Integrative view of pathogenetic mechanisms in reflux nephropa-thy. Abnormalities of ureteral embryogenesis may result in a defective antireflux mechanism, permitting vesicoureteral reflux (VUR), incomplete bladder emptying, urinary stasis, and infection. Bacterial virulence factors modify the pathogenicity of different bacterial strains. Bacterial surface appendages such as fimbriae may interact with epithelial cell receptors of the urinary tract, enhancing bacterial adhesion to urothelium. Endotoxin is capable of inhibiting ureteral peristalsis, contributing to the extension of the infection into the upper urinary tract even in the absence of VUR. Inoculation of the renal parenchyma with bacteria produces an acute inflammatory response, resulting in the release of inflammatory mediators into the surrounding tissue. The acute inflammatory response elicited by the presence of infecting bacteria is responsible for the subsequent renal parenchymal injury. In addition, it is possible that immune complexes, bacterial fragments, and endotoxin resulting from infection may produce a glomerulopathy.

Even in the absence of urinary tract infection, VUR associated with elevated intravesical pressure is capable of producing renal parenchymal scars. The developing kidney appears to be particularly susceptible. Renal tubular distention resulting from high intrapelvic pressure may exert an injurious effect on renal tubular epithelium. Compression of the surrounding peritubular capillary network by distended renal tubules may produce ischemia. During micturition, elevated intravesical pressure is transmitted to the renal pelvis and renal tubule. This transient pressure elevation may produce tubular disruption. Extravasation of urine into the surrounding parenchyma results in an immune-mediated interstitial nephritis and further renal injury.

The reduction in functional renal mass produced by the interaction of the pathogenetic factors listed here induces compensatory hemo-dynamic changes in renal blood flow and the glomerular filtration rate. Over time, these compensatory changes may be maladaptive, may produce hyperfiltration and glomerulosclerosis, and may eventuate in renal insufficiency. (From Kramer [16]; with permission.)

How To Reduce Acne Scarring

How To Reduce Acne Scarring

Acne is a name that is famous in its own right, but for all of the wrong reasons. Most teenagers know, and dread, the very word, as it so prevalently wrecks havoc on their faces throughout their adolescent years.

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