Fibulin Levels in Autosomal Dominant Polycystic Kidney Disease and Its Relationship to Arterial Stiffness.

BACKGROUND: The objective of the present study was to evaluate fibulin 1 levels in different stages of patients with autosomal dominant polycystic kidney disease (ADPKD) and investigate possible connections between fibulin-1 and arterial stiffness. METHODS: For this cross-sectional study, we included 74 patients with ADPKD (mean age, 50.92 ± 15.70 years) and 32 healthy controls (mean age, 49.53 ± 7.32 years). Patients with ADPKD were classified based on CKD epidemiology collaboration (CKD-EPI) equation assessments of estimated glomerular filtration rate (eGFR). Blood levels of fibulin 1 and creatinine levels were analyzed. We measured brachial artery PWV (baPWV), augmentation index (AIx), and pulse pressure (PP) for the assessment of arterial stiffness and systolic and diastolic blood pressures (SBP and DBP, respectively). RESULTS: Fibulin 1 was significantly higher in the patient group (p < 0.001). SBP, DBP, MAP, PP, and baPWV levels were also significantly higher in the patient group. A statistically significant positive correlation was found between fibulin 1 and creatinine (r = 0.377, p = 0.001). No significant correlation was found between the fibulin 1 levels and age, SBP, DBP, MAP, baPWV, and AIx. CONCLUSIONS: Plasma concentrations of fibulin 1 increased in patients with ADPKD. Arterial stiffness measured by baPWV increased in patients with ADPKD, but it was not related to fibulin 1 levels.

Management of hypertriglyceridemia induced acute pancreatitis and therapeutic plasmapheresis : Report of nine cases and review of literature.

Hypertriglyceridemia is one of the rare causes of the acute pancreatitis. The prevalance of hypertriglyceridemia has increased recently due to the changing eating habits, sedentary lifestyle, alcohol consumption, obesity and concomitant diabetes mellitus. Therefore, the frequency of the acute pancreatitis due to hypertriglyceridemia may increase in coming years. Diagnosis of the acute pancreatitis by hypertriglyceridemia can be overlooked easily and may be very severe if untreated accurately on time. In addition to the standard management of pancreatitis, specific treatment for hypertriglyceridemia that is insulin, heparin and anti-hypertriglyceridemic drugs are used. Therapeutic plasmapheresis is the last treatment option and seems the most effective one in this subject through developing device and membrane technologies when we review the current literature. Not only triglycerides but also proinflammatory cytokines and adhesion molecules that play an active role in pathogenesis are removed by plasmapheresis. So, the effectiveness of treatment appears promising. However, the exact pathophysiology of hypertriglyceridemia-induced pancreatitis could not be fully understood and the majority of published experience comes from the case reports and the benefit of randomized clinical trials is not available. Therefore, there are no data about what are the exact indications and when we start therapeutic plasmapheresis in literature. This manuscript describes our hospital experience with treatment options and analyzes reports published recently about plasmapheresis as a treatment modality for hypertriglyceridemia induced acute pancreatitis.

Soluble Klotho levels in diabetic nephropathy: relationship with arterial stiffness.

OBJECTIVE: In this cross-sectional study, we investigate the relationship between soluble Klotho (s-Klotho) levels, markers of bone mineral metabolism and arterial stiffness in 109 diabetic nephropathy patients (median age 61.00± 9.77 years) and 32 healthy controls (median age 49.23 ± 7.32 years). PATIENTS AND METHODS: Blood samples were collected to measure the levels of s-Klotho, and FGF23, serum creatinine, Calcium (Ca), Phosphorus (P), 25-hydroxyvitamin D3 (25hD) and parathyroid hormone (PTH). Pulse wave velocity (PWV) and blood pressure were also measured using a combined monitor. RESULTS: s-Klotho, FGF23 and PTH levels were significantly higher and 25hD was significantly lower in the patients than in controls (p < 0.001). Systolic blood pressure, pulse pressure and PWV were also significantly higher in the patients (p < 0.001). s-Klotho, FGF23 and 25hD levels significantly varied between sub-groups according to CKD stages, defined according to the CKD epidemiology collaboration equation. A strong positive correlation was found between s-Klotho and FGF23 (r = 0.768, p = 0.001) levels, but not with other bone mineral metabolism, blood pressure or arterial stiffness parameters. Creatinine levels significantly differed (p = 0.009) between three s-Klotho-level sub-groups, with the high creatinine levels in the sub-group with the lowest s-Klotho levels and estimated glomerular filtration rate (eGFR). CONCLUSIONS: There was no correlation between eGFR and s-Klotho levels. Arterial stiffness increased in CKD but was not related to s-Klotho or FGF23 levels. Among all parameters, FGF23 levels had the greatest effect on s-Klotho levels.