review (N=194), 15 (8%) of the patients had hormonal syndromes, in which CS being the most frequent (7/15). Large tumor size and presence of metastasis were associated with shorter patients’ survival (p<0.01). RenNETs present as large tumors with metastases.
CS-RenNETs difer through ACTH production and solid-eosinophilic histology from the non-functioning trabecular RenNETs that produce pancreas-related hormones and express ISL1 and SATB2. MEN1 or DAXX/ARTX abnormalities and fusion genes are not detected in RenNETs, indicating a distinct yet unknown molecular pathogenesis.
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