Acute glomerulonephritis is characterized by the sudden appearance of hematuria,proteinuria, red blood cell casts in the urine, edema, and

hypertension with or without oliguria. It can follow streptococcal infections. This illness was first recognized as a complication of the convalescence period of scarlet fever in the 18th century.[1] A link between hemolytic streptococci and acute glomerulonephritis was recognized in the 20th century.
Diagram of a nephron.

Although the incidence of poststreptococcal glomerulonephritis has declined in the United States, it continues to have high incidence in other parts of the world, especially in areas with tropical climates where skin infections are common.[2, 3]

Recent studies
In a study of leukocytes and glomeruli obtained from 22 pediatric patients with acute poststreptococcal glomerulonephritis (APSGN), Wu et al found evidence that in cases of nephritis, the 15-lipoxygenase derivatives lipoxin A 4 (LXA 4 ) and 15-S-hyroxyeicosatetraenoic acid (15-S-HETE) have anti-inflammatory effects. The authors found up-regulation of LXA 4 and 15-LO expression in patients' leukocytes and glomeruli during the acute phase of glomerulonephritis and for 6-8 weeks after the disease's onset. Moreover, blood and urinary concentrations of leukotriene B 4 (LTB 4 ) peaked during the acute phase of glomerulonephritis and fell during the disease's resolution phase, with the number of glomerular polymorphonuclear leukocytes also rising and falling during the acute and resolution phases, respectively. In addition, the investigators found that in vitro, the introduction of 15-S-HETE and LXA 4 inhibited LTB 4 induced chemotaxis of polymorphonuclear leukocytes; inhibition of LTB 4 production from the leukocytes of patients with APSGN was also noted.[4]