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| Acute Pyelonephritis |
| Etiology |
•Bacterial,
especially colonic flora such as Escherichia coli, Proteus and
Klebsiella. |
| Pathogenesis |
•Most cases are due to ascending infections from urine flow
abnormalities. •Urinary outflow obstruction results in urine stasis providing an environment for bacterial proliferation.
•Obstruction also predisposes to vesicoureteral reflux which can enable bacteria to reach the kidney.
•Less common is seeding of the kidney by circulating bacteria (affecting already damaged parenchyma) or septic emboli from valvular vegetations in endocarditis. |
| Epidemiology |
•Most cases are related to pre-existing urine outflow
abnormalities such as pregnancy, tumor, calculi, prostatic hypertrophy,
neurogenic bladder and vesicoureteral reflux. •Women are more prone than
men, possibly due to differences in urethral anatomy. |
| Clinical |
•Symptoms and signs may include fever, chills, and costovertebral area
tenderness. •Laboratory tests may show leukocytosis, pyuria and white
cell casts in the urine sediment. |
| General Gross Description |
•Renal parenchymal involvement tends to be regional, not universal,
commonly upper and lower poles. •Cortical surfaces show suppurative
abscesses. •Since many cases are associated with urine outflow
obstruction, dilatation of pelvis and calyces may be present. |
| General Micro Description |
•Histologic changes are predominantly seen in the tubular and interstitial
compartments. •Neutrophils are the dominant inflammatory cell type and
are seen in widened interstitium and in the lumens of tubules. |
| Reference |
• Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 967-972. • Harrison^s Principles of Internal Medicine, 13th Ed: Isselbach et. al. (eds). New York, McGraw-Hill, 1994, pp. 538-543.
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