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

Transplantation Proceedings
|November 18, 2008
PubMed

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.

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