Linked Life Data

188961

Source:http://linkedlifedata.com/resource/pubmed/id/188961

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1977-3-15
pubmed:abstractText
A unique 53-year-old male patient is described in whom aldosterone-refractory hyperkalemia and renal tubular acidosis/RTA/ was due to chronic interstitial nephritis associated with peritubular hyaline deposits in the distal nephron. Hyperkalemia was not caused by an adrenal disorder or acidosis and could not be abolished by interventions enhancing K clearance; saline infusions, high doses of furosemide, cortisone, cortisol, long-acting synthetic ACTH and excessive doses of aldosterone. Glucocorticoids induced a marked decrease in sodium excreting capacity probably by an action on the ascending limb of Henle's loop while aldosterone elicited a paradoxical natriuretic response by unknown mechanism. The results of our experimental studies carried out on the hyperkalemic RTA patient as well as on various control subjects and patients suggest 1. a specific defect in renal K excretion associated with decreased aldosterone responsiveness of the tubules presumably due to the peritubular pathology, and 2. a disturbance in the cellular regulation of K distribution between fluid compartments of unknown origin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0025-7850
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
481-510
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1976
pubmed:articleTitle
Hyperkalemia unresponsive to massive doses of aldosterone and renal tubular acidosis in a patient with chronic interstitial nephritis: clinical and experimental studies.
pubmed:publicationType
Journal Article, Case Reports