Spironolactone to Prevent Peritoneal Fibrosis in Peritoneal Dialysis Patients: A Randomized Controlled Trial

Vázquez-Rangel, Armando; Soto, Virgilia; Escalona, Marco; Toledo, Rafael; Castillo, Edgar; Flores, Nasser Abdel Polanco; Falcon-Chavez, Ilse; Madero, Magdalena

doi:10.1053/j.ajkd.2014.01.426

Cited by 18 publications

(11 citation statements)

References 7 publications

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“…Moreover, fibrosis is increasingly appreciated as a major player in adipose tissue dysfunction (Divoux and Clement, 2011). Recent reports indicate that spironolactone limits peritoneal fibrosis in rats, opening up the possibility to improve the efficiency of peritoneal dialysis (Vazquez-Rangel et al, 2014;Yelken et al, 2014;Zhang et al, 2014). In addition, spironolactone may be beneficial for the cardiovascular function of these patients (Ito et al, 2014).…”

Section: Mineralocorticoid Receptor Activation Leads To Fibrosismentioning

confidence: 99%

Emerging Roles of the Mineralocorticoid Receptor in Pathology: Toward New Paradigms in Clinical Pharmacology

2015

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Section: Mineralocorticoid Receptor Activation Leads To Fibrosismentioning

confidence: 99%

Emerging Roles of the Mineralocorticoid Receptor in Pathology: Toward New Paradigms in Clinical Pharmacology

2015

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“…Vazquez-Rangel et al [73] 9 PD patients Spironolactone 25 mg/day 6 months CD20 and collagen IV levels in peritoneal biopsy specimens decreased.…”

Section: Effects Of Mr Antagonists In Peritoneal Dialysis Patients Camentioning

confidence: 97%

“…After spironolactone administration, mean dialysate cancer antigen 125 significantly increased (P = 0.028), while the potassium level did not change significantly (4.3 ± 0.5 at baseline vs 4.4 ± 0.6 mEq/l after 6 months, P = 0.488). Vazquez-Rangel et al [73] conducted a randomized, double-blinded, placebo-controlled study. Nine PD patients received spironolactone at 25 mg/day for 6 months and underwent peritoneal biopsies when the PD catheter was placed and at the conclusion of follow-up.…”

Section: Protective Effects On the Peritoneal Membrane In Pd Patientsmentioning

confidence: 99%

Mineralocorticoid receptor antagonists in dialysis patients

et al. 2016

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Mineralocorticoid receptor (MR) antagonists are known to have beneficial effects in patients with cardiovascular disease without renal failure. However, there have been few published studies on the effectiveness of MR antagonists in dialysis patients, and most of the studies were small-sized. The present review focuses on the effectiveness of MR antagonists and the risk of hyperkalemia in dialysis patients. Severe hyperkalemia due to treatment with MR antagonists in dialysis patients is not common, particularly in peritoneal dialysis (PD) patients, and the prospect of cardioprotective effects has been hopeful in both hemodialysis (HD) and PD patients. Further studies are required to establish optimal protocols for the use of MR antagonists in these patients without adverse effects.

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“…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]. Notably, there are also reported a substantial number of studies showing that spironolactone does not cause significantly higher levels of serum potassium in patients on hemodialysis [47][48][49] or peritoneal dialysis therapy [50,51,67,68], when compared with placebo (Table 1). Taken together, the use of aldosterone blockers is teleologically reasonable in terms of cardiovascular protection, although the adverse effect of these blockers might hamper the wide-spread use of this type of agents in patients with CKD.…”

Section: Aldosterone Blockade In Ckdmentioning

confidence: 99%

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

Hayashi

Suzuki²,

Sakamaki

et al. 2018

Ren Replace Ther

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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.

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Spironolactone to Prevent Peritoneal Fibrosis in Peritoneal Dialysis Patients: A Randomized Controlled Trial

Cited by 18 publications

References 7 publications

Emerging Roles of the Mineralocorticoid Receptor in Pathology: Toward New Paradigms in Clinical Pharmacology

Emerging Roles of the Mineralocorticoid Receptor in Pathology: Toward New Paradigms in Clinical Pharmacology

Mineralocorticoid receptor antagonists in dialysis patients

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

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