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Parathyroid/Bone Disorders

(19.15) Hypercalcemia Due to Renal Lymphoma in a Patient with History of Renal Cancer After Nephrectomy

Saturday, May 11, 2024
10:30 AM – 10:45 AM CDT
Location: ePoster Showcase, Empire Ballroom Foyer, Level 2

    Submitter(s)

  • Aneeqa Saif, MD

    Endocrine Fellow
    MedStar Union Memorial Hospital, United States

Introduction : Malignancy-associated hypercalcemia is the number one cause of hypercalcemia in hospitalized patients. The major underlying mechanisms include osteoclast-mediated bone resorption, humoral hypercalcemia of malignancy (HHM) secondary to parathyroid hormone-related peptide (PTHrP), or excess 1,25-dihydroxy vitamin D production. Here we describe a patient who presented with hypercalcemia and was found to have a renal mass that was initially thought to be renal cell cancer causing HHM; however, biopsy results later revealed it to be renal lymphoma.

Case(s) Description :

A 77-year-old male with past medical history of left renal cancer status post nephrectomy in 2008 presented with calcium (Ca) level of 15.4 and albumin 4.0 on outpatient labs done by his primary care physician on the day of admission.

In the ED, his vital signs remained stable. CT abdomen/pelvis showed a large mass at the superior pole of the right kidney with satellite lesions along the retroperitoneum, and two pulmonary nodules. He was given 1 L normal saline bolus and admitted for further management.

The patient received zoledronic acid, was started on calcitonin and normal saline at 200 cc/hr. Parathyroid hormone (PTH) was 34.6 and 25 OH vitamin D was 25.4.

CT-guided biopsy of the right renal mass showed large B-cell lymphoma. PTHrP was slightly elevated at 2.6 and 1,25(OH)2 D was elevated at 115.
His Ca decreased over the next few days to 10.7 at discharge with plan for outpatient oncology follow up.

Discussion :

HHM is the mechanism of hypercalcemia in approximately 80% of cancer patients. This was the initial presumed mechanism of hypercalcemia in our patient in the setting of a renal mass as kidneys are rarely the tissue of origin in lymphomas. Our patient did have mildly elevated PTHrP level, and the presence of simultaneous elevation of 1,25(OH)2 D and PTHrP has previously been reported in a patient with renal cell cancer who responded better to glucocorticoids than to the conventional bisphosphonate therapy.

Isolated renal lymphoma causing hypercalcemia has previously been described in case reports, but the mechanism was thought to be due to elevated PTHrP and not 1,25(OH)2 D excess.

Despite severely elevated calcium levels, his PTH level was also not suppressed, raising questions about the concurrent presence of primary hyperparathyroidism contributing to his hypercalcemia. Ectopic secretion of PTH by tumor cells has also previously been described in malignancies; however, it remains a rare cause.

This case shows the need to consider multiple etiologies in the work up of severe hypercalcemia, including rare causes such as renal lymphoma which may affect treatment.