• Diabetic retinopathy
• Dialysis
• Hypertensive retinopathy
• Kidney transplantation
• Pre-emptive transplant

• Humans
• Kidney Transplantation/adverse effects
• Female
• Male
• Middle Aged
• Adult
• Eye Diseases/etiology
• Visual Acuity
• Postoperative Complications/etiology
• Aged
• Diabetic Retinopathy/etiology
• Intraocular Pressure
• Hypertension

• Humans
• Glomerulonephritis, Membranous
• Anti-Glomerular Basement Membrane Disease
• Autoantibodies
• Immunoglobulin M
• Receptors, Phospholipase A2

Increased lipoprotein (a) [lp (a)] has proinflammatory effects, which increase the risk of coronary artery disease. However, the association between lp (a) variability and follow-up C-reactive protein (CRP) level in patients undergoing percutaneous coronary intervention (PCI) has not been investigated.

To explore the association between lp (a) variability and mean CRP levels within the 1^st year post-PCI.

Results of lp (a) and CRP measurements from at least three follow-up visits of patients who had received PCI were retrospectively analyzed. Standard deviation (SD), coefficient of variation (CV), and variability independent of the mean (VIM) are presented for the variability for lp (a) and linear regression analysis was conducted to correlate lp (a) variability and mean follow-up CRP level. The relationship of lp (a) variability and inflammation status was analyzed by restricted cubic spline analysis. Finally, exploratory analysis was performed to test the consistency of results in different populations.

A total of 2712 patients were enrolled. Patients with higher variability of lp (a) had a higher level of mean follow-up CRP (P < 0.001). lp (a) variability was positively correlated with the mean follow-up CRP (SD: β = 0.023, P < 0.001; CV: β = 0.929, P < 0.001; VIM: β = 1.648, P < 0.001) by multivariable linear regression analysis. Exploratory analysis showed that the positive association remained consistent in most subpopulations.

Lp (a) variability correlated with mean follow-up CRP level and high variability could be considered an independent risk factor for increased post-PCI CRP level.

• Lipoprotein (a)
• Variability
• C-reactive protein
• Coronary artery disease
• Percutaneous coronary intervention

• ApoB/ApoA-Ι ratio
• Contrast-induced acute kidney injury
• Lipoprotein(a) level

• Average nucleotide identity
• Peritoneal dialysis-associated peritonitis
• Rhodococcus kroppenstedtii
• Whole genome sequencing

The glomerular diseases after renal transplantation can occur de novo, i.e., with no relation to the native kidney disease, or more frequently occur as a recurrence of the original disease in the native kidney. There may not be any difference in clinical features and histological pattern between de novo glomerular disease and recurrence of original glomerular disease. However, structural alterations in transplanted kidney add to dilemma in diagnosis. These changes in architecture of histopathology can happen due to: (1) exposure to the immunosuppression specifically the calcineurin inhibitors (CNI); (2) in vascular and tubulointerstitial alterations as a result of antibody mediated or cell-mediated immunological onslaught; (3) post-transplant viral infections; (4) ischemia-reperfusion injury; and (5) hyperfiltration injury. The pathogenesis of the de novo glomerular diseases differs with each type. Stimulation of B-cell clones with subsequent production of the monoclonal IgG, particularly IgG3 subtype that has higher affinity to the negatively charged glomerular tissue, is suggested to be included in PGNMID pathogenesis. De novo membranous nephropathy can be seen after exposure to the cryptogenic podocyte antigens. The role of the toxic effects of CNI including tissue fibrosis and the hemodynamic alterations may be involved in the de novo FSGS pathophysiology. The well-known deleterious effects of HCV infection and its relation to MPGN disease are frequently reported. The new concepts have emerged that demonstrate the role of dysregulation of alternative complement pathway in evolution of MPGN that led to classifying into two subgroups, immune complex mediated MPGN and complement-mediated MPGN. The latter comprises of the dense deposit disease and the C3 GN disease. De novo C3 disease is rather rare. Prognosis of de novo diseases varies with each type and their management continues to be empirical to a large extent.

• De novo glomerulonephritis
• Renal transplantation
• New concepts of therapy

Patients with chronic kidney disease (CKD) have an extremely poor cardiovascular outcome. Arterial stiffness, a strong independent predictor of survival in CKD, is connected to arterial media calcification. A huge number of different factors contribute to the increased arterial calcification and stiffening in CKD, a process which is in parallel with impaired bone metabolism. This coincidence was demonstrated to be part of the direct inhibition of calcification in the vessels, which is a counterbalancing effect but also leads to low bone turnover. Due to the growing evidence, the definition of “CKD mineral bone disorder” was created recently, underlining the strong connection of the two phenomena. In this review, we aim to demonstrate the mechanisms leading to increased arterial stiffness and the up-to date data of the bone-vascular axis in CKD. We overview a list of the different factors, including inhibitors of bone metabolism like osteoprotegerin, fetuin-A, pyrophosphates, matrix Gla protein, osteopontin, fibroblast growth factor 23 and bone morphogenic protein, which seem to play role in the progression of vascular calcification and we evaluate their connection to impaired arterial stiffness in the mirror of recent scientific results.

• Arterial stiffness
• Vascular calcification
• Bone metabolism
• Chronic kidney disease