Association of elevated serum PO(4), Ca x PO(4) product, and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients.
Hyperphosphatemia is highly prevalent among patients with end-stage renal disease (ESRD) and is associated with increased mortality risk in hemodialysis (HD) patients. The mechanism through which this mortality risk is mediated is unclear. Data from two national random samples of HD patients (n = 12,833) was used to test the hypothesis that elevated serum PO(4) contributes mainly to cardiac causes of death. During a 2-yr follow-up, the cause-specific relative risk (RR) of death for patients was analyzed separately for several categories of cause of death, including coronary artery disease (CAD), sudden death, and other cardiac causes, cerebrovascular and infection. Cox regression models were fit for each of the eight cause of death categories, adjusting for patient demographics and non-cardiovascular comorbid conditions. Time at risk for each cause-specific model was censored at death that resulted from any of the other causes. Higher mortality risk was seen for patients in the high PO(4) group (>6.5mg/dl) compared with the lower PO(4) group (< or =6.5mg/dl) for death resulting from CAD (RR 1.41; P < 0.0005), sudden death (RR 1.20; P < 0.01), infection (RR 1.20; P < 0.05), and unknown causes (RR 1.25; P < 0.05). Patients in the high PO(4) group also had non-significantly increased RR of death from other cardiac and cerebrovascular causes of death. The RR of sudden death was also strongly associated with elevated Ca x PO(4) product (RR 1.07 per 10 mg(2)/dl(2); P < 0.005) and serum parathyroid hormone levels greater than 495 pg/ml (RR 1.25; P < 0.05). This study identifies strong relationships between elevated serum PO(4), Ca x PO(4) product, and parathyroid hormone and cardiac causes of death in HD patients, especially deaths resulting from CAD and sudden death. More vigorous measures to reduce the prevalence of these factors in HD patients may result in improved survival.
Ganesh
Santhi K
SK
Division of Nephrology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan.
Stack
Austin G
AG
Division of Nephrology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan.|Renal Research Institute, New York, New York.|Kidney, Epidemiology, and Cost Center, University of Michigan, Ann Arbor, Michigan.
Levin
Nathan W
NW
Renal Research Institute, New York, New York.
Hulbert-Shearon
Tempie
T
Kidney, Epidemiology, and Cost Center, University of Michigan, Ann Arbor, Michigan.
Port
Friedrich K
FK
Division of Nephrology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan.|Renal Research Institute, New York, New York.|Kidney, Epidemiology, and Cost Center, University of Michigan, Ann Arbor, Michigan.
D000328:Adult; D000368:Aged; D002130:Calcium Phosphates / Q000097:blood*; D003327:Coronary Disease / Q000401:mortality; D016757:Death, Sudden, Cardiac; D005260:Female; D006331:Heart Diseases / Q000209:etiology* / Q000401:mortality*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood*; D010710:Phosphates / Q000097:blood*; D006435:Renal Dialysis / Q000009:adverse effects*; D012307:Risk Factors; D013997:Time Factors
D002130:Calcium Phosphates; D010281:Parathyroid Hormone; D010710:Phosphates; C485828:alpha-tricalcium phosphate; C485830:tetracalcium phosphate; C485838:calcium phosphate, monobasic, anhydrous; C020243:calcium phosphate; C485829:calcium phosphate, dibasic, anhydrous