Increased Secretion of Potassium in the Rectum of Humans With Chronic Renal Failure

Martín, Roció Belén; Panese, Sergio A; Virginillo, Mirta; Gimenez, Marisa; Litardo, Maria; Arrizurieta, Elvira; Hayslett, John P.

doi:10.1016/s0272-6386(86)80120-2

Cited by 82 publications

(49 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, high serum potassium levels induce aldosterone release from adrenal cortical gland. In addition, previous studies demonstrated that plasma aldosterone concentrations were elevated in CKD [15,[26][27][28][29][30] and were correlated inversely with renal function [15] (Fig. 1).…”

Section: Aldosterone In Ckdmentioning

confidence: 70%

“…In subjects with intact kidney function, approximately 90% of potassium is excreted from the kidney where aldosterone contributes importantly to potassium excretion, and only 10% of potassium is secreted from the intestine. In patients with end-stage kidney disease, including dialysis patients, however, potassium secretion from the large intestine is considerably increased [29,34,35], in which K Ca 1.1 (BK) channels are largely involved [36]. Whereas aldosterone is shown to enhance the colonic BK channel activity [37,38] and contributes at least partly to the increased colonic potassium excretion [39], there are also reported several studies showing a modest role of aldosterone in colonic potassium secretion in both predialysis [29,40] and dialysis CKD patients [35].…”

Section: Aldosterone In Ckdmentioning

confidence: 99%

“…Caveat is in order, however, because of the potential risk for hyperkalemia when the blockers are given to CKD patients. Thus, potassium secretion from the intestine is increased in patients with advanced CKD or on dialysis therapy [29,34,35], and mineralocorticoid receptor blockers are reported to suppress this mechanism [38]. Indeed, several studies have reported that the administration of spironolactone is associated with increased incidence of hyperkalemia in patients on maintenance hemodialysis therapy [63][64][65] although pronounced hyperkalemia (serum potassium ≥ 6 mEq/L) does not occur commonly [66].…”

Section: Aldosterone Blockade In Ckdmentioning

confidence: 99%

See 2 more Smart Citations

Cardiac hypertrophy in chronic kidney disease—role of Aldosterone and FGF23

Hayashi

Suzuki²,

Sakamaki

et al. 2018

Ren Replace Ther

View full text Add to dashboard Cite

Cardiac hypertrophy is a life-threatening disorder and is frequently observed in patients with chronic kidney disease (CKD). Much attention has been focused on the derangement in hormonal factors, including aldosterone and FGF23, as novel causes of cardiac hypertrophy in CKD. Plasma aldosterone concentrations are elevated as renal function declines. Although aldosterone antagonists are available for the treatment of hypertension with cardiac hypertrophy, concern remains regarding the possible occurrence of serious hyperkalemia. Alternatively, certain types of calcium channel blockers suppress aldosterone synthesis or exert blocking action for mineralocorticoid receptors and could halt the progression of cardiac dysfunction. Recently, FGF23 is shown to be elevated as CKD progresses and may be responsible for the development of cardiac hypertrophy and heart failure. Furthermore, FGF23 not only inhibits the renal expression of angiotensin converting enzyme 2 but also enhances renin gene transcription, both of which could accelerate renin-angiotensin-aldosterone system. Although the increase in serum phosphate concentrations is a pivotal stimulus for FGF23 production, recent studies suggest that reduced iron status and elevated aldosterone levels, frequently seen in patients with CKD or on dialysis, might also contribute to the elevation in serum FGF23 levels. Conversely, phosphate binders and appropriate iron status could reduce serum FGF23, potentially leading to the alleviation of cardiac hypertrophy and heart failure. In conclusion, novel therapeutic strategies associated with aldosterone and FGF23 may confer a benefit in the management of cardiac disorders in CKD.

show abstract

Section: Aldosterone In Ckdmentioning

confidence: 70%

Section: Aldosterone In Ckdmentioning

confidence: 99%

Section: Aldosterone Blockade In Ckdmentioning

confidence: 99%

See 1 more Smart Citation

Cardiac hypertrophy in chronic kidney disease—role of Aldosterone and FGF23

Hayashi

Suzuki²,

Sakamaki

et al. 2018

Ren Replace Ther

View full text Add to dashboard Cite

show abstract

“…69 When uraemia develops, gastrointestinal secretion of potassium increases. 19,20,[205][206][207] When creatinine clearance is <20% normal, gastrointestinal potassium loss can approach 20% of intake. ~9 With progressive acidosis during uraemia, even mild extracellular shift forces can cause rapid hyperkalaemia.…”

Section: Renal Failurementioning

confidence: 99%

Potassium and anaesthesia

1993

View full text Add to dashboard Cite

show abstract

“…Colonic secretion of potassium also rises [7][8][9] in an adaptive response involving upregulation of the number of BK channels (i.e. 'big potassium' channels) present on the surface of colonic epithelial cells [10,11].…”

Section: Introductionmentioning

confidence: 99%

Recent advances in pharmacological treatments of hyperkalemia: focus on patiromer

Epstein

Pitt

2016

Expert Opinion on Pharmacotherapy

View full text Add to dashboard Cite

Introduction: Hyperkalemia is a common electrolyte disorder, especially among patients with chronic kidney disease (CKD), diabetes mellitus, or heart failure, and is associated with a significantly increased risk for all-cause mortality. Hyperkalemia remains a vexing and challenging problem for clinicians, particularly in the management of patients with chronic kidney disease and congestive heart failure. Several observational and retrospective studies have reported a large gap between recommendations in guidelines and real-world practice in the implementation of RAASi therapies. RAASi treatment regimens are frequently down-titrated or discontinued following hyperkalemia events, with consequent worse outcomes than patients who remain on maximum doses. Areas covered: This review covers the preclinical and clinical studies that led to the approval of patiromer for the treatment of hyperkalemia. A literature search on patiromer was carried out using the PubMed database up to December 2015. Expert opinion: Recently, patiromer was approved by the FDA as the first new potassium binder for the treatment of hyperkalemia in over 50 years. Based on the results of phase II and phase III studies, we conclude that patiromer is a well-tolerated and predictable medication to consistently and safely reduce serum potassium levels and to sustain normokalemia for periods up to 52 weeks in patients with diverse underlying diseases including congestive heart failure, and chronic kidney disease. Future research questions that should be evaluated are: the role of patiromer in treating hyperkalemia and the potential to thereby allow the optimal management of resistant hypertension and the use of high dose MRAs in patients with acute decompensated heart failure. Additional research is also warranted in the potential safety benefits of reducing potassium fluctuations in patients on hemodialysis as a result of treatment of hyperkalemia with patiromer. ARTICLE HISTORY

show abstract

Increased Secretion of Potassium in the Rectum of Humans With Chronic Renal Failure

Cited by 82 publications

References 13 publications

Cardiac hypertrophy in chronic kidney disease—role of Aldosterone and FGF23

Cardiac hypertrophy in chronic kidney disease—role of Aldosterone and FGF23

Potassium and anaesthesia

Recent advances in pharmacological treatments of hyperkalemia: focus on patiromer

Contact Info

Product

Resources

About