Metabolic syndrome after kidney transplantation

Česká verzia

Authors: Marta Nedbálková ¹; Jan Svojanovský ¹; Karel Trnavský ¹; Milan Kuman ²; Jiří Jarkovský ³; Michal Karpíšek ⁴; Miroslav Souček ¹
Authors place of work: II. interní klinika LF MU a FN u sv. Anny Brno, přednosta prof. MUDr. Miroslav Souček, CSc. ¹; Centrum kardiovaskulární a transplantační chirurgie Brno, ředitel doc. MUDr. Petr Němec, CSc., MBA, FETCS ²; Institut biostatistiky a analýz LF MU Brno, ředitel doc. RNDr. Ladislav Dušek, Ph. D. ³; BioVendor – Laboratorní medicína a. s., Brno, obchodní ředitel RNDr. Pavel Koupil, CSc. ⁴
Published in the journal: Vnitř Lék 2014; 60(3): 196-204
Category: Original Contributions

Summary

Introduction:
Metabolic syndrome is a risk factor for cardiovascular diseases. Higher risk of the metabolic syndrome and its components in patients after kidney transplantation is caused by immunosuppressive therapy. The aim of our study was to evaluate the prevalence of the metabolic syndrome and its components in kidney transplant recipients and to analyse their influence on allograft function and albuminuria.

Patients, method and results:
In the study we monitored 69 patients after cadaveric kidney transplantation. The prevalence of the metabolic syndrome was 61.3 % 3 years after kidney transplantation. The prevalence of new onset diabetes mellitus after transplantation was 27 % and that of abdominal obesity 59.7 % of patients. The age of kidney transplant recipients with the metabolic syndrome was higher than of these without it, but not statistically significant. The age of kidney transplant recipients with new onset diabetes mellitus after transplantation was significantly higher, 54.0 (35.0; 69.0) years, than in patients without it, 45.5 (27.0; 60.0) years, OR (95% IS) 1.116 (1.031; 1.207), p = 0.006.The number of components of the metabolic syndrome was negatively correlated with the graft function (rs -0,275, p = 0,031). In patients with impaired renal function with estimated glomerular filtration (using MDRD equation) < 1 ml/s 3 years after kidney transplantation the prevalence of the metabolic syndrome and hypertriglyceridaemia was significantly higher. Chronic allograft dysfunction was predicted by donor age, delayed allograft function, rejection, low level of HDL-cholesterol, hypertriglyceridaemia and hyperuricaemia. Hyperuricaemia was the only significant predictor of allograft dysfunction independently of the presence of delayed allograft function, rejection episodes and donor age. The metabolic syndrome, elevation of apolipoprotein B and nonHDL-cholesterol and increased systolic blood pressure were associated with albuminuria. Higher levels of apolipoprotein B and total cholesterol were independent predictors of increased albumin-creatinine ratio. Obesity had no impact on graft function nor on albuminuria, the influence of the new onset diabetes mellitus after transplantation was not significant independently on other factors. We confirmed the correlation of the presence of the metabolic syndrome with increased levels of AFABP (adipocyte fatty acid-binding protein) and leptin. Increased level of AFABP predicted allograft dysfunction 3 years after kidney transplantation.

Conclusion:
The influence of imunosuppressive treatment on new onset diabetes mellitus after transplantation is well documented. However, we conclude that age is an important additional risk factor for the development of diabetes mellitus in kidney transplant recipients group and it is recommended to follow mainly older patients. Early detection of metabolic abnormalities and dietary and therapeutic intervention in kidney transplant recipients may help to prevent chronic allograft dysfunction.

Key words:
abdominal obesity – albuminuria – allograft dysfunction – dyslipidaemia – kidney transplantation – metabolic syndrome – new-onset diabetes mellitus after transplantation

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