Patients with chronic kidney disease (CKD) have an increased risk of developing vascular calcifications, as well as bone dynamics impairment, leading to a poor quality of life and increased mortality. Certain vitamin K dependent proteins (VKDPs) act mainly as calcification inhibitors, but their involvement in the onset and progression of CKD are not completely elucidated. This review is an update of the current state of knowledge about the relationship between CKD and four extrahepatic VKDPs: matrix Gla protein, osteocalcin, growth-arrest specific protein 6 and Gla-rich protein. Based on published literature in the last ten years, the purpose of this review is to address fundamental aspects about the link between CKD and circulating VKDPs levels as well as to raise new topics about how the interplay between molecular weight and charge could influence the modifications of circulating VKDPs at the glomerular level, or whether distinct renal etiologies have effect on VKDPs. This review is the output of a systematic literature search and may open future research avenues in this niche domain.

Objective Osteoarthritis (OA) commonly affects weight-bearing joints and is characterized by articular cartilage breakdown combined with osteophyte formation at the joint margins and chronic nonspecific inflammation of synovium. Understanding the profile of inflammation in a patient population is an essential starting point to predict or prevent OA progression. The aim of this study was to identify the profile of selected biomolecules in synovial fluid (SF) and investigate the correlation according to gender, age, and severity of the disease within patients from among the general knee OA population. Design In our study SF samples were aspirated from the knees of 65 OA patients (46 patients with early knee OA and 19 patients with end-stage knee OA according to the Kellgren-Lawrence grading scale). The concentration of interleukins (IL-6, IL-8), matrix metalloproteinases (MMP-1, MMP-3, MMP-13), MMPs inhibitors (TIMP-1, TIMP-2), cartilage oligomeric matrix protein (COMP), and adiponectin was analyzed using a multiplex ELISA-based approach. Conclusions Our results indicate significant linear correlation of MMP-13 and COMP concentration with age ( P < 0.05), but not with OA severity. In fact, 3 of the examined biomolecules, MMP-3 ( P < 0.01), TIMP-1 ( P < 0.01), and COMP ( P < 0.05) significantly correlate with the grade of knee OA and might be associated with OA severity.

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A single dose of clomipramine, 10 mg i.v., or desipramine, 25 mg i.m., was administered to seven healthy young sibling pairs in a randomized cross-over experiment. The response of serum growth hormone, prolactin and cortisol was measured. The main findings were (1) sex differences in the growth hormone and cortisol response to desipramine and (2) a significant genetic component of the prolactin and cortisol response to desipramine as indicated by significantly (p < 0.05) lower within-pair than between-pair variance in the sibling pairs but not random pairs of the experimental subjects.

The aim of this study was to detect the concentrations of PCSK9 in various subclinical stages of atherosclerosis and to highlight its relationship with inflammation. One hundred and fifty-nine healthy patients were divided into three groups, based on the extent of atherosclerotic changes in the carotid artery: a group without identifiable atherosclerosis, cIMT>75‰ and an asymptomatic plaque group. The PCSK9 was measured by ELISA and hsCRP by the immunoturbidimetric method. Vascular changes were identified by a carotid ultrasound. PCSK9 was elevated, when comparing the healthy group with the cIMT>75‰ group; however, no significant increase was detected between cIMT>75‰ and the asymptomatic plaque group. A positive linear correlation of the PCSK9 concentration and atherosclerotic changes was found; however, after the re-analysis in each group, this correlation persisted only in the group with still normal values. Additionally, a significant linear correlation was found between the PCSK9 concentrations and lipid parameters. However, no significant association was found with hsCRP. PCSK9 was found to be elevated only in cIMT>75‰, but not in the later plaque stage. A linear correlation of PCSK9 values was detected only in the group with still reference values. Based on this fact, we assumed the direct linear role of PCSK9 in initiating atherosclerosis; however, in the later phases, the relationship, which highlights other risk factors such as inflammation, is not linear.