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Poststreptococcal glomerulonephritis

INTRODUCTION

Poststreptococcal glomerulonephritis (PSGN) is caused by prior infection with specific nephritogenic strains of group A beta-hemolytic streptococcus. The clinical presentation of PSGN varies from asymptomatic, microscopic hematuria to the full-blown acute nephritic syndrome, characterized by red to brown urine, proteinuria (which can reach the nephrotic range), edema, hypertension, and acute kidney injury. The prognosis is generally favorable, especially in children, but in some cases, the long-term prognosis is not benign.

The clinical manifestations, diagnosis, management, course of disease, and prognosis of PSGN will be reviewed here.

EPIDEMIOLOGY

Although PSGN continues to be the most common cause of acute nephritis in children globally, it primarily occurs in developing countries. Of the estimated 470,000 new annual cases of PSGN worldwide, 97 percent occur in regions of the world with poor socioeconomic status, with an annual incidence that ranges from 9.5 to 28.5 per 100,000 individuals [1,2].

In more developed and industrialized countries, the incidence has decreased over the past three decades [2-4]. Based upon data from the Italian Biopsy registry, the estimated annual incidence was 0.3 per 100,000 individuals between 1992 and 1994 [5]. The risk of PSGN is increased in older patients (greater than 60 years of age) and in children between 5 and 12 years of age [5,6]. PSGN is uncommon in children less than three years of age.

PSGN can present as a sporadic case or during an epidemic of group A streptococcal (GAS) infection (ie, skin and throat infections) [2]. The incidence of clinically detectable PSGN in children infected during a GAS epidemic is about 5 to 10 percent with pharyngitis and 25 percent with skin infections [7,8].

                     

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Literature review current through: Jul 2014. | This topic last updated: Jul 18, 2014.
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