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How abnormal calcium, phosphate, and parathyroid hormone relate to cardiovascular disease. (Continuing Education).

Mortality from cardiovascular disease in dialysis patients is 10 to 20 times higher than in the general population, with the relative risk being higher in younger patients and declining with age (see Figure 1), suggesting that cardiovascular disease develops prematurely (Levey & Eknoyan, 1999). As an example, patients with end stage renal disease (ESRD) aged 25-34 years are at similar absolute risk of death from cardiovascular disease as individuals without kidney disease aged 7.5 years. Cardiovascular mortality for ESRD patients far exceeds that predicted by classic risk factors, such as age, sex, hypertension, lipid abnormalities, cigarette smoking, and glucose intolerance. Other factors specific for renal disease are, therefore, likely to contribute to the high incidence of cardiovascular mortality.


The purpose of this article is to review the current literature relating abnormal calcium, phosphate and parathyroid hormone (PTH) to the development of cardiovascular disease in patients with chronic kidney disease (CKD).

Abnormal Calcium, Phosphate, and PTH in CKD

PTH starts to rise very early in the course of kidney disease (glomerular filtration rate less than 80 ml/min) (see Figure 2) (Martinez, Saracho, Montenegro, & Llach, 1997; Rix, Andreassen, Eskildsen, Langdahl, & Olgaard, 1999). As kidney disease progresses, plasma levels of vitamin D and calcium begin to decline, thus contributing to greater secretion of PTH. In addition, the retention of phosphate further increases PTH secretion independent of calcium and vitamin D levels. Continued stimulation of PTH secretion leads to irreversible parathyroid gland hyperplasia (Slatopolsky, Brown, & Dusso, 1999).


In a retrospective study of 6,407 patients on hemodialysis (Block, Hulbert-Shearon, Levin, & Port, 1998), serum phosphate levels greater than 6.5 mg/dl were observed in 39% of the patients, and products of serum calcium and phosphate above 72 [mg.sup.2]/[dl.sup.2] were observed in 20% of the patients. A serum phosphate level greater than 6.5 mg/dl was associated with a 27% higher mortality risk (see Figure 3), and a calcium-phosphate product greater than 72 [mg.sup.2]/[dl.sup.2] was associated with a 34% higher risk of death (see Figure 4).


In a separate study of 612 hemodialysis patients (Salem, 1997), 50% had PTH levels more than three times normal (mean 622 pg/ml), and in a Spanish study (Diaz-Corte et al., 1998) a nearly similar fraction of dialysis patients (approximately 40%) exhibited elevated PTH levels (greater than 250 pg/ml).

In the large study by Block et al. (1998), patients with PTH in the highest quintile (PTH > 511 pg/ml) appeared to have an 18% higher mortality risk than those with PTH between 34 and 91 pg/ml. To extend this relationship, Chertow et al. (2000) presented data from more than 40,000 hemodialysis patients that demonstrated a direct, linear relationship between PTH and mortality, with the highest risk found in the high PTH group. Avram et al. (2001) have reported, on the other hand, that an enrollment PTH level less than 65 pg/ml was an independent predictor of mortality in a study of 537 patients on hemodialysis and 422 patients on peritoneal dialysis. Furthermore, Coco and Rush (2000) found in a study of 1,272 patients on dialysis that patients with lower PTH levels had an earlier mortality than patients with higher PTH levels. Thus, it is still controversial how PTH levels relate to mortality rates in patients with CKD.

Cardiovascular Disease in Patients Who Have CKD

In a Canadian study of 433 patients (mean age 51 years) followed for a mean of 41 months from the start of ESRD therapy, clinical and echocardiographical cardiovascular disease was already present in a high proportion of the patients at the start of renal replacement therapy (Foley et al., 1995). Fourteen percent had verified coronary artery disease (a history of myocardial infarction, coronary artery bypass surgery, or percutaneous transluminal angioplasty), 19% had angina pectoris, 31% had cardiac failure, 7% had rhythm disorders requiring therapy, and 8% had peripheral vascular disease. The echocardiographic study revealed an even greater prevalence of cardiac abnormalities: 74% had left ventricular hypertrophy, 36% had left ventricular dilatation, and 15% had systolic dysfunction.

