Key result
Insulin resistance is not linked to worse GFR or major renal endpoints in non-diabetic CKD.
Why the study?
Does insulin resistance increase the risk of CKD progression in non-diabetic CKD stage 2-4 patients?
Cohort (n=73)
Does insulin resistance increase the risk of CKD progression in non-diabetic CKD stage 2-4 patients?
Absolute Event Rate: 21.6% vs 25%
Insulin resistance does not appear to be a significant risk factor for the progression of chronic kidney disease in non-diabetic patients.
Insulin resistance should not guide risk stratification in non-diabetic CKD; leaves open whether IR-targeted interventions modify progression.
BACKGROUND: The aim of this research was to establish whether there is a link between insulin resistance (IR) and glomerular filtration rate (GFR), and assess whether insulin-resistant subjects experience a more rapid deterioration in GFR. METHODS: We enrolled 73 non-diabetic chronic kidney disease (CKD) stage 2-4 patients. All blood samples were taken after 10 h of overnight fasting. Fasting blood glucose (FBG), creatinine, uric acid, albumin, cholesterol, triglyceride, insulin, HbA1c, high-sensitivity C-reactive protein (hs-CRP) and intact parathyroid hormone (iPTH) levels as well as proteinuria were analyzed. Patients were followed up for a mean of 30 (24-35) months and renal and metabolic parameters were compared in conjunction with a homeostasis model assessment of IR (HOMA-IR) between the entry and the end of the study period. CKD progression was assessed by recording renal endpoints, which included end-stage renal disease, requiring renal replacement therapy, or overall mortality. RESULTS: The study patients were divided into group 1 (n = 36), without IR, and group 2 (n = 37), with IR. Group 2 patients had a higher FBG (p = 0.003) and insulin level (p = 0.001) compared to group 1. The baseline and end of study systolic (p = 0.007) and diastolic (p = 0.001) blood pressures were decreased in group 1. In group 2, FBG (p = 0.008), HbA1c (p = 0.009), systolic (p = 0.024) and diastolic (p = 0.001) blood pressures and CRP (p = 0.047) were decreased. In group 2, 8 patients reached renal endpoints while in group 1, 9 patients reached study endpoints. HOMA-IR was not significantly higher among 17 patients who reached the renal endpoint than among the 56 who did not. At baseline, those patients who reached the renal endpoint showed lower GFR (p = 0.001), higher iPTH (p = 0.004) and hs-CRP (p = 0.002) levels. CONCLUSION: There was no significant difference in GFR at the end of the study between patients who had or did not have IR. Furthermore, HOMA-IR was not significantly different in patients with or without renal endpoints.
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Baştürk et al. (2011) conducted a cohort in non-diabetic chronic kidney disease (CKD) stage 2-4 (n=73). Insulin resistance vs. No insulin resistance was evaluated on Renal endpoints (end-stage renal disease, requiring renal replacement therapy, or overall mortality). Insulin resistance was not associated with a significant difference in GFR at the end of the study or the incidence of renal endpoints (21.6% vs 25.0%) in non-diabetic patients with CKD.
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