Calcium Deposits in Kidneys Common in Hypoparathyroidism
Calcium deposits — known as calcifications — in the kidneys and higher-than-normal levels of calcium in urine are common in people with chronic hypoparathyroidism, according to a small Danish study.
Notably, the presence of these calcifications was neither significantly associated with the levels of calcium in the urine or blood, nor with daily doses of vitamin D or calcium supplements, according to the study results.
Further studies are needed to confirm these findings and to better understand what contributes to such kidney calcium deposits in this patient population, the researchers said.
The study, “Determinants of hypercalciuria and renal calcifications in chronic hypoparathyroidism: A cross‐sectional study,” was published in the journal Clinical Endocrinology.
Hypoparathyroidism is caused by abnormally low levels of the parathyroid hormone, called PTH, which results in vitamin D deficiency, low levels of calcium, and high levels of phosphorus in the blood.
Current treatment typically includes calcium and vitamin D supplements, as well as PTH replacement therapy. But many patients still experience fluctuations in calcium levels and excessive calcium loss in the urine — called hypercalciuria — which increases the risk of chronic kidney disease.
In addition, chronic hypoparathyroidism is associated with the buildup of calcium deposits, most often in blood vessels and in the brain, but also in the kidneys, which may impair their function.
Researchers in Denmark have now evaluated the frequency of hypercalciuria and kidney calcifications in 166 patients with chronic hypoparathyroidism. These patients, followed at the Aarhus University Hospital, in Denmark, each underwent a 24 hour-urine collection for measuring calcium urine excretion between July 2008 and February 2020.
Potential links between factors of known importance to kidney function and the presence of kidney calcium deposits also were assessed, with investigators hypothesizing that hypercalciuria would contribute to kidney calcifications in these patients.
The team retrospectively analyzed demographic, clinical, and lab data from 165 adults and one adolescent with chronic hypoparathyroidism, with a median age of 53 years (range of 14.2–79.9 years).
Most patients were women (79.5%) and had developed the disease following neck surgery (75.3%), most often performed due to goiter, an abnormal enlargement of the thyroid gland.
The results showed that 65.7% of the patients had hypercalciuria. That frequency reached 74% if the 17 patients who were on thiazide diuretics — which help to reduce the amount of calcium lost through urine — during the 24 hour-test were excluded from the analysis.
When adjusted for several potential influencing factors, hypercalciuria was significantly associated with lower PTH blood levels, higher levels of vitamin D and calcium in the blood, and higher 24 hour-phosphate levels in urine. All these factors are known to be important to urinary calcium levels in healthy people, the team noted.
A significant association also was found between hypercalciuria and being a woman and having post-surgery hypoparathyroidism.
“Hypercalciuria is to a large extent explained by indices of known physiological importance to [urinary calcium],” the team wrote, adding that the data also suggest “that any remaining parathyroid function might help to reduce urinary calcium in [hypoparathyroidism].”
In addition, chronic kidney disease was present in 18.3% of the patients, and kidney calcifications in 23 (42.6%) of the 54 patients whose kidneys were examined by imaging tests.
The team noted, however, that the high frequency of calcium deposits in the kidneys should be interpreted with caution, since only half of the included patients had undergone such imaging tests.
“If assuming that none of those not examined by [kidney] imaging had [kidney] stones, the prevalence is rather 23 patients among the entire group of 166 patients (14%),” the researchers wrote, adding that the “true prevalence is probably somewhere in-between 14% and 42.6%.”
Based on this and previous studies, the team hypothesized that kidney calcifications likely occur in 20–30% of chronic hypoparathyroidism patients, which is “a much higher prevalence than the 10% reported in cross-sectional studies from the general population.”
These findings suggest that “hypercalciuria, impaired renal [kidney] function and renal calcifications are common in hypoparathyroidism,” the researchers added.
Notably, contrary to their hypothesis, high calcium levels in the urine were not significantly associated with kidney function or kidney calcifications, the researchers found. Blood calcium levels and daily doses of vitamin D or calcium supplements also were not major contributors to these calcifications.
Calcium deposits were only significantly associated with lower phosphate levels and lower calcium x phosphate product in the blood.
Given the study’s limitations, such as its retrospective and one-time assessment nature, further studies are needed, particularly ones that follow patients over time. Such studies will allow scientists to better evaluate “how changes in treatment of the disease and biochemical measures affects … risk of calcifications in chronic hypoparathyroidism,” the researchers wrote.
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