Abstract
The dogma is that the higher risk of pyelonephritis in pregnant women is explained entirely by anatomic/obstructive changes. If so, gestational pyelonephritis should be caused by random, nonpathogenic bacteria. Instead, gestational pyelonephritis is associated with a narrow group of genetically related Escherichia coli and virulence factors, implicating a more complex pathophysiology. Current concepts in the pathogenesis of nongestational urinary tract infections propose receptor-mediated ascending infection. A pathogen with capacity to recognize various receptors may use receptors in the lower, rather than upper urinary tract, and ascend even the lumen of renal tubules. The immune system of a pregnant mother is modified to accommodate a semiallogeneic fetus. Gestational physiologic/immune adaptations may become additional risk factors, increasing sensitivity to urogenital infection. One could argue that it is not primarily the so-called "obstruction," but rather specific changes in the immune system and host receptors that act in concert with--or become exploited by--bacterial virulence that allow for infection in pregnancy to occur.
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