Erratum for Chang et al. High dietary phosphorus intake is associated with all-cause mortality: results from NHANES III. Am J Clin Nutr 2014;99:320–7.
In the published article, Tables 3 and 4 contain errors. The coefficients and P values above the knots actually represent the marginal change (i.e., the change in the slope from the preceding interval). For instance, it was incorrectly stated that phosphorus density ≥0.35 mg/kcal was associated with cardiovascular mortality (Table 4). Rather, the coefficients and P values show that the relation between phosphorus density and cardiovascular mortality significantly changes with phosphorus density ≥0.35 mg/kcal compared with phosphorus density <0.35 mg/kcal. However, there was no significant association between phosphorus density and cardiovascular mortality above 0.35 mg/kcal (corrected Table 4).
CORRECTED TABLE 3.
Adjusted HRs (95% CIs) of all-cause and CVD mortality according to absolute phosphorus intake1
| Model 1 |
Model 2 |
|||
| Adjusted HR (95% CI) | P | Adjusted HR (95% CI) | P | |
| All-cause mortality2 | ||||
| Below ln (1400 mg/d) | 0.78 (0.51, 1.20) | 0.2 | 0.96 (0.64, 1.43) | 0.8 |
| At or above ln (1400 mg/d) | 1.75 (1.05, 2.94) | 0.03 | 1.89 (1.03, 3.46) | 0.04 |
| CVD mortality2 | ||||
| Below ln (1400 mg/d) | 0.89 (0.42, 1.88) | 0.8 | 0.99 (0.46, 2.14) | 1.0 |
| At or above ln (1400 mg/d) | 0.94 (0.26, 3.37) | 0.9 | 1.02 (0.29, 3.58) | 1.0 |
Cox proportional hazards regression was used to estimate HRs of mortality by absolute phosphorus intake. Absolute phosphorus intake was log-transformed to achieve a more normal distribution and modeled continuously by using linear splines with a knot at ln (1400 mg/d) on the basis of evidence of a nonlinear relation. Model 1 was adjusted for age, sex, race, ethnicity, poverty:income ratio, and total energy intake. Model 2 was adjusted as for model 1 covariates and for BMI, systolic blood pressure, current and former smoking, physical activity, non-HDL cholesterol, log albumin:creatinine ratio, estimated glomerular filtration rate, and low vitamin D concentration. CVD, cardiovascular disease.
Continuous [per 1-unit increase in ln (phosphorus intake, mg/d)].
CORRECTED TABLE 4.
Adjusted HRs (95% CIs) of all-cause and CVD mortality according to phosphorus density1
| Model 1 |
Model 2 |
|||
| Adjusted HR (95% CI) | P | Adjusted HR (95% CI) | P | |
| All-cause mortality2 | ||||
| <0.35 mg/kcal | 0.36 (0.20, 0.66) | 0.001 | 0.46 (0.24, 0.89) | 0.02 |
| ≥0.35 mg/kcal | 1.03 (0.99,1.08) | 0.2 | 1.05 (1.01, 1.10) | 0.01 |
| CVD mortality2 | ||||
| <0.35 mg/kcal | 0.22 (0.10, 0.48) | <0.001 | 0.30 (0.13, 0.73) | 0.01 |
| ≥0.35 mg/kcal | 1.02 (0.94, 1.11) | 0.6 | 1.02 (0.93, 1.12) | 0.6 |
Cox proportional hazards regression was used to estimate HRs of mortality by phosphorus density. Phosphorus density was modeled as a continuous variable by using linear splines (knot at 0.35 mg/kcal, which corresponds to 700 mg for a 2000-kcal diet) on the basis of a visual inspection of locally weighted smoothing plots. Model 1 was adjusted for age, sex, race, ethnicity, poverty:income ratio, and total energy intake. Model 2 was adjusted as for model 1 covariates and for BMI, systolic blood pressure, current and former smoking, physical activity, non-HDL cholesterol, log albumin:creatinine ratio, estimated glomerular filtration rate, and low vitamin D concentration. CVD, cardiovascular disease.
Continuous [per 0.1-unit increase in phosphorus density (mg/kcal)].
The corrected Tables 3 and 4 are presented below. The figures and the remainder of the analyses remain correct.