Among the 149 deaths observed during the follow-up period, 58% were attributed to cardiovascular disease: myocardial infarction (10%), sudden death (26%), other cardiac causes (11%), and other vascular disease (11%). It is evident from this study that cardiovascular disease is a primary cause of mortality in ESRD patients. Moreover, cardiovascular disease is already well established in patients at the start of dialytic therapy.

In a study of 94 autopsied cases of CKD (all non-diabetic), Clyne, Lins, and Pehrsson (1986) concluded that fatal myocardial infarction was not more common in the uremic patients than in the general population. Rather, most deaths among the patients were related to heart failure. The few angiographic studies of ESRD patients considered for renal transplantation have shown a great variation in the prevalence of significant coronary artery disease, ranging from 31% of asymptomatic hemodialysis patients (Ikram, Lynn, Bailey, & Little, 1983) to 88% of asymptomatic diabetic patients (Manske, Thomas, Wang, & Wilson, 1993). Interestingly, both Roig et al. (1981) in a study of 9 patients, and Rostand, Kirk, and Rutsky (1984) in a study of 34 patients made the observation that nearly 50% of ESRD patients with symptomatic ischemic heart disease had patent coronary arteries on angiography. Clearly, the pathogenesis of cardiovascular disease in CKD is more complex than in the general population.

Relationship of Abnormal Calcium, Phosphate, and PTH to Cardiovascular Disease

In addition to atherosclerosis, CKD is characterized by premature arterial stiffening. Blacher et al. (1999), who followed a cohort of 241 patients on hemodialysis for 11 years, showed that increased aortic stiffness (as assessed by pulse-wave velocity measurements) was a strong predictor of cardiovascular mortality. Stiffness of the aorta is associated with increased systolic blood pressure and decreased diastolic blood pressure, resulting in increased cardiac workload and reduced perfusion of the coronary arteries. Further, Guerin et al. (2000) found (by ultrasonography and pulse-wave velocity measurements) that arterial and aortic wall stiffness in 120 patients treated with hemodialysis was directly related to the presence and extent of arterial calcifications. Among the factors associated with increased wall stiffness was the prescribed dose of calcium-containing phosphate binder.

Recently, by using the technique of electron beam computed tomography, Goodman et al. (2000) and Braun et al.(1996) demonstrated a surprisingly large extent of calcification of coronary arteries in young and adult patients with ESRD as compared to age- and sex-matched non-ESRD controls, including those with angiographically-proven coronary artery disease. Moreover, calcifications progressed more quickly in the dialysis patients than in matched controls. The patients with the most extensive coronary artery calcifications in the study by Goodman et al. (2000) had higher serum levels of phosphate and higher calcium-phosphate products and were ingesting twice as much calcium in the form of calcium-containing phosphate binders than those without detectable calcium deposits. In the study by Braun et al. (1996), patients with the highest coronary calcium scores had higher PTH levels than those with lower scores, and the coronary calcium score was inversely correlated with bone mass in the dialysis patients. Coronary calcification is a strong predictor of coronary artery disease in persons without kidney disease. Although available evidence suggests that coronary artery calcification may be harmful in ESRD patients as well, this remains to be proven.

Valvular disease. Several studies have demonstrated a high prevalence of cardiac valve calcification in dialysis patients. In an echocardiographic study by Ribeiro et al. (1998), mitral calcification was seen in 45% of 92 hemodialysis patients as compared to 10% of normal subjects, and aortic calcification was noted in ,52% of dialysis patients as compared to 4% of controls. The prevalence of valvular insufficiency was 29.3% in patients with mitral calcification versus 5.8% in patients without mitral calcification, and 22% in patients with aortic calcificication versus 6% in patients without calcification. Mitral calcification was frequently associated with rhythm and cardiac conduction defects. Furthermore, dialysis patients with mitral valve (but not aortic valve) calcification had a significantly higher calcium-phosphate product than patients without calcification. In another study (Mazzaferro et al., 1993), mitral annulus calcification was detected in 39% of 225 hemodialysis patients and 16% of 67 CKD patients not yet on dialysis treatment, as compared to 9% of 67 normal controls. Like the Ribeiro et al. (1998) study, mitral calcification was again associated with an increased frequency of rhythm and conduction defects. In dialysis patients (but not predialysis patients), mitral annulus calcification was correlated to higher PTH levels. Huting (1994) similarly reported calcification of the mitral valves in 44% and of the aortic valves in 35% of 55 peritoneal dialysis patients. Mitral calcification was associated with valve regurgitation, reduced systolic left ventricular function, left ventricular dilatation, and higher calcium-phosphate product levels. Surprisingly, the mean calcium-phosphate product in those with mitral calcification was only 55 [mg.sup.2]/[dl.sup.2].

