Blood pressure and phosphate level in diabetic and non-diabetic kidney disease: Results of the cross-sectional “Low Clearance Consultation” study

Mendes, Margarida; Resende, Luís; Teixeira, Alves; Correia, J.; Silva, Gil

doi:10.1016/j.pbj.2017.02.005

Cited by 7 publications

(8 citation statements)

References 14 publications

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“…An increasing number of publications has revealed a detrimental role of inorganic phosphate in promoting hypertension in otherwise healthy individuals. Cross-sectional studies in patients with end-stage renal disease showed that the presence of hyperphosphatemia was significantly associated with high blood pressure ( Mendes et al, 2017 ). Hyperphosphatemia was associated with a blunted decline in nocturnal blood pressure in hypertensive patients without CKD ( Wang et al, 2018 ).…”

Section: The Role Of Phosphate In Cvdmentioning

confidence: 99%

“…Adeney et al analyzed 439 patients with moderate to severe CKD and found that the incidence of calcification in the coronary artery and descending aorta increased by 21 and 33%, respectively, with the increase of blood phosphate every 1 mg/dL ( Sarnak et al, 2019 ). The prospective cohort study, CRIC, included 1,123 patients with mild to moderate CKD (EGFR 20–70 ml/min/1.73 m 2 ), and demonstrated that serum phosphate > 3.9 mg/dL was significantly associated with coronary artery calcification ( Mendes et al, 2017 ; Bundy et al, 2018 ). Shang et al (2017) selected 70 peritoneal dialysis patients without coronary artery calcification as the research objects, followed up for at least 3 years, and revealed that hyperphosphatemia was an independent risk factor for coronary artery calcification in dialysis patients.…”

Section: The Role Of Phosphate In Cvdmentioning

confidence: 99%

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Hyperphosphatemia and Cardiovascular Disease

Zhou

Shi

Ouyang

et al. 2021

Front. Cell Dev. Biol.

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Hyperphosphatemia or even serum phosphate levels within the “normal laboratory range” are highly associated with increased cardiovascular disease risk and mortality in the general population and patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the development of hypertension, vascular calcification, cardiac valvular calcification, atherosclerosis, left ventricular hypertrophy and myocardial fibrosis by distinct mechanisms. Therefore, phosphate is considered as a promising therapeutic target to improve the cardiovascular outcome in CKD patients. The current therapeutic strategies are based on dietary and pharmacological reduction of serum phosphate levels to prevent hyperphosphatemia in CKD patients. Large randomized clinical trials with hard endpoints are urgently needed to establish a causal relationship between phosphate excess and cardiovascular disease (CVD) and to determine if lowering serum phosphate constitutes an effective intervention for the prevention and treatment of CVD.

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Section: The Role Of Phosphate In Cvdmentioning

confidence: 99%

Section: The Role Of Phosphate In Cvdmentioning

confidence: 99%

Hyperphosphatemia and Cardiovascular Disease

Zhou

Shi

Ouyang

et al. 2021

Front. Cell Dev. Biol.

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“…The prevalence of hypertension increases with decreasing GFR in CKD patients [44]. This is at least partly because of high FGF23 and phosphate levels, as several clinical studies showed an association between increased serum FGF23 or phosphate and the presence of hypertension in CKD patients, as well as in non-CKD populations [45,46,47,48,49]. The ARIC (Atherosclerosis Risk in Communities) study evaluated the correlation of serum intact FGF23 levels and the development of hypertension in a large cohort of 7948 middle-aged (45–64 years) participants without previous hypertension during a median follow-up of 5.9 years.…”

Section: The Role Of Fgf23 and Phosphate In Ckd-associated Cardiovmentioning

confidence: 99%

“…However, this study did not allow any conclusions on whether serum phosphate levels directly correlate with hypertension, because only baseline phosphate levels were measured in the beginning of the study [55]. In a small study of 30 diabetic CKD and 23 non-diabetic CKD patients, serum phosphate levels correlated with increased systolic and diastolic BP in diabetic CKD, but not in non-diabetic CKD patients [48]. Recently, a prospective randomized study investigated the effects of controlled inorganic phosphate (P i ) uptake on BP in 20 healthy young adults.…”

Section: The Role Of Fgf23 and Phosphate In Ckd-associated Cardiovmentioning

confidence: 99%

FGF23 and Phosphate–Cardiovascular Toxins in CKD

Vogt

Haffner

Leifheit-Nestler

2019

Toxins

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Elevated levels of fibroblast growth factor 23 (FGF23) and phosphate are highly associated with increased cardiovascular disease and mortality in patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the secretion of the phosphaturic hormone FGF23. In early stages of CKD, FGF23 prevents the increase of serum phosphate levels and thereby attenuates phosphate-induced vascular calcification, whereas in end-stage kidney disease, FGF23 fails to maintain phosphate homeostasis. Both hyperphosphatemia and elevated FGF23 levels promote the development of hypertension, vascular calcification, and left ventricular hypertrophy by distinct mechanisms. Therefore, FGF23 and phosphate are considered promising therapeutic targets to improve the cardiovascular outcome in CKD patients. Previous therapeutic strategies are based on dietary and pharmacological reduction of serum phosphate, and consequently FGF23 levels. However, clinical trials proving the effects on the cardiovascular outcome are lacking. Recent publications provide evidence for new promising therapeutic interventions, such as magnesium supplementation and direct targeting of phosphate and FGF receptors to prevent toxicity of FGF23 and hyperphosphatemia in CKD patients.

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“…Cross-sectional studies in patients with end-stage renal disease showed that the presence of hyperphosphatemia was significantly associated with high BP [14], LV hypertrophy [15], LV diastolic dysfunction [15], heart failure with preserved ejection fraction [16], as well as stroke [17]. A meta-analysis of 7 cohort studies also has demonstrated an association between elevated serum Pi and increased risk of all-cause mortality in the CKD population [18*].…”

Section: Role Of Dietary Pi Excess In Bp Regulationmentioning

confidence: 99%

Phosphate, the forgotten mineral in hypertension

Kim¹,

Mizuno²,

Vongpatanasin

2019

Current Opinion in Nephrology and Hypertension

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Purpose of review: To review the current literature related to the role of inorganic phosphate (Pi) in the pathogenesis of hypertension Recent findings: An increasing number of publications has revealed a detrimental role of inorganic Pi, which is commonly used as a flavor enhancer or preservative in the processed food, in promoting hypertension in otherwise healthy individuals. Animal experimental data indicate that dietary Pi excess engages multiple mechanisms that promote hypertension, including overactivation of the sympathetic nervous system, increased vascular stiffness, impaired endothelium-dependent vasodilation, as well as increased renal sodium absorption or renal injury. These effects may be explained by direct effects of high extracellular Pi levels or increase in phosphaturic hormones such as fibroblast growth factor 23 (FGF23), or downregulation of klotho, a transmembrane protein expressed in multiple organs which possess anti-aging property. Summary: Dietary Pi, particularly inorganic Pi, is an emerging risk factor for hypertension which is ubiquitous in the western diet. Large randomized clinical trials are needed to determine if lowering dietary Pi content constitutes an effective nonpharmacologic intervention for prevention and treatment of hypertension.

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Blood pressure and phosphate level in diabetic and non-diabetic kidney disease: Results of the cross-sectional “Low Clearance Consultation” study

Cited by 7 publications

References 14 publications

Hyperphosphatemia and Cardiovascular Disease

Hyperphosphatemia and Cardiovascular Disease

FGF23 and Phosphate–Cardiovascular Toxins in CKD

Phosphate, the forgotten mineral in hypertension

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