Among adult patients with recurrent kidney stones, primary hyperparathyroidism has a reported prevalence of approximately 5%.91 Primary hyperparathyroidism is associated with a significantly elevated risk of stones, with a reported 40-fold increased incidence of stone disease in those with untreated primary hyperparathyroidism compared with normal controls.92 Serum PTH represents the cornerstone in the identification of primary hyperparathyroidism. For expediency in adults, clinicians may obtain serum PTH at initial screening or may consider obtaining serum PTH in follow-up if other findings (e.g., hypercalcemia, predominantly calcium phosphate [hydroxyapatite or brushite] stone composition, marked hypercalciuria, and/or medullary nephrocalcinosis) suggest possible underlying primary hyperparathyroidism.93 Primary hyperparathyroidism is much less common in children and adolescents than in adults; therefore, there is insufficient evidence to support routine PTH measurement as part of the initial metabolic evaluation in all pediatric stone formers. In pediatric patients, PTH testing should be obtained when hypercalcemia or other features (e.g., hypercalcemia, pure calcium phosphate stone composition, marked hypercalciuria, and/or medullary nephrocalcinosis) raise suspicion for primary hyperparathyroidism. Primary hyperparathyroidism is obvious in the setting of hypercalcemia, hypercalciuria, and elevated serum PTH; however, nuances in diagnosis abound. Serum PTH levels are normally regulated in a homeostasis-maintaining negative feedback loop, with low serum calcium serving as an important stimulator for PTH secretion, while higher serum calcium reduces PTH secretion. Therefore, PTH should be obtained with serum calcium to evaluate PTH in the context of serum calcium. Of note, normocalcemic primary hyperparathyroidism should be considered in those with serum calcium approaching the upper limits of normal in the setting of inappropriately elevated or high-normal (thus inadequately suppressed) serum PTH.94 This can be elicited with a thiazide challenge, by which thiazide-induced calcium reabsorption fails to suppress PTH and unmasks primary hyperparathyroidism by revealing persistent/dysregulated hyperparathyroidism despite reduction in hypercalciuric calcium loss.95 Whereas primary hyperparathyroidism arises from dysregulated PTH secretion, elevated PTH may also occur as a secondary, appropriate response to factors including CKD, vitamin D deficiency, and calcium loss from hypercalciuria. Vitamin D deficiency with subsequent impaired GI calcium absorption may induce secondary hyperparathyroidism, and as such, serum 25-hydroxy vitamin D should be measured. If vitamin D levels are low, a trial of vitamin D supplementation may allow appropriate suppression of PTH.96 Likewise, calcium loss associated with hypercalciuria may induce elevated PTH and can be distinguished from primary hyperparathyroidism with a thiazide challenge.96   If primary hyperparathyroidism is diagnosed in patients with kidney stones, appropriate referral for evaluation for parathyroidectomy should be initiated.