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Relationship of High-Density Lipoprotein Cholesterol With Renal Function in Patients Treated With Atorvastatin
Kwok Leung Ong1, David D Waters2, Rana Fayyad3
1School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia kwokleung.ong@unsw.edu.au.
Insights
In patients taking atorvastatin, higher high-density lipoprotein (HDL) cholesterol levels protected against kidney function decline in those with normal baseline kidney function. Further research is needed to confirm a causal link between HDL and renal health.
Area of Science:
- Cardiology
- Nephrology
- Pharmacology
Background:
- The relationship between high-density lipoprotein (HDL) cholesterol and renal function in patients receiving statins is not well understood.
- Investigating this association is crucial for understanding cardiovascular and renal health outcomes in statin-treated populations.
Purpose of the Study:
- To determine if HDL cholesterol levels predict renal function in patients treated with atorvastatin.
- To analyze the impact of HDL cholesterol on estimated glomerular filtration rate (eGFR) decline within the Treating to New Targets (TNT) trial.
Main Methods:
- Analysis of 9542 participants from the TNT trial.
- Assessment of renal function using estimated glomerular filtration rate (eGFR).
- Measurement of HDL cholesterol levels at month 3, when they stabilize during atorvastatin treatment.
Main Results:
- In patients with normal baseline eGFR (≥60 mL/min per 1.73 m²), higher HDL cholesterol levels at month 3 were significantly associated with a lower risk of eGFR decline.
- For participants with normal baseline eGFR, increasing HDL cholesterol quintiles showed a trend towards reduced risk of renal function decline (P for trend=0.006).
- In patients with impaired baseline eGFR (<60 mL/min per 1.73 m²), HDL cholesterol levels had a less pronounced impact on eGFR during follow-up, with significance only observed when analyzed continuously (P=0.043).
Conclusions:
- Higher HDL cholesterol levels are linked to a reduced risk of kidney function decline in atorvastatin-treated patients with normal baseline renal function.
- The study suggests a protective role of HDL cholesterol in maintaining renal function in this cohort.
- Further investigation is required to establish a causal relationship between HDL cholesterol and renal function preservation.
Background:
It is not known whether the concentration of high-density lipoprotein (HDL) cholesterol is related to renal function in statin-treated patients. We therefore investigated whether HDL cholesterol levels predicted renal function in atorvastatin-treated patients in the TNT (Treating to New Targets) trial.
Methods And Results:
A total of 9542 participants were included in this analysis. Renal function was assessed by estimated glomerular filtration rate (eGFR). HDL cholesterol levels at month 3 were used as this is the time point at which on-treatment HDL cholesterol levels became stable. Among 6319 participants with a normal eGFR (≥60 mL/min per 1.73 m2) at baseline, higher HDL cholesterol levels at month 3 were significantly associated with lower risk of decline in eGFR (ie, having eGFR <60 mL/min per 1.73 m2) during follow-up (HR of 1.04, 0.88, 0.85, and 0.77 for HDL cholesterol quintiles 2, 3, 4, and 5, respectively, relative to quintile 1, P for trend=0.006). Among 3223 participants with an eGFR (<60 mL/min per 1.73 m2) at baseline, higher HDL cholesterol levels at month 3 had less impact on eGFR during follow-up, with statistical significance observed only when analyzing HDL cholesterol levels as a continuous variable (P=0.043), but not as a categorical quintile variable (P for trend=0.27).
Conclusions:
In patients treated with atorvastatin, higher HDL cholesterol levels were associated with lower risk of eGFR decline in patients with normal eGFR at baseline. However, further study is needed to establish whether there is any causal relationship between HDLs and renal function.
Clinical Trial Registration:
URL: https://www.clinicaltrials.gov. Unique identifier: NCT00327691.
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