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1/lab called to report a serum Ca jump to 12.6 (normal albumin) along with hypokalemia and high serum CO2. PTH 21 (down from 129!), 25 vit D 30. So a PTH-independent case. Pt feels fine and is active. Pt not on calcitriol, vitamin D or thiazide. SPEP and fLC normal.
2/neg skeletal survey; calcitriol level comes back normal 5 days later, so does PTH-rp. As noticed, K and CO2 were also remarkably off. Pt had diabetic nephropathy and was taking ARB and patiromer 16.8 g Qd. So, initial plan was to stop patiromer & repeat labs next day
3/I was drawn by the idea of milk-alkali syndrome and malignancy causes and initially saw the K/CO2 as a separate problem, but work up was coming back unrevealing and the pt had not taken anything (trust me, I pushed). To my surprise, the serum Ca the next day dropped to 11.2.
4/wait a second, patiromer stopped and hyperCa improves (even faster than hypokalemia!)? That took me immediately to PubMed...
5/ and this is what I found
6/One case from the great M Emmett. Duh! A cation exchange resin after all. Once again postmarketing reveals drug adverse effects that keeps us nephrologists busy.
7/ met alkalosis was likely due to hypokalemia. Ca and K normalized in 2 days. CO2 took longer, 6 days, likely due to CKD. Conclusion: add patiromer to your differential diagnosis of PTH-independent hypercalcemia #MedEd #nephrocentric #InternalMedicineRounds
