Serum complement C3 predicts renal arteriolosclerosis in non-diabetic chronic kidney disease.

AIM: Complement C3 (C3) is one of the major mediators of inflammation. Serum C3 has been shown to be correlated with the presence of atherosclerosis. We examined whether the serum C3 level might be correlated with the severity of renal arteriolosclerosis in patients with chronic kidney disease (CKD). METHODS: Non-diabetic CKD (stages 1-3) patients who underwent renal biopsy were enrolled in this study. Renal arteriolosclerosis was defined by the presence of hyaline changes and vessel wall thickening in the renal biopsy specimens. We examined whether the serum C3 level might be correlated with the severity of renal arteriolosclerosis in CKD patients. RESULTS: A total of 208 CKD patients (age 36.0±13.6 years; 94 male) who underwent renal biopsy were included. Univariate analysis showed that the serum C3 level was positively correlated with age, body mass index, blood pressure and the serum triglyceride, LDL cholesterol and CRP (p<0.001). The serum C3 level was also inversely correlated with serum HDL cholesterol (p<0.001). Multiple regression analysis identified that the serum C3 (p=0.043) as well as age (p<0.001), serum uric acid (p=0.009) and eGFR (p= 0.025) were independently associated with the severity of renal arteriolosclerosis. CONCLUSION: Our results suggest that the serum C3 level is a reliable marker of renal arteriolosclerosis. Components of metabolic syndrome were also correlated with the serum C3 level. Inflammation or metabolic syndrome may contribute to CKD through influencing the rate of progression of renal arteriolosclerosis.

Red blood cell survival in long-term dialysis patients.

BACKGROUND: Shortening of red blood cell (RBC) survival contributes to the anemia of chronic kidney disease. The toxic uremic environment accounts for the decreased RBC life span. The contribution of mechanical damage caused by hemodialysis to the shortened life span is unclear. Reductions up to 70% in RBC survival have been reported in uremic patients. To date, no accurate well-controlled RBC survival data exist in dialysis patients treated using different dialysis modalities and receiving erythropoiesis-stimulating agent (ESA) therapy. The aim of this study was to determine RBC survival in hemodialysis (HD) and peritoneal dialysis (PD) patients compared with healthy persons. STUDY DESIGN: Observational study. SETTING & PARTICIPANTS: 14 HD patients and 5 PD patients were recruited from the dialysis unit. Healthy volunteers (n = 14) age- and sex-matched to HD participants were included. All dialysis patients received either ESA therapy or regular iron supplementation. PREDICTOR: Dialysis patients versus age- and sex-matched healthy controls. OUTCOMES: RBC survival. MEASUREMENTS: RBC survival was determined using radioactive chromium labeling. RESULTS: More than 85% of dialysis patients were anemic (hemoglobin, 12.0 ± 1.1 g/dL); hemoglobin concentrations were not significantly different between HD and PD patients. Median RBC survival was significantly decreased by 20% in HD patients compared with healthy controls: 58.1 (25th-75th percentile, 54.6-71.2) versus 72.9 (25th-75th percentile, 63.4-87.8) days (P = 0.02). No difference was shown between the PD and HD groups: 55.3 (25th-75th percentile, 49.0-60.2) versus 58.1 (25th-75th percentile, 54.6-71.2) days (P = 0.2). LIMITATIONS: Label loss from RBCs associated with the chromium 51 labeling technique needs to be accounted for in the interpretation of RBC survival data. CONCLUSIONS: Despite current ESA therapy, decreased RBC survival contributes to chronic kidney disease-related anemia, although the reduction is less than previously reported. There does not appear to be net mechanical damage associated with HD therapy resulting in decreased RBC life span.

Postprandial hyperglycemia and hyperinsulinemia associated with renal arterio-arteriolosclerosis in chronic kidney disease.

