A Case of Anti-Glomerular Basement Membrane Antibody-Positive Systemic Lupus Erythematosus with Pulmonary Hemorrhage Successfully Treated at an Early Stage of the Disease.

We report here a case of systemic lupus erythematosus (SLE) with pulmonary hemorrhage and anti-glomerular basement membrane (anti-GBM) antibodies. A 42-year-old woman was admitted to our hospital with complaints of exanthema, arthralgia, shortness of breath, and hemoptysis. Plain chest computed tomography (CT) scan revealed pericardial effusion, bilateral pleural effusions, and pulmonary hemorrhage.

Impact of anti-glomerular basement membrane antibodies and glomerular neutrophil activation on glomerulonephritis in experimental myeloperoxidase-antineutrophil cytoplasmic antibody vasculitis.

Background: Antineutrophil cytoplasmic antibody (ANCA) and neutrophil interactions play important roles in ANCA-associated vasculitis (AAV) pathogenesis. However, mechanisms underlying the pathogenesis of crescent formation in ANCA-associated vasculitis have not been completely elucidated. To ascertain the involvement of these interactions in necrotizing crescentic glomerulonephritis (NCGN), we used an AAV rat model and investigated the effects of the anti-myeloperoxidase (MPO) antibody (Ab) titer, tumor necrosis factor α (TNF-α), granulocyte colony-stimulating factor (G-CSF) and subnephritogenic anti-glomerular basement membrane (GBM) Abs, as proinflammatory stimuli.

Glomerular capillary and endothelial cell injury is associated with the formation of necrotizing and crescentic lesions in crescentic glomerulonephritis.

Background: The associations of glomerular capillary and endothelial injury with the formation of necrotizing and crescentic lesions in cases of crescentic glomerulonephritis (GN) have not been evaluated in detail.

Methods: Glomerular capillary and endothelial cell injury were assessed in renal biopsy specimens of crescentic GN, including those from patients with anti-neutrophil cytoplasmic autoantibodies (ANCA) -associated GN (n=45), anti-glomerular basement membrane (GBM) GN (n=7), lupus GN (n=21), and purpura GN (n=45) with light and electron microscopy and immunostaining for CD34.

Results: In ANCA-associated GN, anti-GBM GN, lupus GN, and purpura GN, almost all active necrotizing glomerular lesions began as a loss of individual CD34-positive endothelial cells in glomerular capillaries, with or without leukocyte infiltration.

Acute graft-versus-host disease of the kidney in allogeneic rat bone marrow transplantation.

Allogeneic hematopoietic cell or bone marrow transplantation (BMT) causes graft-versus-host-disease (GVHD). However, the involvement of the kidney in acute GVHD is not well-understood. Acute GVHD was induced in Lewis rats (RT1l) by transplantation of Dark Agouti (DA) rat (RT1(a)) bone marrow cells (6.

A case of secondary focal segmental glomerulosclerosis associated with malignant hypertension.

Focal segmental glomerulosclerosis (FSGS) is associated with various clinicopathological conditions, including hypertension. We report here a case of secondary FSGS associated with malignant hypertension. A 33-year-old man with a 1-month history of visual impairment and headache visited the Department of Ophthalmology at our hospital and was found to have hypertensive retinopathy and severe hypertension (230/160 mmHg).

Proliferative glomerulonephritis with monoclonal immunoglobulin G3κ deposits in association with parvovirus B19 infection.

Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits is a recently described disease entity, characterized by nonorganized electron-dense deposits in glomeruli and immunofluorescence findings indicating monoclonal immunoglobulin G deposits. The pathogenesis of many cases of proliferative glomerulonephritis with monoclonal immunoglobulin G deposits remains unknown. We herein report 2 patients with parvovirus B19 infection who developed acute nephritic syndrome with hypocomplementemia (patient 1) or persistent proteinuria and congestive heart failure (patient 2); however, neither patient had detectable levels of serum monoclonal immunoglobulin G.

Caspase-3-independent internucleosomal DNA fragmentation in ischemic acute kidney injury.

Background/aims: Renal tubular cell death in ischemia-reperfusion does not follow the classical apoptosis or necrosis phenotype. We characterized the morphological and biochemical features of injured tubular epithelial cells in ischemic acute kidney injury (AKI).

Methods: Ischemic AKI was induced in rats by 60 min of ischemia followed by 24 h of reperfusion.

Development of lymphatic vasculature and morphological characterization in rat kidney.

Background: The mechanisms and morphological characteristics of lymphatic vascular development in embryonic kidneys remain uncertain.

Methods: We examined the distribution and characteristics of lymphatic vessels in developing rat kidneys using immunostaining for podoplanin, prox-1, Ki-67, type IV collagen (basement membrane: BM), and α-smooth muscle actin (αSMA: pericytes or mural cells). We also examined the expression of VEGF-C.

Successful treatment of icodextrin-single peritoneal dialysis for refractory nephrotic syndrome induced by idiopathic membranous nephropathy.

The patient was a 76-year-old male who developed nephrotic syndrome. Idiopathic membranous nephropathy was diagnosed by renal biopsy and clinical findings. The patient had been refractory to predonisolone and cyclosporine A therapies, and overhydration recurred repeatedly during the clinical course.

A patient with idiopathic cholesterol crystal embolization: effectiveness of early detection and treatment.

A 72-year-old man was admitted to our hospital because of progressive renal dysfunction persisting for 1.5 months. Physical examination showed livedo reticularis of the toes of both feet, peripheral edema, and gait disturbance due to the toe pain.

Focal segmental glomerulosclerosis after renal transplantation.

Focal segmental glomerulosclerosis (FSGS) is a clinicopathologic syndrome of proteinuria, usually of nephrotic range, associated with focal and segmental sclerotic glomerular lesions. Therefore, FSGS is diagnosed by clinical features and histopathological examination of renal biopsy. The natural history of the condition varies, and although it may respond to treatment, FSGS is an important disease in the etiology of end-stage renal disease (ESRD).