Background: There are recent claims that high dietary BCAA may improve insulin resistance although this conflicts with the recommendation that low protein/BCAA diet may confer renoprotection in patients with chronic kidney disease (CKD) stages 3-5. Type 2 diabetes (T2D) has dysregulated energy metabolism where excessive BCAA intake can be harmful. We examined the risk association of BCAA and rate of estimated glomerular filtration rate (eGFR) decline in a prospective T2D cohort.

Method: We measured serum BCAA in 2340 adults with CKD stages 1-2 at baseline with available stored sera. By using linear regression analysis, we examined the association of serum BCAA with annual change in eGFR, which was estimated from a linear mixed model using at least three eGFR measurements from baseline until the onset of CKD or data censored on June 2017.

Results: In this study cohort with mean±SD follow-up of 10.0±5.3 years (age 55.2±11.2 years, BMI 25.4±4.3 kg/m2, HbA1c 7.6±1.7%, annual change in eGFR -1.37±1.28 ml/min/1.73m2), patients with incident CKD had higher serum BCAA (median [IQR]: 622.7 [540.3-730] vs. 595.8 [518.3-680.3] µM; P<0.001) and usage of blood pressure (BP)-lowering drugs (56.2% vs. 33.7%; P<0.001) at baseline than those without CKD. Every doubling of serum BCAA was associated with faster eGFR decline (β -0.24 [95% CI -0.34, -0.14]; P<0.001) that remained significant after adjusting for age, sex and diabetes duration (β -0.27 [-0.37, -0.18]; P<0.001). The effect was attenuated by further adjustment of HbA1c, BMI, lipids, BP and related drug usage (β -0.16 [-0.27, -0.05]; P=0.003), as well as by retinopathy, albuminuria and eGFR at baseline (β -0.13 [-0.23, -0.02]; P=0.016). There was no significant BCAA-sex interaction.

Conclusions: In Chinese T2D patients with CKD stages 1-2, high serum BCAA was independently associated with a modest decline in eGFR, suggesting the renoprotective effect of a low BCAA diet may be extended to early CKD with careful monitoring.


L. Lim: Research Support; Self; AstraZeneca. Speaker's Bureau; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Merck & Co., Inc. E.S. Lau: None. H. Lee: None. C.H. Tam: None. C.K. Lim: None. A. Luk: None. E. Chow: Research Support; Self; Powder Pharmaceuticals Inc., Sanofi-Aventis. R.C. Ma: Advisory Panel; Self; Boehringer Ingelheim International GmbH. Research Support; Self; AstraZeneca, Bayer AG, Pfizer Inc. Stock/Shareholder; Self; GemVCare. Other Relationship; Self; AstraZeneca. J.C. Chan: Board Member; Self; Asia Diabetes Foundation. Consultant; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Lilly Diabetes, Medtronic, Merck Sharp & Dohme Corp., Sanofi-Aventis. Research Support; Self; Amgen Inc., AstraZeneca, Lee Powder, Lilly Diabetes, Pfizer Inc., Sanofi-Aventis. Speaker's Bureau; Self; Ascensia Diabetes Care. Stock/Shareholder; Self; GemVCare. A.P. Kong: Advisory Panel; Self; Lilly Diabetes. Research Support; Self; AstraZeneca, Lilly Diabetes. Speaker's Bureau; Self; Abbott. Other Relationship; Self; AstraZeneca, Novartis Pharmaceuticals Corporation, Sanofi.


Hong Kong Society of Endocrinology, Metabolism and Reproduction; Hong Kong Association for the Study of Obesity

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at