1936
DOI: 10.1016/s0140-6736(00)79080-5
|View full text |Cite
|
Sign up to set email alerts
|

Death in Addison's Disease (Functional Renal Failure)

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
4
0

Year Published

1945
1945
2008
2008

Publication Types

Select...
4
3
1

Relationship

0
8

Authors

Journals

citations
Cited by 28 publications
(4 citation statements)
references
References 4 publications
0
4
0
Order By: Relevance
“…Since aldosterone facilitates renal acid excretion, its deficiency would be expected to result in renal acidification defects and, indeed, metabolic acidosis has been described in some patients with Addison's disease and in several with SHHH [4,5,10], The pathogenesis of this acidosis has not been studied systematically. That it may be related to mineralocorticoid deficiency is suggested by studies in adrenalectomized animals demonstrating defects in renal acidification that are corrected by desoxycorticosterone [7,8], Further indirect evidence for a mineralocorticoid deficiency-induced impairment of renal acidification has been obtained from the study of the effect of aldosterone antagonists [33], S ar to r iu s et al [8] and Y o sh im ur a et al [7] showed impaired excretion of titratable acid and ammonium in response to an acid load in adrenalectomized animals in spite of the excretion of urine of low pH (albeit somewhat higher than that of controls).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Since aldosterone facilitates renal acid excretion, its deficiency would be expected to result in renal acidification defects and, indeed, metabolic acidosis has been described in some patients with Addison's disease and in several with SHHH [4,5,10], The pathogenesis of this acidosis has not been studied systematically. That it may be related to mineralocorticoid deficiency is suggested by studies in adrenalectomized animals demonstrating defects in renal acidification that are corrected by desoxycorticosterone [7,8], Further indirect evidence for a mineralocorticoid deficiency-induced impairment of renal acidification has been obtained from the study of the effect of aldosterone antagonists [33], S ar to r iu s et al [8] and Y o sh im ur a et al [7] showed impaired excretion of titratable acid and ammonium in response to an acid load in adrenalectomized animals in spite of the excretion of urine of low pH (albeit somewhat higher than that of controls).…”
Section: Discussionmentioning
confidence: 99%
“…Mild to moderate metabolic acidosis may occur in patients with untreated Addison's disease [4,5], Although it has been suggested that these patients manifest impaired renal ammonium excretion [5], the pathogenesis of their acidosis has not been studied systematically. In adrenalectomized animals the capacity to excrete net acid and/or to generate steep urine to blood hydrogen ion gradients [6][7][8] is impaired while bicarbonate reabsorption is not de pressed [6].…”
Section: Introductionmentioning
confidence: 99%
“…Chan: First of all, should the hyperkalemia be come extremely severe, cardiac arrest may occur and indeed as early as 1936 sudden death was reported in Addison's disease [46], In addition, the long-term effects of persistent hyperchloremic metabolic acidosis, hypona tremia and hyperkalemia lead to complex metabolic changes resulting in growth failure. Although the serious ness of the electrolyte disorder may regress with age.…”
Section: Questions and Answersmentioning
confidence: 99%
“…In adrenalectomized animals or in patients with Addison's disease there is: (a) a marked decrease in liver glycogen (4,48); (b) an increased carbohydrate utilization (13,46,63); (c) a decreased deaminization in kidney tissue (32,53), a decreased rate of formation of carbohydrate from amino acids (45); a normal rate of deaminization (14,45), in the liver and a normal rate of formation of carbohydrate from glutamic acid (45); (d) a decreased conversion in the liver of lactic acid (7), pyruvate or succinate (45, 63) to glycogen; a normal rate of conversion of succinic and pyruvic acid to carbohydrate in the kidney (53); (e) a decreased rate of oxidation of pyruvate and succinate by liver (64) and kidney (53) slices; and (f) a decreased muscle performance (23).…”
Section: Fig 5 Response Inmentioning
confidence: 99%