Albuminuria predicts early neurological deterioration in patients with acute ischemic stroke.

BACKGROUND: Reduced glomerular filtration rate (GFR) and albuminuria have been independently associated with an increased risk of stroke and unfavorable long-term outcomes. However, the association between GFR, albuminuria, and early neurological deterioration (END) in patients with ischemic stroke has not been well studied to date. We therefore investigated the ability of estimated GFR (eGFR) and albuminuria to predict END in patients with acute ischemic stroke. METHODS: We retrospectively enrolled 294 patients that were admitted to our stroke center with acute ischemic stroke between January 2011 and September 2012. General blood and urine examinations, including eGFR and urinary albumin/creatinine ratio (UACR) measurements, were performed on admission. Kidney dysfunction was defined by a low eGFR value (<60mL/min/1.73m2) and/or increased albuminuria (≥30mg/g creatinine). END was defined as a ≥2-point increase in the National Institutes of Health Stroke Scale (NIHSS) score within 7days after admission. RESULTS: Kidney dysfunction was diagnosed in 200 of the 294 patients (68.0%). END was observed in 60 patients (20.4%). Age, blood glucose level on admission, UACR on admission, and NIHSS score on admission were significantly associated with END, while no relationship between eGFR on admission and END was identified. A multivariable logistic regression analysis showed that END was positively associated with high UACR (≥39.6mg/g creatinine) and a high NIHSS score (≥6 points). CONCLUSIONS: Our data suggest that high UACR on admission may predict END in patients with acute ischemic stroke. Larger prospective studies are required to validate the correlation between albuminuria and END.

Multiple cerebral lesions as the unique complication of idiopathic retroperitoneal fibrosis.

We present a case of idiopathic retroperitoneal fibrosis (IRF) complicated by severe renal failure and multiple intracranial lesions, which are probable results of cerebral vasculitis. IRF is an idiopathic hyperplasia of the retroperitoneal tissue that often entraps the ureters and causes post-renal failure. While the etiology of IRF is unclear, researchers consider IRF a systemic autoimmune disease complicated by immune-mediated vasculitides. The chief complaints of the patient were cognitive disorders, and brain MRI findings revealed multiple intracranial lesions with accompanying central degeneration. Given that vasogenic cerebral edemas derive from uremia, we speculated that the lesions in our case were related to more destructive changes such as aortic and periaortic inflammation. Details on this case manifesting rare cerebrovascular complications may help elucidate the pathogenesis of IRF.

A case of multicentric Castleman's disease with membranoproliferative glomerulonephritis type 3-like lesion.

Renal involvement is a significant complication of multicentric Castleman's disease (MCD) and various glomerular involvements have been reported. A 45-year-old Japanese man presented with persistent proteinuria, with lymphadenopathy and hypergammaglobulinemia. He had been diagnosed 4 years previously with MCD. As his renal impairment had progressed to renal failure, he underwent a renal biopsy. Histology revealed diffuse and global membranous lesions with large and heterogeneous epimembranous deposits. In addition, mesangial cell proliferation and focal extracapillary lesions were found. Under immunofluorescence, granular staining for anti-IgG, IgG1, IgG2 and IgA was strongly positive in the capillary loop, and weakly positive in the mesangium. As such, there was a diversity of histological features. Our perspective with regard to pathogenesis is that the formation of the immune-complex contributed to the membranoproliferative glomerulonephritis type 3-like lesion. This histological multiform with MCD is valuable for increasing our understanding of the mechanism for onset of immune-complex glomerular deposition and cellular proliferation of glomerulonephritis.

Secondary membranous glomerulonephritis associated with recipient residual lymphoma cells after allogeneic bone marrow transplantation.

A 29-year-old man with malignant lymphoma developed membranous nephropathy (MN) after allogeneic bone-marrow transplantation (BMT). There had been no obvious findings of graft versus host diseases (GVHD) after BMT, and the dosage of immunosuppressant drugs had not been reduced during this period. At the onset of MN, a few lymphoma cells still remained in the bone marrow; the patient achieved complete remission of MN after the disappearance of the lymphoma cells. In this case it is suggested that immune complexes including antigens expressed by lymphoma cells might induce MN. Therefore, this is a significant case that may reveal an alternative mechanism of the onset of MN related to BMT.