Objective: The insulin-like growth factor-I (IGF-I) is involved in glucose metabolism and may contribute to the accelerated cardiovascular disease. The aim of the study was to assess IGF-I level in diabetic patients with resistant hypertension (RHTN) and to evaluate its association with glucose metabolism and cardiac, renal and brain tissues. Design and method: The study included 19 diabetic patients with RHTN (mean age 58.9 ± 7.6 years, five men, mean office BP (systolic/diastolic) 174.8 ± 20.7/94.6 ± 15mmHg, mean HbA1c 7 ± 0.8%) and 21 age- and sex-matched patients with RHTN without diabetes mellitus (DM). Office BP, echocardiography, kidney and brain MRI, lab tests (IGF-1, plasma glucose and insulin levels, HOMA-index, HbA1c, serum creatinine, serum cystatin, eGFR (MDRD formula) and 24 h microalbuminuria) were performed in all patients. On average, patients were taking 4.2 ± 0.8 antihypertensive drugs. Results: IGF-I level was in the normal range in 18 (95%) patients with DM+RHTN and in 100% of patients with RHTN without DM, one diabetic patient with RHTN had elevated IGF-I levels. The mean IGF-I values in hypertensive patients with DM and those without DM were the same. In diabetic patients with RHTN the IGF-I level was inversely correlated to HOMA-IR index (R = -0.87, P = 0.002), but had a direct correlation with basal glucose level (R = 0.48, P = 0.04). In addition, increase in IGF-I level was associated with both of left ventricular mass (R = 0.49, P = 0.03), and the end-diastolic interventricular septum thickness (R = 0.59, P = 0.008), with decreased renal function (R = 0.64, P = 0.003 for serum creatinine; R = 0.76, p = 0.01 for serum cystatin; R = -0.50, P = 0.03 for eGFR), microalbuminuria level (R = 0.61, P = 0.03), as well as with structural kidney damage (R = -0.67, P = 0.04 for the medulla volume according to kidney MRI) and brain damage (R = 0.89, P = 0.015 for Evans’ index as a MRI- sign of brain atrophy) Conclusions: Most diabetic patients with RHTN have a normal IGF-I level, which does not differ from that in patients with RHT without DM. Although an increase in IGF-I level is associated with a decrease in insulin resistance, our data suggest the possible participation of IGF-I in the development of myocardial hypertrophy, the progression both of chronic kidney disease and brain atrophy.