Please use this identifier to cite or link to this item: https://hdl.handle.net/1/140
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dc.contributor.authorBency, Rosammaen
dc.contributor.authorRoger, Simon Den
dc.contributor.authorElder, Grahame Jen
dc.date2011-03en
dc.date.accessioned2015-03-30T23:50:22Zen
dc.date.available2015-03-30T23:50:22Zen
dc.date.issued2011-05en
dc.identifier.citationVolume 26, Issue 5, pp. 1740-1742en
dc.identifier.issn0931-0509en
dc.identifier.urihttps://elibrary.cclhd.health.nsw.gov.au/cclhdjspui/handle/1/140en
dc.descriptionOpen Access: http://ndt.oxfordjournals.org/content/26/5/1740.shorten
dc.description.abstractFollowing renal transplantation, hypercalcaemia is frequently caused by persisting hyperparathyroidism. Unregulated extrarenal 1,25-dihydroxyvitamin D (1,25(OH)2D) synthesis, which is well recognized as a cause of hypercalcaemia in granulomatous diseases, may also occur after kidney transplantation. This mechanism is also likely to be responsible for hypercalcaemia reported during treatment of cytomegalovirus and associated with acute symptomatic pneumocystis jivorecii pneumonia (PCP). Hypercalcaemia as a prodromal feature of indolent PCP has not been described. We report a renal transplant recipient who developed hypercalcaemia 30 months post-transplant due to extrarenal production of 1,25(OH)2D. Two months later, PCP was diagnosed and hypercalcaemia resolved after initiation of treatment.en
dc.subjectKidney Transplanten
dc.titleHypercalcaemia as a prodromal feature of indolent pneumocystis jivorecii after renal transplantationen
dc.typeJournal Articleen
dc.identifier.doi10.1093/ndt/gfr051en
dc.description.pubmedurihttp://www.ncbi.nlm.nih.gov/pubmed/21378150en
dc.identifier.journaltitleNephrology Dialysis Transplantationen
dc.originaltypeTexten
item.cerifentitytypePublications-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
Appears in Collections:Renal Medicine
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