Introduction:
We present a descriptive study of symptomatic hypercalcemia patients from a tertiary care nephrology centre.
Methods:
All patients with hypercalcemia [corrected serum calcium (S.Ca) greater than 10.5 mg/dl] with any one of the following symptoms - altered sensorium, recent deterioration of renal function, recurrent vomiting and/or pancreatitis admitted between Jan 2022 to Aug 2024 were included. They were followed up for a period of 30 days. Statistical analysis was performed using R statistic (ver4.4.1). Mann Whitney U test was used for quantitative analysis.
Results:
Mean age of the 27 patients studied was 54.1 +/- 14.2 years with 59% females. Etiologies included plasma cell dyscrasia (30%), malignancies (30%), iatrogenic (22%), autoimmune (11%) and tuberculosis (7%). The average S.Ca was 12.9 +/-1.8 mg/dl and serum phosphate (S.PO4) was 3.6 +/ 1.7 mg/dl. M band by serum protein electrophoresis was detected in 6 patients (22%) and 10 (37%) patients had preexisting chronic kidney disease (CKD). The commonest symptoms noted were nausea and vomiting (82%), fatigue (67%), abdominal pain (63%), neurological manifestations (11%), bony pain (11%) and pancreatitis (11%). We found significantly higher alkaline phosphatase levels in the 8 patients who had malignancy related hypercalcemia compared to the rest (360+/-234 vs 160+/-65 IU/L, p=0.01). The intact parathyroid hormone (iPTH) levels were expectedly higher in the 6 patients with PTH adenomas compared to the rest (mean 1041+/-884 vs 32+/-46 pg/ml, P<0.001). iPTH levels were markedly lower in patients with iatrogenic hypercalcemia, although not reaching statistical significance (mean 75 vs 336 pg/dl, P = 0.36).
Amongst the 17 patients without preexisting CKD, 16 had acute kidney injury (AKI) attributable to hypercalcemia (mean creatinine 3.39+/-1.9 mg/dl). 88% of these patients with AKI completely recovered by day 30. S.PO4 levels were significantly lower in plasma cell dyscrasias (3.9 +/- 1.9 vs 2.8+/-0.4 mg/dl, p=0.03). We hypothesize that this is probably due to Fanconi’s syndrome secondary to plasma cell dyscrasia. While two deaths were related to malignancy, one succumbed to calciphylaxis.
Treatment strategies in patients without CKD included furosemide with IV fluids (88%), salmon calcitonin (35%), bisphosphonate (30%), hemodialysis (17%) and cinacalcet (12%). All patients with PTH adenoma were successfully treated with resection surgery. Majority of hypercalcemia in CKD patients was due to unmonitored consumption of calcium based phosphate binders and vitamin D supplements. Treatment in these patients mainly involved usage of non-calcium based phosphate binders, cinacalcet and low calcium bath hemodialysis. However, two patients with CKD were detected to have tuberculosis and hypercalcemia resolved after anti-tubercular treatment.
Conclusions:
Lower phosphate levels, high PTH levels, suppressed PTH and high alkaline phosphatase levels in hypercalcemia should raise suspicion of plasma cell dyscrasias, non myelomatous malignancies, iatrogenic causes and malignancies respectively. The use of calcium based phosphate binders and vitamin D supplements in CKD should be appropriately monitored. Tuberculosis in developing countries is a readily treatable cause of hypercalcemia.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.