Key result
Higher serum phosphate independently predicted a greater decline in eGFR (0.34 mL/min/month steeper decline per 1 mmol/L increment, P=0.02) in patients with early chronic kidney disease.
Why the study?
Do serum phosphate and markers of arterial stiffness predict progression of renal dysfunction in patients with early CKD?
Cohort (n=225)
No
Do serum phosphate and markers of arterial stiffness predict progression of renal dysfunction in patients with early CKD?
Effect estimate: 0.34 mL/min/month steeper decline per 1 mmol/L increment
p-value: p=0.02
Phosphate may aid risk stratification in early CKD; hypothesis-generating and should not yet change practice or support stiffness assessment.
BACKGROUND: The rate of decline in kidney function is a powerful predictor of cardiovascular risk in patients with chronic kidney disease (CKD). Serum phosphate and increased arterial stiffness are associated with elevated cardiovascular risk in CKD and the general population. We sought to determine whether serum phosphate and markers of arterial stiffness predict progression of renal dysfunction in patients with early CKD. METHODS: Two hundred and twenty-five patients with Stage II-IV CKD were prospectively followed up at University Hospital Birmingham. Serum phosphate was measured at baseline and arterial stiffness was determined through measurement of aortic pulse wave velocity (PWV) and augmentation index (AIx). Progression of renal dysfunction was defined as the slope of estimated glomerular filtration rate (eGFR) against time. We determined the associations between possible predictors and rate of progression and also examined a combined end point of start of dialysis or ≥ 25% decline in eGFR. RESULTS: Mean baseline eGFR was 43 ± 19 mL/min/1.73 m(2) and serum phosphate 1.22 ± 0.27 mmol/L. Median follow-up was 924 days. Serum phosphate independently predicted a greater decline in eGFR; a 1 mmol/L increment in serum phosphate was associated with a 0.34 mL/min/month steeper decline (P = 0.02). Brachial and aortic systolic pressure independently predicted the rate of renal function decline but aortic PWV and AIx had no significant influence. Forty-one patients (18%) reached the combined end point; serum phosphate was significantly higher in this group (1.32 ± 0.36 versus 1.19 ± 0.24 mmol/L, P = 0.04) and was an independent predictor for the combined end point. CONCLUSIONS: Serum phosphate independently predicts decline in renal function in early CKD. Further studies are required to determine the mechanisms involved and to investigate the potential benefits of phosphate lowering on preserving kidney function.
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Chue et al. (2011) conducted a cohort in Stage II-IV chronic kidney disease (n=225). Serum phosphate vs. Lower serum phosphate was evaluated on Progression of renal dysfunction (slope of eGFR against time) (0.34 mL/min/month steeper decline per 1 mmol/L increment, p=0.02). Higher serum phosphate independently predicted a greater decline in eGFR (0.34 mL/min/month steeper decline per 1 mmol/L increment, P=0.02) in patients with early chronic kidney disease.
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