The term acute glomerulonephritis (AGN) implies a temporal sequence of the rapid onset of renal disease characterized by proliferation of cells within the glomerulus and exudation of leukocytes within the glomerulus. The process is immunologically mediated. In its typical form, AGN is characterized by hematuria, proteinuria, reduced urine output, and volume overload. Often, but not always, there is reduction in glomerular filtration rate, as well as hypertension. AGN is usually postinfectious in origin, and of the postinfectious causes, acute poststreptococcal glomerulonephritis (APSGN) is the most common. Infectious etiologies that have been reported as causing AGN are listed in Table 1 (1). The differential diagnosis of APSGN is presented in Table 2 (2). These diseases have many of the features of APSGN presenting with either 1) acute nephritic onset characterized by hematuria, proteinuria, reduced urine volume, and volume overload or 2) gross hematuria, with or without proteinuria. The clinical features and therapy of these other diseases are discussed elsewhere in this book. This chapter will discuss the clinical manifestations, complications, therapy, and possible prevention of APSGN (1,2).
KeywordsGlomerular Filtration Rate Infective Endocarditis Fluid Overload Total Body Water Hypertensive Encephalopathy
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