Post-streptococcal acute glomerulonephritis in children: clinical features and pathogenesis.

10:59 EST 23rd November 2014 | BioPortfolio

Summary of "Post-streptococcal acute glomerulonephritis in children: clinical features and pathogenesis."

Post-streptococcal acute glomerulonephritis (PSAGN) is one of the most important and intriguing conditions in the discipline of pediatric nephrology. Although the eventual outcome is excellent in most cases, PSAGN remains an important cause of acute renal failure and hospitalization for children in both developed and underdeveloped areas. The purpose of this review is to describe both the typical and less common clinical features of PSAGN, to outline the changes in the epidemiology of PSAGN over the past 50 years, and to explore studies on the pathogenesis of the condition with an emphasis on the search for the elusive nephritogenic antigen.

Affiliation

Division of Pediatric Nephrology, Department of Pediatrics, University of Tennessee Health Science Center, and the Children's Foundation Research Center at Le Bonheur Children's Medical Center, Room 301 WPT, 50 North Dunlap, Memphis, TN, 38103, USA.

Journal Details

This article was published in the following journal.

Name: Pediatric nephrology (Berlin, Germany)
ISSN: 1432-198X
Pages:

Links

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Medical and Biotech [MESH] Definitions

A chronic form of glomerulonephritis characterized by deposits of predominantly IMMUNOGLOBULIN A in the mesangial area (GLOMERULAR MESANGIUM). Deposits of COMPLEMENT C3 and IMMUNOGLOBULIN G are also often found. Clinical features may progress from asymptomatic HEMATURIA to END-STAGE KIDNEY DISEASE.

Bacterial infections of the leptomeninges and subarachnoid space, frequently involving the cerebral cortex, cranial nerves, cerebral blood vessels, spinal cord, and nerve roots. The type of causative organism varies with age and clinical status (e.g., post-operative, immunodeficient, or post-traumatic states). Clinical manifestations include the acute onset of fever, stiff neck, altered mentation, seizures, and focal neurologic deficits. Death may occur within 24 hours of disease onset. Pathologic features include a purulent exudate in the subarachnoid space, and diffuse inflammation of neural and vascular structures. (From Joynt, Clinical Neurology, 1994, Ch24, pp1-5)

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Vaccines or candidate vaccines used to prevent STREPTOCOCCAL INFECTIONS.

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