Fatores de risco para o desenvolvimento de diabetes mellitus pós-transplante renal

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Abstract

Avaliamos retrospectivamente os prontuários de 34 pacientes com diabetes pós-transplante renal (DMPT) (grupo 1) e 68 transplantados sem DMPT (grupo 0) com objetivo de determinar a prevalência de fatores de risco conhecidos para desenvolvimento da doença em pacientes acompanhados no Hospital Universitário Pedro Ernesto. Observamos uma prevalência de DMPT de 7,4%. O grupo 1 apresentou maior idade no momento da coleta dos dados (p<0,005), maior idade no transplante (p<0,005), maior freqüência de doador cadáver de rim (p= 0,023) e de hipercolesterolemia (p=0,006) e menor freqüência de hipertensão arterial sistêmica (p<0,0001). Houve uma tendência à maior freqüência de sorologia positiva para hepatite C (p= 0,0573) e de uso de tacrolimus (p= 0,069). Pela regressão logística, os fatores de risco mais importantes para evolução para DMPT foram idade ao receber transplante [OR= 1,099, IC 95% (1,045-1,156), p= 0,0001] e sorologia positiva para hepatite C [OR= 3,338, IC 95% (1,205-9,248), p= 0,020]. Concluímos que a prevalência de DMPT em nosso hospital está nos parâmetros descritos na literatura convencional e que nossos pacientes com DMPT apresentaram maior prevalência dos fatores de risco tradicionais para DMPT, como idade avançada e sorologia positiva para hepatite C, em relação aos controles.

Translated abstract

We evaluated retrospectively 34 patients with post-kidney transplant diabetes (PTDM) (group 1) and 68 submitted to renal transplant without PTDM (group 0) to determine the prevalence and risk factors for developing PTDM in patients followed at the Hospital Universitário Pedro Ernesto. The prevalence of PTDM was 7.4%. Group 1 patients were older at data collection (p<0.005) and at transplantation (p<0.005). Among them there was a higher frequency of cadaver donors (p= 0.023) and hypercholesterolemia (p= 0.006), and a lower frequency of arterial hypertension (p<0.0001). We observed a trend to higher frequency of positive sorology for C hepatitis (p= 0.057) and use of tacrolimus (p= 0.069) in group 1 as compared to group 0. The most important risk factors for developing PTDM (by logistic regression) were the age at renal transplant [OR= 1.099, IC 95% (1.045-1.156), p= 0.0001] and positive sorology for C hepatitis [OR= 3.338, IC 95% (1.205-9.248), p= 0.020]. We conclude that the prevalence of PTDM in our hospital was similar to that found in the literature and that the patients who developed PTDM presented a higher prevalence of traditional risk factors for PTDM, like older age and positive C virus hepatitis sorology, comparing to controls.

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Most cited references 22

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The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes.

S E Kahn (2003)

The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes have been debated extensively. The concept that a feedback loop governs the interaction of the insulin-sensitive tissues and the beta cell as well as the elucidation of the hyperbolic relationship between insulin sensitivity and insulin secretion explains why insulin-resistant subjects exhibit markedly increased insulin responses while those who are insulin-sensitive have low responses. Consideration of this hyperbolic relationship has helped identify the critical role of beta-cell dysfunction in the development of Type 2 diabetes and the demonstration of reduced beta-cell function in high risk subjects. Furthermore, assessments in a number of ethnic groups emphasise that beta-cell function is a major determinant of oral glucose tolerance in subjects with normal and reduced glucose tolerance and that in all populations the progression from normal to impaired glucose tolerance and subsequently to Type 2 diabetes is associated with declining insulin sensitivity and beta-cell function. The genetic and molecular basis for these reductions in insulin sensitivity and beta-cell function are not fully understood but it does seem that body-fat distribution and especially intra-abdominal fat are major determinants of insulin resistance while reductions in beta-cell mass contribute to beta-cell dysfunction. Based on our greater understanding of the relative roles of insulin resistance and beta-cell dysfunction in Type 2 diabetes, we can anticipate advances in the identification of genes contributing to the development of the disease as well as approaches to the treatment and prevention of Type 2 diabetes.