Myocardial disease. Congestive heart failure is a frequent complication of CKD. Rostand et al. (1988) utilized energy subtraction radiography of the chest to demonstrate that 43 dialysis patients had greater myocardial calcium content than control subjects. There was a strong positive correlation between myocardial calcium content and vascular calcification, previous parathyroidectomy, and calcium-phosphate product. Those patients with the highest myocardial calcium content had the lowest left ventricular ejection fraction values. Moreover, decreased ejection fraction was significantly associated with elevated PTH levels. Drueke et al. (1980) in a study of 23 hemodialysis patients found some improvement of the left ventricular myocardial function after parathyroidectomy.

Elevated PTH levels may contribute to cardiovascular morbidity and mortality in several additional ways. In rats, Baczynski et al. (1985) showed that long-term exposure to excess PTH was associated with severe abnormalities of myocardial energy metabolism. Further, Amann et al. (1994, 1995) demonstrated that parathyroidectomy prevented (and PTH administration restored) thickening of cardiac arteriolar walls and myocardial interstitial fibrosis in uremic rats. Arteriolar wall thickening may adversely affect the ability to vasodilate appropriately in response to a need for increased cardiac perfusion. Myocardial interstitial fibrosis may reduce cardiac compliance and predispose patients to intradialytic hypotension, pulmonary edema, and ventricular arrhythmias. Extensive myocardial interstitial fibrosis has previously been reported to be present in a large proportion of uremic patients (Mall, Huther, Schneider, Lundin, & Ritz, 1990). The limited effect of parathyroidectomy observed in some dialysis patients may in fact be related to irreversible changes such as myocardial fibrosis and arteriolar wall thickening.

Effect of parathyroid hormone on traditional cardiovascular risk factors. Elevated PTH levels in patients with CKD are associated with glucose intolerance, lipid abnormalities, and anemia (Bro & Olgaard, 1997), which are known cardiovascular risk factors in the general population. Thus, through these effects elevated PTH levels may indirectly worsen the cardiovascular risk profile in patients with CKD.

Conclusion and Recommendations

Elevated plasma phosphate, calcium-phosphate product, and PTH, and excess calcium load from long-term ingestion of high doses of calcium-containing phosphate binders are associated with an increased incidence of cardiovascular calcification and cardiovascular disease in patients with CKD. Further, elevated plasma phosphate and calcium-phosphate product are associated with increased mortality in these patients.

This new evidence suggests that an intensive approach to the prevention and treatment of these abnormalities may contribute to improved survival of patients with CKD. Evidently, current management shows limited effectiveness. Further, it also seems that the current recommendations for upper acceptable levels of phosphate, calcium-phosphate product, and PTH are inappropriate when it comes to cardiovascular health. Although it remains to be proven that the high incidence of cardiovascular disease in CKD may be reduced by early and more effective control of abnormal calcium, phosphate, and PTH, the results of these studies should not be awaited before starting to improve management. Until The National Kidney Foundation Dialysis Outcomes Quality Initiative (K/DOQI) develops new treatment goals and algorithms, it is advisable to follow the recent recommendations by Block and Port (2000) for plasma calcium, phosphate, calcium-phosphate product, and PTH levels (see Table 1). Block and Port view these levels as upper limits of acceptability, with optimal levels being as close to normal plasma values as can be achieved.

