Parathyroid gland function in subgroups of metabolically mediated urolithiasis as evaluated by serum parathyroid hormone, and urinary and nephrogenous cyclic nucleotides

Schwille, P. O.; Scholz, D.; Schwille, K.; Engelhardt, W; Schreiber, B. Charlotte; Goldberg, I. J. L.; Sigel, A.

doi:10.1007/bf01728341

Cited by 5 publications

(2 citation statements)

References 17 publications

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“…Parathyroid gland function in non-pHPT stone disease, especially in R-HC, is generally not elevated, although elevation has been reported [31]. Normal or low parathyroid gland func tion has been confirmed by others [32], but it may appear falsely elevated in non-pHPT subgroups when an antibody recognizing the bioinactive midregional part of the PTH molecule is used [33]. There is much confusion in the pertinent literature concerning phosphate metabolism (phosphate in serum, urine, renal threshold concentration) in calcium stone disease studied under widely varying cir cumstances.…”

Section: Classification and Metabolic State O F Participantsmentioning

confidence: 98%

Citrate in Urine and Serum and Associated Variables in Subgroups of Urolithiasis

Schwille

Scholz

Schwille

et al. 1982

Nephron

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Outpatient renal stone formers belonging to the established urolithiasis subgroups and controls were examined with respect to urinary and serum citrate (Cit) and several associated variables. Only in the normocalciuric majority of calcium and in uric acid stone formers was Cit in 24-hour urine decreased, but was normal in 2-hour fasting morning, and in 3-hour postprandial urine following a Cit-free test meal. Serum Cit was elevated in normocalciuria, renal and resorptive hypercalciuria. This Cit constellation was associated with either normal (absorptive, renal hypercalciuria) or low (normocalciuria, uric acid stone formers) parathyroid gland function as assessed by serum parathyroid hormone and nephrogenous urinary cyclic AMP, except in patients with primary hyperparathyroidism. In 2-hour morning urine the magnesium/creatinine ratio (normocalciuria) and ammonia excretion (uric acid stone formers) were decreased, while ammonia in 24-hour urine was low in all stone formers. It is suggested that Cit metabolism is altered in renal stone disease in general, and that in normocalciuria, stone inhibitors (Cit; magnesium) may be deficient.

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Section: Classification and Metabolic State O F Participantsmentioning

confidence: 98%

Citrate in Urine and Serum and Associated Variables in Subgroups of Urolithiasis

Schwille

Scholz

Schwille

et al. 1982

Nephron

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“…idiopathic recurrent calcium urolithiasis (RCT.J) with its two main calciuria subtypes (normocalciuria, NC; idiopathic hypercalciuria, I-HC) is not thoroughly understood. There are especially controversies with respect to serum parathyroid hormone (PTH) (Coe et al, 1973;Sutton and Walker, 1980), calcitonin (Kestenbaum et al, 1984) and calcium (Evans et al, 1984;Schwille et al, 1982) in I-HC, Differences in sex, age, body weight, dietary pretreatment in the populations studied as well as in the investigation tools may account for these discrepancies. There is agreement that oral loading with calcium leads to both suppression of PTH and stimulation of calcitonin secretion, and that the associated serum calcium reflects the body's tolerance toward exogenous calcium.…”

Section: Introductionmentioning

confidence: 99%

Fasting and Post-Calcium Load Serum Calcium, Parathyroid Hormone, Calcitonin, in Male Idiopathic Calcium Urolithiasis - Evidence for a Basic Disturbance in Calcium Metabolism

Schwille

Rümenapf²,

Schmidtler³

et al. 2009

Exp Clin Endocrinol Diabetes

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In male healthy controls (n = 12), male renal calcium stone patients with either normocalciuria (NC; n = 12) or idiopathic hypercalciuria (I-HC; n = 12), all ideally matched for age and body weight, the response of variables of mineral metabolism to a calcium-rich oral test meal was evaluated. In all groups the postprandial urinary cyclic AMP is decreased as compared with fasting urine, indicating that the parathyroid glands are suppressible by oral calcium. However, in I-HC serum total calcium was significantly higher than in controls both basally and in the postprandial period; the associated mid-regional (bioinactive) serum parathyroid hormone was also elevated, but serum parathyroid hormone recognizing the amino terminal (bioactive) region of the molecule was significantly decreased. Also in I-HC, serum alkaline phosphatase is elevated, whereas urinary hydroxyproline in both fasting and postprandial urine is unchanged. The NC group holds an intermediate position between I-HC and controls. It can be concluded that I-HC subjects may suffer from a more basic disturbance of calcium metabolism which may help explain the nature of their hypercalciuria.

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Postprandiale Hyperkalzurie und Hyperoxalurie bei rezidivierender Kalzium-Urolithiasis — Ausdruck einer Störung gastro-entero-pankreatischer Hormone?

Schwille

Hanisch

Scholz

et al. 1984

Pathogenese Und Klinik Der Harnsteine X

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Parathyroid gland function in subgroups of metabolically mediated urolithiasis as evaluated by serum parathyroid hormone, and urinary and nephrogenous cyclic nucleotides

Cited by 5 publications

References 17 publications

Citrate in Urine and Serum and Associated Variables in Subgroups of Urolithiasis

Citrate in Urine and Serum and Associated Variables in Subgroups of Urolithiasis

Fasting and Post-Calcium Load Serum Calcium, Parathyroid Hormone, Calcitonin, in Male Idiopathic Calcium Urolithiasis - Evidence for a Basic Disturbance in Calcium Metabolism

Postprandiale Hyperkalzurie und Hyperoxalurie bei rezidivierender Kalzium-Urolithiasis — Ausdruck einer Störung gastro-entero-pankreatischer Hormone?

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