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Dr. Kory  Tray  Md image

Dr. Kory Tray Md

85 Seymour St Ste 900
Hartford CT 06106
860 410-0700
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: 040113
NPI: 1336248368
Taxonomy Codes:
207RN0300X

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Publications

Idiopathic Infantile Hypercalcemia, Presenting in Adulthood--No Longer Idiopathic Nor Infantile: Two Case Reports and Review. - Connecticut medicine
We present two unrelated cases of young adults with hypercalcemia, hypercalciuria, and nephrocalcinosis. Both had suppressed intact parathyroid hormone levels and high 1,25 vitamin D levels after only brief, low-dose, over-the-counter vitamin supplementation. Neither had evidence of a granulomatous disorder. Their presentation mimicked that of 1,25 hydroxy vitamin D intoxication. In both patients, the diagnosis of idiopathic infantile hypercalcemia was confirmed with immeasurably low 24,25 vitamin D levels. Both were found to have a loss-of-function mutation in the CYP24A1 gene, which encodes the vitamin D-metabolizing enzyme 25-hydroxyvitamin D 24-hydroxylase.
Hepatic resection-related hypophosphatemia is of renal origin as manifested by isolated hyperphosphaturia. - Annals of surgery
The objective of this study was to elucidate and define the pathophysiological mechanism(s) responsible for the clinically relevant phenomenon of posthepatic resection hypophosphatemia.Although biochemically significant hypophosphatemia has been described after major hepatic resection, no mechanism or validated scientific explanation exists. The phenomenon is of considerable clinical relevance because numerous patients, after hepatic resection, develop significant hypophosphatemia requiring large doses of phosphate replacement to maintain metabolic homeostasis. This event has previously been empirically ascribed to amplified phosphate utilization of regenerating hepatocytes, although no rigorous data attest to this postulate. Recent data identifying a novel mechanism of phosphaturia in X-linked hypophosphatemic rickets, autosomal-dominant hypophosphatemic rickets, and oncogenic osteomalacia demonstrate that elevated levels of novel circulating phosphaturic factors such as fibroblast growth factor 23 (FGF-23) and PHEX are responsible for phosphate wasting. We hypothesize that posthepatectomy hypophosphatemia reflects a derangement of normal hepatorenal messaging and is the result of a disruption of renal phosphate handling consequent on aberrations in the metabolism of an as yet unrecognized chemical messenger(s) responsible for tubular phosphate homeostasis. This postulate has not previously been proposed or examined.Twenty patients undergoing hepatic resection were studied prospectively with respect to serum phosphate, phosphate requirements, as well as renal phosphate handling. Fractional excretion of phosphate was calculated on a daily basis. To confirm the relationship between phosphate loss and a circulating renal-targeted messenger, the plasma levels of the circulating phosphaturic factor FGF-23 were measured using a c-terminal assay both pre- and postoperatively.All patients developed hypophosphatemia with a nadir on postoperative day 2 (average drop of 47% despite phosphate administration). This phenomenon was associated with hyperphosphaturia (mean +/- standard error) with high fractional excretion of phosphate. A consistent change in FGF-23 was not identified.Hypophosphatemia after hepatic resection is a frequent occurrence. Transient isolated hyperphosphaturia and not increased phosphate utilization is the predominant cause of this phenomenon, although the identity of the agent involved remains to be identified.

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85 Seymour St Ste 900 Hartford, CT 06106
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