Insulin resistance, inflammatory biomarkers, and adipokines in patients with chronic kidney disease : Effects of angiotensin II blockade

• Published in: Journal of the American Society of Nephrology Vol. 17; no. 12 Suppl 3; pp. S206 - S212
• Main Authors: GARCIA DE VINUESA, Soledad, GOICOECHEA, Marian, KANTER, Julia, PUERTA, Marta, CACHOFEIRO, Victoria, LAHERA, Vicente, GOMEZ-CAMPDERA, Francisco, LUNO, José
• Format: Conference Proceeding Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01-12-2006
• Subjects: Adipokines - blood; Adiponectin - blood; Adult; Aged; Aged, 80 and over; Angiotensin II Type 1 Receptor Blockers - therapeutic use; Biological and medical sciences; C-Reactive Protein - metabolism; Chronic Disease; Female; Humans; Imidazoles - therapeutic use; Inflammation - blood; Insulin - blood; Insulin Resistance - physiology; Interleukin-6 - blood; Kidney Diseases - blood; Kidney Diseases - drug therapy; Kidney Diseases - physiopathology; Kidneys; Leptin - blood; Male; Medical sciences; Metabolic Syndrome - blood; Metabolic Syndrome - physiopathology; Middle Aged; Nephrology. Urinary tract diseases; Olmesartan Medoxomil; Pharmacology. Drug treatments; Tetrazoles - therapeutic use; Urinary system; Urinary system involvement in other diseases. Miscellaneous; Waist-Hip Ratio; Endocrinopathy; Pancreatic hormone; Tetrazole derivatives; Nephrology; Peptide hormone; Biological marker; Olmesartan medoxomil; Urology; Octapeptide; Antagonist; Angiotensin II; Kidney disease; Human; Urinary system disease; Biological indicator; Inflammation; Chronic kidney disease; AT1 angiotensin receptor; Adipokine; Insulin; Target tissue resistance; Renin angiotensin system; Chemotherapy; Treatment; Renal failure; Angiotensin antagonist
• ISSN: 1046-6673; 1533-3450
• DOI: 10.1681/ASN.2006080916

Patients with chronic kidney disease (CKD) present a high prevalence of insulin resistance (IR). Some studies suggest that angiotensin II may influence some cellular pathways that contribute to the pathogenesis of IR and stimulate the release of proinflammatory cytokines. Fifty-two patients who had stages 3 and 4 CKD and no diabetes were administered an angiotensin receptor blocker (ARB), olmesartan (40 mg), for 16 wk. Before and after ARB treatment, metabolic and inflammatory parameters and adipokines were measured. IR was calculated by Homeostasis Model Assessment (HOMA) index. Baseline data were compared with data that were obtained from 25 healthy control individuals of similar age and normal renal function. Compared with control subjects, patients with CKD presented significantly higher BP and waist circumference, higher triglycerides and lower HDL levels, higher insulin levels, and higher mean HOMA index (6.0 +/- 2.7 versus 2.9 +/- 2.2 muU/ml x mmol/L; P < 0.001). In addition, patients with CKD had increased levels of high-sensitivity C-reactive protein, TNF-alpha, and IL-6. In patients with CKD, leptin was positively correlated to abdominal obesity, insulin levels, and IL-6, and adiponectin was inversely correlated to abdominal obesity and insulin levels. Olmesartan treatment resulted in a significant decrease of BP, urinary protein excretion, plasma glucose (99 +/- 16 versus 92 +/- 14 mg/dl; P < 0.05), insulin (23.1 +/- 8.8 versus 19.9 +/- 9; P < 0.05), HOMA index (6.0 +/- 2.7 versus 4.7 +/- 2.8; P < 0.05), and glycated hemoglobin (5.33 +/- 0.58 versus 4.85 +/- 0.81%; P < 0.01). At the same time, there was a significant reduction of high-sensitivity C-reactive protein levels, from 4.45 mg/L (2.45 to 9.00) to 3.55 mg/L (1.80 to 5.40; P < 0.05) and fibrinogen (412 +/- 100 versus 370 +/- 105 mg/dl; P < 0.05). There were no significant differences in adipokine levels after olmesartan treatment. These data demonstrate that patients with CKD have a high prevalence of IR, metabolic syndrome, and chronic inflammation and that the administration of the ARB olmesartan improves IR and inflammation markers in these patients. Plasma adipokine levels that are related to several metabolic risk factors in patients with CKD were not modified by ARB therapy.