Repeated analysis of estimated insulin resistance using the HOMAIR index in nondiabetic patients on peritoneal dialysis and its relationship with cardiovascular disease and mortality.

Terminal chronic renal failure patients show early insulin resistance (IR), characterised by alterations in the hydrocarbon metabolism and hyperinsulinaemia generally associated with dyslipidaemia and a proinflammatory condition. Cardiovascular disease (CVD) is the main cause of mortality in patients on dialysis. There is a strong association between IR, hyperinsulinism and CV disease. The objective of this study was to evaluate the effect of peritoneal dialysis (PD) on IR and its effects on the subsequent CVD morbidity and mortality in nondiabetic uraemic patients. It involved 69 nondiabetic patients on PD, 35 incident patients (≤ 3 months on PD) and 34 prevalent patients (>3 months on PD), with 2 estimated insulin resistance measurements 12 months apart using the insulin resistance index (HOMAIR). The mean HOMAIR value in incident patients was 1.8 ± 1.3 and 2.2 ± 2.1 at baseline situation and at 12 months respectively (not significant [NS]). In prevalent patients these values were 2.3 ± 1.3 and 2.5 ± 2.2 (NS). In our study, the mean glucose, insulin and IR concentrations measured by the HOMAIR and QUICKI indexes (the latter being a quantitative control for insulin sensitivity control) were similar at baseline situation and the following year, in both incident and prevalent patients. We did not find any significant differences in relation to CVD comorbidity, ischaemic heart disease, heart failure or cerebrovascular or peripheral comorbidity neither in the HOMAIR index or insulin levels. To conclude, nondiabetic patients on PD do not display a significant increase in HOMAIR levels and this remains the case over time when on dialysis. This, in turn, suggests that PD is not an IR risk factor. The fact that the IR indexes are not associated with CVD morbidity or mortality seems to suggest that this is a less significant factor in the field of PD.