vitamin-k-semiquinone-radical and Glomerulonephritis

The product of growth arrest-specific gene 6 (Gas6) is a unique vitamin K-dependent autocrine growth factor for mesangial cells, and warfarin inhibits mesangial cell proliferation by interfering with the activation process of Gas6. A recent series of studies has revealed the in vivo roles of Gas6 and its receptor Axl in the progression of acute and chronic glomerulonephritis, diabetic nephropathy, chronic allograft rejection, and human kidney diseases. This review summarizes these studies and discusses the possible interventions targeting the Gas6/Axl pathway to prevent the progression of kidney diseases.

Topics: Animals; Diabetic Nephropathies; DNA-Binding Proteins; Glomerular Mesangium; Glomerulonephritis; Graft Rejection; Humans; Intercellular Signaling Peptides and Proteins; Kidney Diseases; Mice; Mice, Knockout; Signal Transduction; STAT3 Transcription Factor; Trans-Activators; Vitamin K; Warfarin

Disturbances in hemostasis are common complications of kidney diseases. Both bleeding diathesis and thromboembolism may complicate the course of chronic uremia. As far as we know, there is a limited data about protein Z in kidney disease.. The aim of our work was to examine plasma protein Z and vitamin K concentrations in nephrotic syndrome (n = 34), glomerulonephritis (n = 48), kidney transplant recipients (n = 80), peritoneally dialyzed patients (n = 42) and in the healthy volunteers (n = 27).. Vitamin K was significantly lower in nephrotic syndrome when compared to non-nephrotic patients, CAPD and healthy volunteers (p < 0.05). Protein Z was the highest in CAPD and kidney transplant recipients when compared to any other group. In nephrotic syndrome protein Z was significantly lower when compared to the healthy volunteers, but it did not differ significantly between two groups of patients with chronic renal failure (with and without nephrotic syndrome). Protein Z correlated only with fibrinogen in CAPD, glomerulonephritis and nephrotic patients. Vitamin K correlated with age and albumin in patients with glomerulonephritis, nephrotic syndrome as well as with albumin in CAPD.. Alterations in protein Z might contribute to the enhanced risk of thromboembolic complications in nephrotic syndrome, CAPD and Tx via different and unknown mechanisms. This phenomenon seems to be unrelated to vitamin K status in these patients.

Topics: Adult; Blood Proteins; Case-Control Studies; Female; Glomerulonephritis; Hemorrhagic Disorders; Humans; Kidney Transplantation; Male; Middle Aged; Nephrotic Syndrome; Peritoneal Dialysis; Risk Factors; Thromboembolism; Vitamin K

Glucocorticoid-induced osteoporosis has been reported to be caused by enhanced bone resorption and suppressed bone formation. To clarify whether administration of vitamin K, which enhances bone formation, prevents prednisolone-induced loss of bone mineral density (BMD), a randomized, prospective, controlled study was conducted on 20 patients with chronic glomerulonephritis scheduled for treatment with prednisolone. All patients were initially treated with 0.8 mg/kg body weight/day of prednisolone (maximum of 40 mg) for 4 weeks, tapering to 20 mg/day over approximately 6 weeks. Ten patients received prednisolone alone (Group 1), and the other 10 patients received prednisolone plus 15 mg of menatetrenone, vitamin K, three times per day (Group 2). BMD of the lumbar spine measured by dual-energy X-ray absorptiometry (DXA) and biochemical markers of bone metabolism in blood and urine were evaluated before and 10 weeks after administration of prednisolone alone or with menatetrenone. In Group 1, treatment with prednisolone significantly reduced BMD of the lumbar spine from 1.14 +/- 0.12 to 1.10 +/- 0.11 g/cm2 (P = 0.0029). Serum intact osteocalcin and procollagen type I C-peptide (PICP) concentrations, biochemical markers of bone formation, were markedly reduced. A biochemical marker of bone resorption, urinary excretion of deoxypyridinoline, was significantly reduced. In Group 2, prednisolone-induced reduction of BMD was prevented by menatetrenone administration (1.09 +/- 0.09 to 1.07 +/- 0.07 g/cm2, P = 0.153). Menatetrenone prevented reduction of PICP concentration by prednisolone but not in serum intact osteocalcin concentration and urinary excretion of deoxypyridinoline. Thus, treatment with prednisolone resulted in loss of BMD of the lumbar spine associated with suppression of both bone formation and bone resorption. Menatetrenone is a useful agent in preventing prednisolone-induced loss of BMD.

Topics: Absorptiometry, Photon; Adolescent; Adult; Anti-Inflammatory Agents; Bone Density; Calcium; Chronic Disease; Drug Therapy, Combination; Female; Glomerulonephritis; Hemostatics; Humans; Male; Middle Aged; Osteoporosis; Phosphates; Prednisolone; Vitamin K; Vitamin K 2

Topics: Biomarkers; Blood Proteins; Glomerulonephritis; Humans; Nephrotic Syndrome; Peritoneal Dialysis; Vitamin K

Topics: Adult; Antibodies, Anti-Idiotypic; Anticoagulants; Antigen-Antibody Reactions; Biopsy; Female; Fibrinogen; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Immune Sera; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Kidney; Kidney Diseases; Kidney Glomerulus; Male; Nephrotic Syndrome; Pregnancy; Vitamin K

Topics: Acute Disease; Age Factors; Ascorbic Acid; Calcium; Cerebral Hemorrhage; Cortisone; Diet Therapy; Glomerulonephritis; Gluconates; Humans; Male; Middle Aged; Purpura; Rheumatic Diseases; Rutin; Vitamin K

Topics: Anti-Glomerular Basement Membrane Disease; Cerebrospinal Fluid Rhinorrhea; Diagnosis, Differential; Glomerulonephritis; Hematuria; Hemoptysis; Hemorrhage; Humans; Hydrocortisone; Lung Diseases; Prednisone; Vitamin K