The cause of maintained hypercalciuria after the surgical cure of primary hyperparathyroidism is a defect in renal calcium reabsorption

Farias, MariaLucia; Delgado, Alvimar G.; Rosenthal, Doris; Vieira, José Gilberto H.; Kasamatsu, Teresa S.; Lazarevitch, M. J.; Pereira, M. Francisco; Lima, Maurício B.

doi:10.1007/bf03347852

Cited by 14 publications

(6 citation statements)

References 33 publications

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“…Farias et al. [16,17] reported hypercalciuria after treatment in HPT, and found reduced tubular calcium reabsorption that they ascribed to hypercalcaemic nephropathy. We have no data to support or contradict their idea, but agree with their findings.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2009

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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.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2009

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“…Longstanding hyperparathyroidism in renal hypercalciuria is thought to eventually evolve to parathyroid adenomas in some cases (29). These patients with renal hypercalciuria and autonomous parathyroid function may have persistent hypercalciuria after parathyroidectomy (30), which is thought to be the underlying etiologic mechanism for persistent hyperparathyroidism after parathyroidectomy (31).…”

Section: Box 1 Causes Of Persistent Parathyroid Hormone Elevation Andmentioning

confidence: 99%

Significance Of Elevated Parathyroid Hormone After Parathyroidectomy For Primary Hyperparathyroidism

Oltmann¹,

Maalouf

Holt³

2011

Endocrine Practice

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“…S ERUM AND URINARY CALCIUM should completely normalize in surgically cured primary hyperparathyroid patients (PHPx). We have previously described persistent hypercalciuria in 6 of 10 PHPx patients, 1 although their glomerular filtration rate (GFR) and filtered load of calcium (FL Ca ) were significantly lower than in control subjects.…”

Section: Introductionmentioning

confidence: 99%

Changes in Renal Hemodynamics and Tubular Function of Surgically Cured Primary Hyperparathyroid Patients Are Probably Due to Chronic Hypercalcemic Nephropathy

Farias

Delgado

Rosenthal

et al. 1998

Journal of Bone and Mineral Research

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To understand the mechanisms responsible for the persistent hypercalciuria and reduced glomerular filtration rate (GFR) previously found in 6 of 10 patients surgically cured of primary hyperparathyroidism (PHPx), the tubular handling of lithium, sodium, calcium, and phosphate as well as the renal hemodynamics were evaluated in these 10 PHPx patients, in 10 control subjects, and in 5 patients with renal hypercalciuria (RH), during fasting and after an oral calcium load. A positive correlation between the fractional excretions of calcium and sodium was found in all groups, but the PHPx patients excreted more calcium for the same amount of sodium than control subjects. The fractional proximal sodium reabsorption (FPR Na ), distal delivery, and fractional phosphate reabsorption were similar in all groups; a significant positive correlation was found between the fractional calcium reabsorption and the FPR Na , indicating that proximal tubular function was preserved and that the urinary calcium losses in RH and in the hypercalciuric PHPx patients (h-PHPx) occurred in the distal nephron. However, only h-PHPx patients had reduced renal plasma flow, renal blood flow, and GFR, as well as a high renal vascular resistance, which was even more evident after the calcium challenge. These findings lead us to conclude that RH and h-PHPx patients are very different, as far as kidney dysfunction is concerned, and that a hypercalcemic nephropathy is the most probable cause of the alterations in distal calcium reabsorption and renal hemodynamics found in the h-PHPx patients. (J Bone Miner Res 1998;13:1679-1686)

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The cause of maintained hypercalciuria after the surgical cure of primary hyperparathyroidism is a defect in renal calcium reabsorption

Cited by 14 publications

References 33 publications

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

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

Significance Of Elevated Parathyroid Hormone After Parathyroidectomy For Primary Hyperparathyroidism

Changes in Renal Hemodynamics and Tubular Function of Surgically Cured Primary Hyperparathyroid Patients Are Probably Due to Chronic Hypercalcemic Nephropathy

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