Renal Effects of Calcitonin

Cochran, M.; Peacock, Munro; Sachs, George; Nordin, B.E.C.

doi:10.1136/bmj.1.5689.135

Cited by 72 publications

(38 citation statements)

References 17 publications

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“…In the pig, only very large doses of CT provoke phosphaturia (9) and no consistent results are obtained after PTX (6,9). Phosphaturia in man was detected by Bijvoet, Van der Sluys Veer, and Jansen (10) and their findings were subsequently confirmed by two groups of investigators (11,12). However, in all these patients secondary parathyroid stimulation may have accounted for the observed increase of phosphate excretion (UP).…”

Section: Introductionmentioning

confidence: 78%

“…After administration of the hormone this P is released immediately into the ECF, with a consequent initial rise of plasma P. In a close temporal relationship to the change of P excretion, all CT peptides produced a significant increase of CNa and CK. The natriuretic effect seems to be a regular finding both in experimental animals (4), in normal subjects, and in patients with metabolic bone disease (10)(11)(12)35). That we are dealing with a true hormonal effect was shown in the two patients given an ammonium phosphate infusion: the same degree of phosphaturia was obtained without significant changes of blood pH and serum cations, but the CP peak was not associated with a relevant increase of cation excretion (Fig.…”

Section: Discussionmentioning

confidence: 99%

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Renal effects of calcitonin and parathyroid extract in man

Haas¹,

Ma²,

Gunčaga³

et al. 1971

J. Clin. Invest.

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A B S T R A C T To clarify the controversial renal action of calcitonin (CT) and a possible interrelationship between CT and parathyroid hormone, eight patients with untreated surgical hypoparathyroidism were studied. Various calcitonins, i.e. extracted porcine, synthetic porcine, synthetic human, and synthetic salmon CT in doses of 150 Medical Research Council U or 1.5 mg were infused over a 3 hr period. Subsequently, six of the same subjects received 500 USP U parathyroid extract (PTE) (Eli Lilly & Co., Indianapolis, Ind.) in 3 hr and later a combination of CT and PTE. In addition, two patients were given an infusion of ammonium phosphate with the aim of producting a phosphaturia of comparable degree as seen after CT and PTE, thus differentiating hormonal from nonhormonal influences on cation excretion. A protocol of serial clearance (C) studies using the patients as their own controls was followed. Serum and urinary inorganic phosphate (P), calcium (Ca), magnesium (Mg), sodium (Na), potassium (K), and creatinine (Cr) were determined and the clearance values calculated.All

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Section: Introductionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Renal effects of calcitonin and parathyroid extract in man

Haas¹,

Ma²,

Gunčaga³

et al. 1971

J. Clin. Invest.

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“…There are certain findings which would indicate that parathormone affects the tubular reabsorption of amino acids. Hillman et al [37] described an infant with neonatal hyperparathyroidism who demonstrated hyperaminoaciduria; similar findings also have been reported in patients with hyperparathyroidism [10,17]. In the first case [10], hyperaminoaciduria disappeared after resection of the adenomas; in the latter [47], however, it persisted despite parathyroidectomy.…”

Section: Discussionmentioning

confidence: 68%

“…This, indeed, has been questioned [21,32]. Phosphaturia can be produced by factors other than parathyroid extract, for example, extracellular volume expansion [24,48,66,67], thyrocalcitonin [2,17,26,61], cortisone [60], infusion of glucose [38,53], sodium bicarbonate [25], or glycine and alanine [7]. Furthermore, calcium might exhibit its inhibitory effect on phosphate excretion by direct action on renal tubules, as suggested by the findings of Lavender and Pullman [44].…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Deficiency Rickets: Renal Handling of Phosphate and Free Amino Acids

