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    Abstract:
    Background Schistosoma mansoni schistosomiasis (SM) remains a public health problem in Brazil. Renal involvement is classically manifested as a glomerulopathy, most often membranoproliferative glomerulonephritis or focal and segmental glomerulosclerosis. We report a case of collapsing glomerulopathy (CG) associated with SM and high-risk APOL1 genotype (HRG). Case report A 35-year-old male was admitted for hypertension and an eight-month history of lower-limb edema, foamy urine, and increased abdominal girth. He had a recent diagnosis of hepatosplenic SM, treated with praziquantel, without clinical improvement. Laboratory tests revealed serum creatinine 1.89mg/dL, blood urea nitrogen (BUN) 24mg/dL, albumin 1.9g/dL, cholesterol 531mg/dL, low-density lipoprotein 426mg/dL, platelets 115000/mm3, normal C3/C4, antinuclear antibody (ANA), rheumatoid factor (RF), and antineutrophil cytoplasmic antibodies (ANCA), negative serologies for hepatitis C virus (HCV) and human immunodeficiency virus (HIV), HBsAg negative and AntiHBc IgG positive, no hematuria or leukocyturia, 24 hour proteinuria 6.56g and negative serum and urinary immunofixation. Kidney biopsy established the diagnosis of CG. A treatment with prednisone was started without therapeutic response, progressing to end-stage kidney disease 19 months later. Molecular genetics investigation revealed an HRG. Conclusions This is the first report of CG associated with SM in the setting of an HRG. This case highlights the two-hit model as a mechanism for CG pathogenesis, where the high-risk APOL1 genotype exerts a susceptibility role and SM infection serves as a trigger to CG.
    Keywords:
    Glomerulopathy
    Podocytic infolding glomerulopathy (PIG) has been proposed as a new disease entity. A 14-year-old girl underwent renal biopsy at our institution because of a chance finding of proteinuria. Light microscopic findings revealed a minor glomerular abnormality, but under a higher magnification, after periodic acid methenamine silver staining, a bubbling appearance in the glomerular basement membrane (GBM) was observed. An electron microscopic examination revealed microspheres in the GBM, which were sparse but global. The patient was diagnosed as having PIG. After 3 years, her urinary protein had increased and a second biopsy was performed, showing focal segmental glomerulosclerosis in addition to a lesser degree of podocytic infolding than at the first biopsy. This is the first report of a case complicated by a different type of glomerulonephritis after being diagnosed as PIG. A few cases of PIG are complicated by focal segmental glomerulosclerosis, suggesting several mechanisms for the disorder.
    Glomerulopathy
    Silver stain
    Citations (14)
    Background. Massive proteinuria is often associated with hypoalbuminaemia in glomerulopathy. However, patients may have normal levels of serum albumin despite heavy proteinuria in many circumstances. This study analysed factors affecting serum levels of albumin in primary glomerulopathy patients with nephrotic-range proteinuria.
    Glomerulopathy
    Serum Albumin
    Citations (16)
    Sickle cell disease is known to cause glomerulopathy, including focal segmental glomerulosclerosis (FSGS). Patients who have sickle cell glomerulopathy with FSGS are thought to have a poorer prognosis than patients who have sickle cell glomerulopathy without this lesion. The former patients are more likely to have persistent proteinuria and eventually develop end-stage renal disease. We present a boy with sickle cell glomerulopathy and FSGS who is younger than patients with similar findings reported previously. The histopathology of his renal lesions is remarkable for segmental ultrastructural changes in the glomerular basement membranes and endothelial cells. We speculate that these changes are precursory to the pathogenesis of glomerular sclerosis in patients with sickle cell disease.
    Glomerulopathy
    Glomerulosclerosis
    Pathogenesis
    Citations (20)
    Collapsing glomerulopathy is an aggressive form of glomerular disease defined for its histopathological features of glomerular collapse, visceral epithelial cell damage and tubulointerstitial changes that are characteristic. Patients with collapsing glomerulopathy present with severe nephrotic syndrome, marked proteinuria, generally more than 10 g/day and rapid progression to chronic renal failure, or death due to complications of nephrotic syndrome, despite any form of treatment. Collapsing glomerulopathy presents as de novo or recurrent disease in the renal allograft. There is slight predominance in males and strong predominance in blacks as renal diseases in general. Collapsing glomerulopathy shares several clinical and histopathological features with focal and segmental glomerulosclerosis and HIV-nephropathy; nevertheless, there is enough evidence to support collapsing glomerulopathy as a different entity. It must be mentioned that collapsing glomerulopathy, focal and segmental glomerulosclerosis and HIV-nephropathy may have a similar pathophysiological mechanism of damage to the visceral epithelial cell.
    Glomerulopathy
    Glomerulosclerosis
    Minimal change disease
    Membranous Nephropathy
    Citations (7)
    Lupus nephritis (LN) is one of the most severe organ manifestations of systemic lupus erythematosus (SLE). Crescentic lupus nephritis rarely presents as rapidly progressive renal failure (RPRF) and needs prompt initiation of treatment. Collapsing glomerulopathy (CG) itself is associated with poor renal survival. Collapsing glomerulopathy's association with lupus nephritis is rarely reported in the literature. It may indicate a severe form of lupus podocytopathy.
    Glomerulopathy
    Nephritis
    Citations (0)
    Glomerulopathy
    Nephritis