Hypertension has an important function in the formation of renal arterio-arteriolosclerosis. However, renal arterio-arteriolosclerosis is sometimes found in biopsy specimens of normotensive patients, which indicates unknown factors may contribute to renal arterio-arteriolosclerosis. In this study, we aimed to evaluate the effects of glucose metabolism/insulin resistance on renal arterio-arteriolosclerosis. Forty-eight patients with biopsy-proven non-diabetic chronic glomerular disease were included. Renal arterio-arteriolosclerosis was evaluated as the percentage of vessels showing hyaline changes or wall thickening. We correlated renal arterio-arteriolosclerosis with clinical parameters including indices obtained by 75 g oral glucose tolerance test. Of the 48 patients, 30 had hypertension. The results of univariate analysis showed significant association of renal arterio-arteriolosclerosis with hypertension, increased serum creatinine (S-Cr), hypertriglyceridemia, increased 2-h plasma glucose (PG) and increased 2-h plasma insulin (PI). In stepwise multiple regression analysis, hypertension (beta=0.344, P=0.009), S-Cr (beta=0.287, P=0.03) and 2-h PG (beta=0.274, P=0.03) were independently associated with renal arterio-arteriolosclerosis. Eleven of the 30 hypertensive patients did not have renal arterio-arteriolosclerosis. The hypertensive patients with renal arterio-arteriolosclerosis showed significantly higher 2-h PG (134+/-25 vs. 106+/-26 mg per 100 ml, P=0.008) and higher 2-h PI (67.7+/-34.9 vs. 48.3+/-30.0 microU ml(-1), P=0.04) compared with those without renal arterio-arteriolosclerosis, but the difference in S-Cr was not significant. Postprandial hyperglycemia and hyperinsulinemia may contribute to the formation of renal arterio-arteriolosclerosis independently of hypertension.

Apo B/Apo A-I ratio in central and peripheral arterial diseases.

BACKGROUND: The apo B/apo A-I ratio represents the balance between atherogenic particles, rich in apo B, and the antiatherogenic ones, apo A-I rich. This study investigated the association between atherosclerotic diseases in different anatomical sites and apo B/apo A-I ratio. METHODS: Lipids, lipoproteins, and apolipoproteins A-I and B were assessed in 30 subjects with coronary artery disease (CAD), 26 with ischemic stroke (IS), 30 with peripheral arterial obstructive disease (PAOD), and 38 healthy subjects (controls). RESULTS: HDLc and Apo A-I were significantly lower in PAOD and CAD groups, respectively, than in other groups. Significantly higher levels of triglycerides were observed for CAD and PAOD groups than for controls. Apo B was significantly higher in IS group than in control and PAOD groups. The apo B/apo A-I ratio showed significantly higher in CAD and IS groups when compared to control and PAOD groups (p < 0.001). CONCLUSION: The apo B/apo A-I ratio was important for identifying an increased trend for coronary and cerebral atherosclerosis. In spite of the increased trend for apo B/apo A-I ratio in IS and CAD groups, the studied variables cannot be considered in an isolated way, given as those parameters were analyzed together by a binary logistic regression, no association has been demonstrated.

Apo B/Apo A-I ratio in central and peripheral arterial diseases

BACKGROUND: The apo B/apo A-I ratio represents the balance between atherogenic particles, rich in apo B, and the antiatherogenic ones, apo A-I rich. This study investigated the association between atherosclerotic diseases in different anatomical sites and apo B/apo A-I ratio. METHODS: Lipids, lipoproteins, and apolipoproteins A-I and B were assessed in 30 subjects with coronary artery disease (CAD), 26 with ischemic stroke (IS), 30 with peripheral arterial obstructive disease (PAOD), and 38 healthy subjects (controls). RESULTS: HDLc and Apo A-I were significantly lower in PAOD and CAD groups, respectively, than in other groups. Significantly higher levels of triglycerides were observed for CAD and PAOD groups than for controls. Apo B was significantly higher in IS group than in control and PAOD groups. The apo B/apo A-I ratio showed significantly higher in CAD and IS groups when compared to control and PAOD groups (p < 0.001). CONCLUSION: The apo B/apo A-I ratio was important for identifying an increased trend for coronary and cerebral atherosclerosis. In spite of the increased trend for apo B/apo A-I ratio in IS and CAD groups, the studied variables cannot be considered in an isolated way, given as those parameters were analyzed together by a binary logistic regression, no association has been demonstrated.

