In this report, we describe 5 patients with cholesterol atheroembolic renal failure. In 3 of the 5 patients, combined therapy with corticosteroids and plasma exchange was performed. These 3 patients survived, with 2 showing an improvement in renal function. The 2 remaining patients died of multifactorial causes. The literature on therapy for cholesterol atheroembolic renal failure is reviewed and the efficacy of combined therapy by use of corticosteroids and plasma exchange is evaluated.

Background. Our aim was to assess plasma neutrophil gelatinase-associated lipocalin (NGAL) as a predictor of cardiovascular (CV) events in patients with chronic kidney disease (CKD) and no history of CV events.Methods. This was a prospective observational cohort study of 252 patients with predialysis CKD. CV events were defined as CV death, acute coronary syndrome, and hospitalization for worsening heart failure, stroke, and aortic dissection.Results. During a median follow-up period of 63 months, 36 CV events occurred. On Cox stepwise multivariate analysis, plasma NGAL and B-type natriuretic peptide (BNP) were significant predictors of CV events. Kaplan-Meier incidence rates of CV event-free survival at 5 years were 96.6%, 92.9%, 85.9%, and 61.3%, respectively, among quartiles of plasma NGAL (P<0.0001). The C-index for the receiver-operating characteristic curves for CV events was greater when plasma NGAL was added to an established risk model (0.801, 95% CI 0.717–0.885), compared to the model without plasma NGAL (0.746, 95% CI 0.653–0.840,P=0.021).Conclusion. Elevated plasma NGAL could predict future CV events in CKD patients with no history of CV events and add incremental value to the established risk model.

Anti-endothelial cell antibodies (AECA) are frequently detected in patients with systemic lupus erythematosus (SLE), but their pathological role remains unclear. We recently developed a solubilized cell surface protein capture enzyme-linked immunosorbent assay (CSP-ELISA) to detect antibodies against membrane proteins involved in autoimmune reactions. In this study, sera from 51 patients with biopsy-proven lupus nephritis (LN), 25 with SLE without renal involvement (non-LN SLE), 42 disease control (DC) subjects, and 80 healthy control (HC) subjects were tested for IgG- and IgA-AECA for human umbilical vein endothelial cells (HUVEC) and human glomerular EC (HGEC) by using CSP-ELISA. IgG- and IgA-AECA titers were significantly higher in LN and non-LN SLE patients than in the DC or HC (P < 0.001) groups. IgG- and IgA-AECA titers for HUVEC corresponded well with those for HGEC. The IgA-AECA level correlated with the SLE disease activity index and with histological evidence of active lesions (cellular proliferations, hyaline thrombi and wire loops, leukocytic infiltration, and fibrinoid necrosis) in LN patients (P < 0.001). The sensitivity of IgA-AECA as a diagnostic test for histological evidence of active lesions in LN patients was 0.92, with a specificity of 0.70. The significant correlation of IgA-AECA with glomerular hypercellularity indicates that IgA-AECA are associated with endothelial damage in LN.

An 81-year-old man was treated with prednisolone, avacopan, and rituximab for microscopic polyangiitis and sulfamethoxazole/trimethoprim (SMX/TMP) and vonoprazan for prophylaxis. The liver enzyme levels were elevated 42 days after avacopan administration. Avacopan, SMX/TMP, and vonoprazan treatment were discontinued. A liver biopsy revealed vanishing bile duct syndrome. The patient was subsequently treated with ursodeoxycholic acid and glucocorticoid. Although vasculitis remained in remission, the patient ultimately died. Autopsy revealed persistent bile ductopenia and progressive liver cell injury confirmed by cytokeratin 7 positivity, severe cholestasis, and portal fibrosis. Further studies are required to elucidate associated mechanisms and risk factors.

The accumulation of amyloid-β protein (Aβ) in the brain signifies a major pathological change of Alzheimer’s disease (AD). Extracorporeal blood Aβ removal system (E-BARS) has been under development as a tool for enhancing the clearance of Aβ from the brain. Previously, we revealed that dialyzers remove blood Aβs effectively, evoking substantial Aβ influx into the blood during hemodialysis sessions as one form of blood Aβ removal by E-BARS, and that postmortem brains of hemodialysis patients exhibited lower Aβ accumulation. Here, we present a case report of a 77-year-old male patient with end-stage renal failure whose Aβ accumulation in the brain declined by initiating and continuing hemodialysis for 6 months. This report suggests that blood Aβ removal by E-BARS could be an effective therapeutic method for AD.