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Left ventricular structure and function in long-term kidney transplantation: the influence of glucose metabolism and
J M Osorio Moratalla1, C Ferreyra Lanatta, Y Baca Morilla
1Department of Nephrology, Hospital Universitario Virgen de las Nieves, Granada, Spain. josem.osorio.sspa@juntadeandalucia.es
Insights
Subclinical glucose metabolism impairment, indicated by HbA1c, may cause diastolic dysfunction in kidney transplant patients. This occurs through impaired oxidative stress, independent of blood pressure or left ventricular hypertrophy.
Area of Science:
- Nephrology
- Cardiology
- Metabolic Research
Background:
- Cardiovascular disease is a major complication in renal transplant recipients, impacting morbidity, mortality, and graft survival.
- Cardiac abnormalities, including impaired structure and function, are prevalent in these patients.
- The roles of glucose metabolism and oxidative stress in these cardiac issues require further elucidation.
Purpose of the Study:
- To investigate factors contributing to cardiac abnormalities in long-term, non-diabetic renal transplant recipients.
- To specifically examine the influence of glucose metabolism and oxidative stress on cardiac function.
Main Methods:
- Echocardiography was performed on 54 non-diabetic renal transplant recipients without valvulopathy.
- Biochemical analyses included lipid profile, hemoglobin A1c (HbA1c), and oxidative stress markers (malondialdehyde, superoxide dismutase, total glutathione, isoprostanes).
- Left ventricular mass index (LVMI), ejection fraction, and E/A ratio (index of diastolic dysfunction) were calculated.
Main Results:
- Diastolic dysfunction (LVDD) was observed in 59.25% of patients.
- The E/A ratio showed a significant negative association with HbA1c and age, and a positive association with total glutathione.
- Multiple regression analysis identified HbA1c as a significant predictor of LVDD, independent of mean blood pressure (MBP) or LVMI.
Conclusions:
- Subclinical glucose metabolism impairment, as indicated by HbA1c, may causally influence diastolic dysfunction in renal transplant recipients.
- Impaired oxidative stress status appears to mediate the relationship between glucose metabolism and diastolic dysfunction.
- These findings suggest that managing glucose metabolism is crucial for preventing cardiac dysfunction post-transplantation, irrespective of blood pressure or LVH severity.
Abstract:
Impaired cardiac structure and function are fundamental components of cardiovascular disease, leading to morbidity, mortality, and graft loss after renal transplantation. The aim of this study was to describe and determine the factors involved in these cardiac abnormalities, paying special attention to the role of glucose metabolism and oxidative stress. We studied 54 long-term, nondiabetic recipients with no valvulopathy who underwent an echocardiographic examination and simultaneous biochemical determinations of lipid profile, hemoglobin A1c (HbA1c), and various oxidative stress parameters: malondialdehyde, superoxide dismutase, total glutathione, and isoprostanes. We calculated the left ventricular mass index (LVMI) and ejection fraction and the peak velocity of early rapid filling to peak velocity of atrial filling (E/A) ratio. Left ventricular hypertrophy (LVH), systolic dysfunction, and diastolic dysfunction (LVDD) were present in 25.9%, 5.6%, and 59.25% of the patients, respectively. The mean blood pressure (MBP) was higher and the hemoglobin lower among patients with LVH, which was related to the age of the patients. We observed a significant negative association of the E/A ratio-used as an index of LVDD-with HbA1c (r = -.448, P = .002) and age (r = -.57, P = .000) and a positive association with the level of total glutathione (r = .322, P = .029). Multiple regression analysis of the E/A ratio showed significance only for HbA1c but not for MBP or LVMI. These results suggested a possible causal influence of subclinical glucose metabolism impairment as detected by HbA1c on the presentation of LVDD via the impaired oxidative stress status, independent of blood pressure control or LVH grade.
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