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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. |
| 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 Microscopic 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. |
| Clinical Correlation •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. |
| References • 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. |
| Acute Pyelonephritis |
| Synopsis by: Harold Yamase M.D. (T71000M41000)[109] |
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