Brodeiil¹,

Kaas²,

Weber³

1971

Pediatr Res

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ExtractHypophosphatemia, hyperphosphatasemia, and phosphate diabetes in vitamin D deficiency rickets are considered to be due to secondary hyperparathyroidism. It is still questionable whether hyperaminoaciduria in rickets also may be due to hyperparathyroidism. In an attempt to clarify the pathomechanism of tubular transport of phosphate and free amino acids in humans with rickets, clearance studies were performed in three infants (3.5-5 months of age) with mild rickets and in six infants (21 -25 months of age) with severe rickets. In three of the six with severe rickets clearance studies were repeated after 58, 70, and 111 days, respectively, of treatment with vitamin D. Glomerular filtration rate was estimated by use of inulin. Free amino acids in serum and urine were determined by ion exchange column chromatography. It was considered essential to use age-matched control values for comparison.Infants with mild and severe rickets had significantly lowered values of serum phosphate, elevated values for phosphate clearance, and a decrease in percentage tubular reabsorption of phosphate. Comparison of both groups revealed that there were no quantitative differences in the degree of disturbed phosphate metabolism between mildly and severely affected infants if the data of each group were related to agematched control values. The glomerular filtration rate was normal or elevated in both groups, with higher values in the group suffering from severe rickets.Concentrations of free amino acids in serum of infants with rickets were not significantly different from those found in normal subjects. Endogenous clearance rates and excretion levels of amino acids into urine were significantly higher than normal values in both groups. The percentage tubular reabsorption was correspondingly lower. The degree of hyperaminoaciduria was much higher in infants with severe rickets than in those with mild rickets when related to age-matched controls.Individual amino acids show great differences of involvement in vitamin D deficiency rickets; there were, however, no differences found between mild and severe rickets in this respect. The transport of the following amino acids was most severely involved: threonine, serine, glycine, cystine, tyrosine, lysine, and histidine. Some amino acids are either not involved or only to a slight degree: valine, isoleucine, leucine, ornithine, and arginine. The actual values of percentage tubular reabsorption were almost the same in the young and older infants with rickets, which demonstrates the influence of age on the degree of hyperaminoaciduria.There was no correlation evident between urinary excretion rates of free amino acids and hypophosphatemia, between the ratio of amino acid clearance to inulin clearance (C AA /C In ) and the serum phosphate level, and between C AA /Ci n and the ratio of phosphate clearance to inulin clearance (C P /C In ). The only significant correlation found was between inulin clearance and amino acid clearance. Clearance studies were repeated in three infants with sever...

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“…Some reports [35] conclude that CT results in increased renal clearance of calcium; other reports [36] conclude that CT results in decreased renal clearance of calcium. Since the latter is inconsistent with its being a factor in the hypocalcemic role of CT, it is presumed that the effect of CT on bone is the major action for CT hypocalcemia.…”

Section: Ct Effects On Bone Citratementioning

confidence: 99%

Untitled

2016

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The homeostatic maintenance of a normal plasma citrate concentration is an important factor in humans and in animals; and is required for many normal physiological activities. Dysregulation of normal plasma citrate presents pathophysiological hypocitricemic or hypercitricemic conditions. This can lead to clinical consequences in many areas of medicine; such as impaired blood clotting, altered acid/base status, impaired neuromuscular/cardiac activities, hypocitraturia and stone formation, bone disorders with loss of bone strength and increased fractures, hypocitricemia of surgical stress. These important implications of citrate relationships have been largely ignored by the contemporary clinical and biomedical community; to the extent that it is not even described in most current textbooks and review papers. This review describes the physiological, endocrine, and metabolic relationships in the normal regulation and maintenance of plasma citrate; and presents some important clinical consequences of its dysfunctional maintenance. The importance of bone, kidney and liver activities in the maintenance of normal plasma citrate is described along with the citricemic roles of parathyroid hormone, calcitonin and vitamin D. These factors and relationships are presented as the contemporary understanding of the integrated regulation of plasma citrate as the basis for its clinical importance in medicine. The exclusion of these citrate relationships leads to misunderstanding and misrepresentation of physiological and clinical conditions in many issues in medicine and paramedicine areas. The intent of this review is to revive the interest and support for research to address the many unknown and speculative issues of plasma citrate regulation and its important clinical implications. This is in the best interest of the medical community and the public-at-large.Keywords: Calcitonin and parathyroid hormone; Citrate and clinical disorders; Liver citrate clearance; Osteoblast citrate production; Plasma citrate regulation; Renal citrate clearance; Surgical stress hypocitricemia; Vitamin D and citrate Citation: Costello LC, Franklin RB (2016) Plasma Citrate Homeostasis: How It Is Regulated; And Its Physiological and Clinical Implications. An Important, But Neglected, Relationship in Medicine. J Hum Endocrinol 1: 005. • the maintenance of normal plasma citrate concentration. This is evident from the normocitricemia that exists despite the large variations in the citrate content of the diets of humans, which often contain minimal citrate. In animals with food supply containing minimal citrate, normocitricemia is well maintained. As such, other sources of citrate must exist, if or when the availability of dietary citrate is insufficient to maintain the normal plasma citrate.Soft tissue metabolic production of citrate as a source of plasma citrate ( Figure 1C): All cells synthesize citrate as the initial metabolic step in the Krebs cycle ( Figure 2). Typically in most cells, citrate is retained in the mitochondria for its entr...

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Renal Effects of Calcitonin

Cited by 72 publications

References 17 publications

Renal effects of calcitonin and parathyroid extract in man

Renal effects of calcitonin and parathyroid extract in man

Vitamin D Deficiency Rickets: Renal Handling of Phosphate and Free Amino Acids

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