Abnormal Calcium Levels Tied to Chronic Kidney Disease: Study

No link between blood phosphate, calcium-phosphate measurements and CKD

Somi Igbene, PhD avatar

by Somi Igbene, PhD |

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A person is seen taking a sip of a drink while their kidneys are highlighted and enlarged to the sides.

People with chronic hypoparathyroidism and blood calcium levels outside the reference range may have higher odds of developing chronic kidney disease, according to a study.

The study, “Association of calcium and phosphate levels with incident chronic kidney disease in patients with hypoparathyroidism: a retrospective case-control study, was published in the International Journal of Endocrinology.

Hypoparathyroidism is caused by insufficient levels of the parathyroid hormone (PTH), which regulates calcium and phosphate blood levels. When calcium drops, PTH stimulates the kidneys to reabsorb it, excrete phosphate and release active vitamin D to reabsorb calcium and phosphate in the gut. Low or absent PTH causes insufficient calcium blood levels and high blood levels of phosphate.

Conventional therapy, including calcium supplements and active vitamin D, can correct calcium levels. But some patients don’t respond well to conventional therapy and may experience high blood calcium. Also, calcium and active vitamin D supplements lack PTH’s effects on the urinary excretion of phosphate, which can lead to temporary high calcium wasting in urine.

Conventional therapy has been linked with kidney damage in hypoparathyroidism, but little is known about what contributes to it.

The researchers hypothesized that frequent changes in blood serum calcium and phosphate might be associated with a higher risk of developing chronic kidney disease (CKD).

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CKD and blood calcium, phosphate changes

To test this, they assessed data from adults (mean age, 57.7) with chronic hypoparathyroidism and CKD and from people without CKD who were matched for factors such as age and sex to serve as controls. All eligible patients were required to have at least one prescription for calcitriol — or active vitamin D — and must have developed CKD after they started it.

Blood calcium (specifically, albumin-corrected serum calcium) was assessed in 300 patients. Blood phosphate and calcium-phosphate product (used to estimate the cardiovascular risk of patients with renal failure) were measured in 80 participants. The reference range of albumin-corrected blood calcium for people with chronic hypoparathyroidism was 2.00–2.25 mmol/L, which is different from the healthy values (2.15–2.55 mmol/L). In contrast, phosphate and calcium-phosphate product reference ranges were the same for patients and healthy populations.

Among participants analyzed for blood calcium, 97.3% had stage 3 CKD, 2% had stage 4, and 0.7% had stage 5, whereas 92.5% and 7.5% of patients in the phosphate and calcium-phosphate group had stage 3 and 4 CKD, respectively. Stage 3 CKD refers to mild to moderate damage, whereas stage 4 refers to moderate to severe damage.

Compared to matched controls, CKD patients had a significantly higher proportion (57.9% vs. 41.2%) of serum calcium levels outside (above or below) the reference range. Patients with at least 67% of blood calcium measurements outside, above, or below the reference range had a 3.5, 2.9 and 2.7 higher risk of CKD, respectively, than those whose levels were under 33% of the reference range.

Similar findings were seen in a sensitivity analysis among 89 participants with CKD and 89 controls.

Patients with 33% to less than 67% of their blood calcium measurements outside, above, or below the reference range in the primary analysis showed a trend toward an increased risk of CKD that wasn’t statistically significant.

The proportion of participants with blood phosphate or calcium-phosphate measurements above the reference range was similar in patients and controls. No link was found between these measurements above the reference range and developing CKD.

The researchers said the infrequent monitoring of phosphate and calcium-phosphate throughout the study was a limitation. This limited the sample size and may have affected the inability to find associations between blood phosphate and calcium-phosphate product and developing CKD.

“Further studies are warranted to explore whether treatment modifications aiming to achieve more stable serum calcium levels within recommended disease management ranges may reduce the risk of CKD development in patients with chronic hypoparathyroidism,” they wrote.