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Glomerular injury is the central basis of renal insufficiency. Accumulated immunohistopathologic evidence from human kidney diseases and experimental glomerular disease models indicates that immunologic mechanisms are often pivotally involved in glomerular injury. Founded on the classical evidence, recent advances in basic immunology, the molecular and cellular biology of intrinsic glomerular cells, and genetic engineering in mice have provided significant clues to understanding the immune mechanisms that target the glomerulus. [ABSTRACT FROM AUTHOR]

In children, the most common cause of nephrotic syndrome is idiopathic nephrotic syndrome (INS), also called nephrosis (1). INS is defined by the combination of a nephrotic syndrome (proteinuria, hypoalbuminemia, hyperlipidemia, and edema) and non-specific histological abnormalities of the kidney including minimal changes, focal and segmental glomerular sclerosis (FSGS), and diffuse mesangial proliferation. Glomeruli show a fusion of epithelial cell foot processes on electron microscopy and no significant deposits of immunoglobulins or complement on immunofluorescence. [ABSTRACT FROM AUTHOR]

Immunoglobulin A (IgA) nephropathy was first described in 1968 by Berger and Hinglais (1) and is now recognized as a distinct clinicopathologic entity with a higher frequency worldwide than any other primary glomerulopathy (2). It was initially considered a benign condition, but extended follow-up of patients indicated that 20–50% of adults would ultimately progress to end-stage renal failure (2, 3). Likewise, the favorable prognosis initially attributed to children with IgA nephropathy must be questioned in the light of studies (4–8). [ABSTRACT FROM AUTHOR]

The term acute postinfectious glomerulonephritis includes a large group of glomerulonephritis that result from a variety of infectious agents. In this chapter we will deal only with the most common glomerulonephritis that result from bacterial infections. The term acute glomerulonephritis defines a pathological process that may be manifested clinically as an acute nephritic syndrome, nephrotic syndrome or rapidly progressive glomerulonephritis. Since post-streptococcal glomerulonephritis is the best known of the acute postinfectious glomerulonephritis and its most frequent clinical picture is the acute nephritic syndrome, the terms poststreptococcal glomerulonephritis, acute glomerulonephritis and acute nephritic syndrome are often, and incorrectly, used interchangeably. [ABSTRACT FROM AUTHOR]

Membranoproliferative glomerulonephritis (MPGN) is characterized on histology by glomerular hypercellulatity, increased mesangial matrix, thickening of the peripheral capillary walls, and a splitting of the glomerular basement membranes (GBMs) due to mesangial interposition in the capillary walls. The term MPGN was originally used by Habib et al. (1) to describe the glomeruli in a group of patients with chronic nephritis. In 1965, this appearance was associated with hypocomplementemia (2, 3). [ABSTRACT FROM AUTHOR]

Membranous nephropathy is a disease that typically presents with nephrotic syndrome, and although more common in the adult population, has been described in children, and even in the newborn. The disease is defined by the presence of subepithelial immune deposits (between the glomerular basement membrane (GBM) and the podocyte) with subsequent expansion of the GBM resulting in a membrane-like (membranous) thickening of the glomerular capillary wall. [ABSTRACT FROM AUTHOR]

The origin of the diagnostic term Hemolytic Uremic Syndrome (HUS) is found in the seminal report of five children by Gasser et al. (1). The children all had micro-angiopathic hemolytic anemia died of renal failure and were discovered to have acute cortical necrosis at post-mortem. From this emerged the triad of clinical features, microangiopathic hemolytic anemia, thrombocytopenia, and renal impairment that are used to diagnose the syndrome. [ABSTRACT FROM AUTHOR]

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease characterized by highly diverse clinical manifestations and the presence in the serum of a variety of autoantibodies reacting with different cell components. The skin, joints, lungs, heart, kidneys, nervous system, and other organs are involved. The role of autoantibodies in the pathogenesis of the disease is subject to debate. Certain autoantibodies, such as those reacting with cell surface determinants or circulating proteins, are directly responsible for specific clinical manifestations of the disease. The clinical course of the disease is characterized by flares, periods of chronic disease and periods of remissions. [ABSTRACT FROM AUTHOR]

Pediatric nephrologists in North America care for children who have a wide variety of acute and chronic kidney diseases. Two registries provide insight into the current state of chronic kidney disease in pediatric patients: the North American Pediatric Renal Trials Cooperative Study (NAPRTCS), previously called the North American Pediatric Renal Transplant Cooperative Study; and the United States Renal Data System (USRDS), which produces an annual report on end stage renal disease that includes pediatric patients. [ABSTRACT FROM AUTHOR]

Africa remains the world's poorest and most underdeveloped continent. The continent includes 53 countries including all the island groups. Despite many similarities, African nations are heterogeneous, with varying cultural and socioeconomic differences. [ABSTRACT FROM AUTHOR]