Clinical and laboratory characteristics of calcium stone‐formers with and without primary hyperparathyroidism

Abstract

OBJECTIVE To compare the clinical presentation, laboratory features and outcome of treatment in stone formers (SF) with primary hyperparathyroidism (HPT) to those without systemic disease. PATIENTS, SUBJECTS AND METHODS We compared 105 (54 female) stone‐formers (SF) with primary hyperparathyroidism (HPT) to 2416 (835 female) common SF with no systemic disease, and 260 normal subjects (NS, 106 female) using pre‐treatment and treatment data from our kidney‐stone programme. All were assessed before treatment, with three 24‐h urine samples, for stone risk factors, each with a corresponding fasting blood sample. Records were reviewed for stone rates and urological stone‐related procedures. RESULTS The hypercalcaemia of HPT was modest, but hypercalciuria was far more marked than in SF because the fractional calcium excretion of HPT exceeded that of SF. Surgical cure of HPT did not completely eradicate either hypercalciuria or hypophosphataemia, suggesting that these patients have some additional mineral disorder. Serum calcium and phosphate, and fractional excretion of calcium, combined into a discriminant function provided the best separation between HPT and SF. However, we present 49 patients for whom the diagnosis (HPT vs SF) has never been resolved, despite years of observation and successful reduction of stone recurrence. Stones in HPT have slightly more phosphate than SF but the difference is not large enough to be of clinical interest. The stone frequency in HPT is about that for SF, and treatment reduces stones in HPT and SF by about the same amount, 10 times. CONCLUSION No study to date has compared HPT with SF and NS, as done here. SF with even slight hypercalcaemia and brisk hypercalciuria probably have this curable disease, and after cure clinicians must be wary of residual hypercalciuria that requires medical treatment. Some patients will never be fully diagnosed and remain, like ours, an enigma, albeit responsive to usual medical treatments. Although stones are modestly enriched with phosphate, most are mainly calcium oxalate, so the stone analysis is not clinically a guide to diagnosis.

A test of the hypothesis that oxalate secretion produces proximal tubule crystallization in primary hyperoxaluria type I

“…We presume this disproportion of damage between papilla and cortex reflects the corresponding disproportion of CaOx SS and crystallization potential. Whereas cortical SS is predicted to be two-threefold (Table 3), urine SS for CaOx is always much higher (40). In idiopathic CaOx stone formers cortical SS is null, as shown in Fig.…”

Mechanism by which shock wave lithotripsy can promote formation of human calcium phosphate stones

“…SWL procedures were more frequent among those ICSF who converted to IPSF (26). Stone CaP% has increased in the past three decades (4,20,21,24,29), which coincides with the introduction of SWL for stone treatment (5,18).…”

Renal stones and calcifications in patients with primary hyperparathyroidism: associations with biochemical variables

“…In the kidneys, PTH stimulates the renal tubular reabsorption of calcium (TRCa%) (8). However, in spite of the increased reabsorption, the renal calcium excretion is typically increased due to an increased filtered load (10). In the bones, the PTH elevates plasma calcium by promoting osteoclastic bone resorption (9,11) and possibly also by enhancing the active transport of calcium over the bone-extracellular fluid barrier mediated by osteocytes and lining cells (12).…”

“…Finally, calcitriol stimulates the intestinal calcium absorption (14) and to some extent promotes the renal TRCa% (15). In addition, PTH decreases the renal tubular reabsorption of phosphate (8), whereas calcitriol increases intestinal phosphate absorption (10).…”