Left Ventricular Hypertrophy

Achinger, Steven G.; Ayus, Juan Carlos

doi:10.1681/asn.2006080923

Cited by 62 publications

(52 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…16 Furthermore, evidence from hemodialysis patients suggests that lowering of serum phosphate may reduce LV mass. 29 These observations led to our hypothesis that, in early stage CKD, when phosphate levels are normal, reducing phosphate exposure using a noncalciumbased phosphate binder would have beneficial effects on both arterial stiffness and LV mass.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Effects of Sevelamer in Stage 3 CKD

Chue

Townend²,

Moody³

et al. 2013

Journal of the American Society of Nephrology

112

View full text Add to dashboard Cite

Serum phosphate independently predicts cardiovascular mortality in the general population and CKD, even when levels are in the normal range. Associations between serum phosphate, arterial stiffness, and left ventricular (LV) mass suggest a possible pathophysiological mechanism, potentially mediated by the phosphaturic hormone fibroblast growth factor-23 . To what extent the phosphate binder sevelamer modulates these effects is not well understood. In this single-center, randomized, double-blind, placebo-controlled trial, we enrolled 120 patients with stage 3 nondiabetic CKD. After a 4-week openlabel run-in period, during which time all patients received sevelamer carbonate, we randomly assigned 109 patients to sevelamer (n=55) or placebo (n=54) for an additional 36 weeks. We assessed LV mass and systolic and diastolic function with cardiovascular magnetic resonance imaging and echocardiography, and we assessed arterial stiffness by carotid-femoral pulse wave velocity. The mean age was 55 years, and the mean eGFR was 50 ml/min per 1.73 m 2 . After 40 weeks, we found no statistically significant differences between sevelamer and placebo with regard to LV mass, systolic and diastolic function, or pulse wave velocity. Only 56% of subjects took $80% of prescribed therapy; in this compliant subgroup, treatment with sevelamer associated with lower urinary phosphate excretion and serum FGF-23 but not serum phosphate, klotho, vitamin D, or cardiovascular-related outcomes of interest. In conclusion, this study does not provide evidence that sevelamer carbonate improves LV mass, LV function, or arterial stiffness in stage 3 nondiabetic CKD. Over the last decade, phosphate has emerged as an important cardiovascular risk factor. 1 Serum phosphate within the normal range independently predicted mortality in the Framingham Offspring Study. 2 CKD is the most common cause of abnormal phosphate handling, and the relationship between phosphate and adverse cardiovascular outcome was first identified in hemodialysis patients. 3,4 Additional studies have shown this relationship in early stage CKD, 5,6 type 2 diabetes mellitus, 7 and patients with coronary artery disease and normal renal function. 8 The strong association between serum phosphate and increased arterial stiffness 9 as well as increased left ventricular (LV) mass [10][11][12] suggests a potential mechanism, although the cellular processes remain unclear. The ability of the kidneys to excrete phosphate is reduced at a GFR below 60 ml/min per 1.73 m 2 . Serum phosphate, however, remains within the normal range until the GFR falls below 30 ml/min per 1.73 m 2 because of increased production of the phosphatonins parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF-23), which promote urinary phosphate excretion. 13,14 Recent data have linked

show abstract

Section: Discussionmentioning

confidence: 99%

Cardiovascular Effects of Sevelamer in Stage 3 CKD

Chue

Townend²,

Moody³

et al. 2013

Journal of the American Society of Nephrology

112

View full text Add to dashboard Cite

show abstract

“…9 Recent data suggest that hyperphosphatemia per se induces LVH and that correction of hyperphosphatemia may reduce LVH via a reversible pathway. 10 Isolated hyperphosphatemia in an animal model of chronic renal failure induced LVM, although no vascular calcification was observed. 11 Several biomarkers, such as B-type natriuretic peptide (BNP), cardiac troponin T (cTnT), and C-reactive protein (CRP), are predictors of mortality in patient with HD, 12, 13 and play an important role in the assessment of cardiovascular risk because each reflects a distinct aspect of the cardiac status.…”

Section: Fgf-23 and Lvh In Hd Patientsmentioning

confidence: 97%

Association Between Fibroblast Growth Factor 23 and Left Ventricular Hypertrophy in Maintenance Hemodialysis Patients - Comparison With B-Type Natriuretic Peptide and Cardiac Troponin T -

Negishi

Kobayashi

Ochiai

et al. 2010

Circ J

View full text Add to dashboard Cite

“…Furthermore, sevelamer and lanthanum are shown to reduce serum phosphate concentrations and ameliorate LV hypertrophy without changes in FGF23 levels in experimental animals [135,136]. Of interest, a strong association between serum phosphate concentrations and LV mass is demonstrated in humans [137,138] and animals [139], and hyperphosphatemia per se could be a potential risk factor causing cardiac hypertrophy [140,141]. Accordingly, the ability of phosphate binders to alleviate cardiac hypertrophy may vary, depending on the responsiveness of serum FGF23 and/or phosphate to these drugs.…”

Section: Ckd Ratsmentioning

confidence: 99%

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

Left Ventricular Hypertrophy

Cited by 62 publications

References 51 publications

Cardiovascular Effects of Sevelamer in Stage 3 CKD

Cardiovascular Effects of Sevelamer in Stage 3 CKD

Association Between Fibroblast Growth Factor 23 and Left Ventricular Hypertrophy in Maintenance Hemodialysis Patients - Comparison With B-Type Natriuretic Peptide and Cardiac Troponin T -

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

Contact Info

Product

Resources

About