Early and continuous control and effective treatment are necessary to prevent secondary hyperparathyroidism and hyperphosphatemia. A phosphate restricted diet in combination with oral phosphate binders can prevent or reverse hyperphosphatemia and moderate degrees of hyperparathyroidism. Therefore, this is recommended as the initial therapy early in CKD (Slatopolsky Brown, & Dusso, 1999). As renal failure progresses, it will often be necessary to supplement with an active vitamin D analog to control the parathyroid gland function. Predialysis patients (and peritoneal dialysis and home hemodialysis patients) can benefit from the convenience of an oral formulation of doxercalciferol (Hectorol[R]) (Maung et al., 2001). The predialysis study by Hamdy et al. (1995) has demonstrated that early treatment with an active vitamin D analog is safe with regard to preservation of the remaining kidney function. For patients with a tendency to hypercalcemia, a non-calcium containing phosphate binder like sevelamer hydrochloride (RenaGel[TM]) should be considered (Slatopolsky, Burke, & Dillon, 1999). Patients on dialysis should be switched to low-calcium dialysis fluids (Bro, Brandi, Daugaard, & Olgaard, 1997). Calcimimetic drugs (i.e., pharmaceuticals that mimic the effect of calcium in suppressing PTH secretion [Andress, 1999]) are now available for patients with secondary hyperparathyroidism resistant or intolerant to conventional therapies.


Elevated plasma phosphate, calcium-phosphate product, and PTH, and excess calcium load from long-term ingestion of high doses of calcium-containing phosphate binders are associated with an increased incidence of cardiovascular calcification and cardiovascular disease in patients with CKD. Further, elevated plasma phosphate and calcium-phosphate product are associated with increased mortality in these patients. Current management show limited effectiveness. It also seems that the current recommendations for upper acceptable levels of phosphate, calcium-phosphate product, and PTH are inappropriate when it comes to cardiovascular health. More vigorous measures to control abnormal calcium, phosphate and PTH may result in improved survival.
Table 1

Revised Treatment Goals in Dialysis Patients

* Lower calcium-phosphate product to less than 55 [mg.sup.2]/[dl.sup.2]
* Lower phosphate range: 2.5-5.5 mg/dl
* Calcium in normal range or 9.2-9.6 mg/dl
* Lower PTH to 100-200 pg/ml

Acknowledgment: Writing of this review article was sponsored by an unrestricted educational grant from Bone Care International.


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Amann, K., Tornig, J., Flechtenmacher, C., Nabokov, A., Mall, G., & Ritz, E. (1995). Blood-pressure-independent wall thickening of intramyocardial arterioles in experimental uraemia: Evidence for a permissive action of PTH. Nephrology, Dialysis, Transplantation, 10, 2043-2048.

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Blacher, J., Guerin, A.P., Pannier, B., Marchais, S.J., Safar, M.E., & London, G.M. (1999). Impact of aortic stiffness on survival in end stage renal disease. Circulation, 99, 2434-2439.

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Coco, M., & Rush, H. (2000). Increased incidence of hip fractures in dialysis patients with low serum parathyroid hormone. American Journal of Kidney Diseases, 36, 1115-1121.

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Slatopolsky, E.A., Burke, S.K., & Dillon, M.A. (1999). RenaGel[TM], a nonabsorbed calcium- and aluminum-free phosphate binder, lowers serum phosphorus and parathyroid hormone. The RenaGel[TM] study group. Kidney International, 55, 299-307.

How Abnormal Calcium, Phosphate, and PTH Relate to Cardiovascular Disease

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Goal: Discuss how long-term imbalances in calcium, phosphate, and parathyroid hormone (PTH) relate to the development of cardiovascular disease in chronic kidney disease (CKD). hormone (PTH)
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   a. Discuss the prevalence of cardiovascular    1    2    3    4    5
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   b. Describe how abnormal plasma calcium,       1    2    3    4    5
      phosphate, and PTH levels affect
      cardiovascular function in patients
      with CKD.
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      phosphate, and PTH levels in patients on
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Susanne Bro, MD, PhD, is a Specialist in Nephrology, Righospitalet, University of Copenhagen, Copenhagen, Denmark.
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Publication:Nephrology Nursing Journal
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Date:Jun 1, 2003
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