Niels Sondergaard Heinrich1, Bernt Johan von Scholten2, Henrik Reinhard3, Frederik Persson4, Tarunveer S Ahluwalia5, Tine Willum Hansen6, Hans-Henrik Parving7, Peter Karl Jacobsen8, Peter Rossing9. 1. Steno Diabetes Center Copenhagen, Niels Steensensvej 2, 2820 Gentofte, Denmark. Electronic address: niels.soendergaard.heinrich@regionh.dk. 2. Steno Diabetes Center Copenhagen, Niels Steensensvej 2, 2820 Gentofte, Denmark. Electronic address: bjos@novonordisk.com. 3. Steno Diabetes Center Copenhagen, Niels Steensensvej 2, 2820 Gentofte, Denmark. Electronic address: hr@executivehealth.es. 4. Steno Diabetes Center Copenhagen, Niels Steensensvej 2, 2820 Gentofte, Denmark. Electronic address: frederik.persson@regionh.dk. 5. Steno Diabetes Center Copenhagen, Niels Steensensvej 2, 2820 Gentofte, Denmark. Electronic address: tarun.veer.singh.ahluwalia@regionh.dk. 6. Steno Diabetes Center Copenhagen, Niels Steensensvej 2, 2820 Gentofte, Denmark. Electronic address: tine.willum.hansen@regionh.dk. 7. Department of Medical Endocrinology, Rigshospitalet, Copenhagen University Hospital, Blegdamsvej 9, 2100 Copenhagen, Denmark; University of Copenhagen, Copenhagen, Denmark. Electronic address: d028916@dadlnet.dk. 8. Department of Cardiology, Rigshospitalet, Copenhagen University Hospital, Blegdamsvej 9, 2100 Copenhagen, Denmark. Electronic address: peter.karl.jacobsen@regionh.dk. 9. Steno Diabetes Center Copenhagen, Niels Steensensvej 2, 2820 Gentofte, Denmark; University of Copenhagen, Copenhagen, Denmark. Electronic address: peter.rossing@regionh.dk.
Abstract
AIMS: Lipoprotein(a)(Lp(a)) has emerged as an independent risk marker for cardiovascular disease (CVD) in the general population and among persons with existing CVD. We investigated associations between serum Lp(a)concentrations and renal function decline, incident CVD and all-cause mortality in individuals with type 2 diabetes (T2D) and microalbuminuria. METHODS: Prospective study including 198 individuals with T2D, microalbuminuria and no CVD. Yearly p-creatinine was measured after baseline in 176 of the participants. The renal endpoint was defined as decline in eGFR of >30% from baseline. CVD events and mortality were tracked from national registries. Cox regression analyses were applied both unadjusted and adjusted for traditional risk factors (sex, age, systolic blood pressure, LDL-cholesterol, smoking, HbA1c, creatinine and urinary albumin creatinine ratio (UAER)). RESULTS: Baseline mean (SD) age was 59 (9)years, eGFR 89 (17) mL/min/1.73 m2, 77% were male, and median [IQR] UAER was 103 [38-242] mg/24-h. Median Lp(a)was 8.04 [3.42-32.3] mg/dL. Median follow-up was 6.1 years; 38 CVD events, 26 deaths and 43 renal events were recorded. For each doubling of baseline Lp(a), the following hazard ratios (95% confidence intervals) were found before and after adjustment respectively: 0.98 (0.84-1.15) and 1.01 (0.87-1.18) for decline in eGFR > 30%, 0.96 (0.81-1.13) and 0.99 (0.82-1.18) for CVD events, 1.04 (0.85-1.27) and 1.06 (0.87-1.30) for all-cause mortality. CONCLUSIONS: In this cohort of individuals with T2D and microalbuminuria, the baseline concentration of Lp(a)was not a risk marker for renal function decline, CVD events or all-cause mortality.
AIMS: Lipoprotein(a)(Lp(a)) has emerged as an independent risk marker for cardiovascular disease (CVD) in the general population and among persons with existing CVD. We investigated associations between serum Lp(a)concentrations and renal function decline, incident CVD and all-cause mortality in individuals with type 2 diabetes (T2D) and microalbuminuria. METHODS: Prospective study including 198 individuals with T2D, microalbuminuria and no CVD. Yearly p-creatinine was measured after baseline in 176 of the participants. The renal endpoint was defined as decline in eGFR of >30% from baseline. CVD events and mortality were tracked from national registries. Cox regression analyses were applied both unadjusted and adjusted for traditional risk factors (sex, age, systolic blood pressure, LDL-cholesterol, smoking, HbA1c, creatinine and urinary albumin creatinine ratio (UAER)). RESULTS: Baseline mean (SD) age was 59 (9)years, eGFR 89 (17) mL/min/1.73 m2, 77% were male, and median [IQR] UAER was 103 [38-242] mg/24-h. Median Lp(a)was 8.04 [3.42-32.3] mg/dL. Median follow-up was 6.1 years; 38 CVD events, 26 deaths and 43 renal events were recorded. For each doubling of baseline Lp(a), the following hazard ratios (95% confidence intervals) were found before and after adjustment respectively: 0.98 (0.84-1.15) and 1.01 (0.87-1.18) for decline in eGFR > 30%, 0.96 (0.81-1.13) and 0.99 (0.82-1.18) for CVD events, 1.04 (0.85-1.27) and 1.06 (0.87-1.30) for all-cause mortality. CONCLUSIONS: In this cohort of individuals with T2D and microalbuminuria, the baseline concentration of Lp(a)was not a risk marker for renal function decline, CVD events or all-cause mortality.