INTRODUÇÃO: O índice apo B/apo A-I representa o balanço entre partículas de colesterol potencialmente aterogênicas ricas em apo B e partículas anti-aterogênicas ricas em apo A-I. O objetivo deste estudo foi investigar a associação entre doenças ateroscleróticas em diferentes sítios anatômicos e o índice apo B/apo A-I. MÉTODOS: Lípides, lipoproteínas e apolipoproteínas A-I e B foram quantificados em 30 indivíduos apresentando doença arterial coronariana (DAC), 26 com acidente vascular cerebral (AVC), 34 apresentando doença arterial obstrutiva periférica (DAOP) e 38 indivíduos hígidos (grupo controle). RESULTADOS: HDLc e apo A-I apresentaram-se significativamente mais baixos nos grupos DAOP e DAC, respectivamente, quando comparados com os demais grupos. Níveis de triglicérides foram significativamente mais elevados nos grupos DAC e PAOD quando comparados com o grupo controle. Apo B foi significativamente mais elevada no grupo AVC quando comparado com os grupos controle e DAOP. O índice apo B/apo A-I se mostrou significativamente elevado nos grupos DAC e AVC quando comparados com os demais (p < 0,001). CONCLUSÃO: O índice apo B/apo A-I foi importante para identificar uma tendência aumentada para aterosclerose coronariana e cerebral. No entanto, os parâmetros avaliados não podem ser considerados de forma isolada, considerando que nenhuma associação foi demonstrada quando os dados foram analisados pelo modelo de regressão logística binária.

Association between serum adiponectin levels and arteriolosclerosis in IgA nephropathy patients.

OBJECTIVE: Adiponectin has attracted great attention because of its anti-atherogenic properties; however, to date the relationship between serum adiponectin and arteriolosclerosis has not been reported. In our study, we aimed to examine whether or not serum adiponectin levels are associated with arteriolosclerosis in patients with IgA nephropathy which is the most common form of chronic glomerulonephritis. MATERIALS AND METHODS: We enrolled 35 patients aged 35.0+/-14.6, who underwent renal biopsy from August 2004 to February 2006 in our hospital, and were confirmed to have IgA nephropathy. We examined serum adiponectin, high-sensitive C-reactive protein, total cholesterol and triglyceride level, urinary protein excretion, body mass index (BMI), and the presence of arteriolosclerosis in the renal specimens. Since the serum adiponectin level is strongly affected by renal function, we classified the patients by creatinine clearance. RESULTS: Multiple regression analysis showed the associations of adiponectin with creatinine clearance (p<0.001), BMI (p<0.001), serum triglyceride (p=0.001) and urinary protein excretion (p=0.001). We observed a positive relation of adiponectin with urinary protein excretion and an inverse relation of adiponectin with creatinine clearance, serum triglyceride, and BMI. We could not detect any relation between the presence of arteriolosclerosis and adiponectin in the IgA nephropathy patients as a whole; however, in patients whose creatinine clearance was 90-120 ml/min/1.73 m2, the serum adiponectin level of patients with arteriolosclerosis was lower than in those without arteriolosclerosis (p=0.025). CONCLUSION: The serum level of adiponectin was related to arteriolosclerosis in IgA nephropathy patients whose renal function was almost normal. Adiponectin may prevent renal arteriolosclerosis.

Serum osteoprotegerin levels in patients with acute atherothrombotic stroke and lacunar infarct.

BACKGROUND: Arterial calcification is associated with increased risk of cardiovascular events. Osteoprotegerin (OPG) is a cytokine involved in the bone metabolism and vascular calcification. Recent data support a relationship between high serum levels of OPG and increased risk for cardiovascular disease in human. The aim of this study was to evaluate the OPG serum levels in acute ischemic stroke. Our study was further designed to detect differences in serum OPG levels between subtypes of ischemic stroke. MATERIALS AND METHODS: The study consisted of 51 patients with acute ischemic stroke and 28 control subjects. Stroke subtypes were defined by the TOAST classifications. Serum OPG levels were measured with the ELISA method. RESULTS: OPG serum levels were significantly higher in patients with ischemic stroke than in control subjects (p<0.001). OPG serum levels were significantly higher in large-vessel disease (LVD) subtype compared with small-vessel disease (SVD) subtype and controls (p<0.001, p<0.001). There was no significant difference in OPG serum levels between SVD group and control subjects. Serum OPG levels were correlated with age (r=0.407, p=0.005) and fasting glucose levels (r=0.542, p=0.001) in ischemic stroke group. Logistic regression analysis showed that plasma OPG levels (OR 2.1, 95% CI, 1.16 to 3.4, p=0.01) associated with presence of stroke independently of the other risk factors. CONCLUSIONS: High serum OPG levels were associated with the LVD stroke subtype, suggesting that OPG levels may play role in pathogenesis of atherothrombotic stroke. The precise mechanism for the role of OPG in atherosclerosis needs to be investigated further.