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Etiology and Pathogenesis.

The dominant etiologic agents, accounting for more than 85% of cases of urinary tract infection, are the Gram-negative bacilli that are normal inhabitants of the intestinal tract.[86] By far

the most common is Escherichia coli, followed by Proteus, Klebsiella, and Enterobacter. Streptococcus faecalis, also of enteric origin, staphylococci, and virtually every other bacterial

and fungal agent can also cause lower urinary tract and renal infection. In immunocompromised patients, particularly those with transplanted organs, viruses such as polyoma virus,

cytomegalovirus, and adenovirus can also be a cause of renal infection.

In most patients with urinary tract infection, the infecting organisms are derived from the patient's own fecal flora. This is thus a form of endogenous infection. There are two routes by

which bacteria can reach the kidneys: (1) through the blood-stream (hematogenous infection) and (2) from the lower urinary tract (ascending infection) ( Fig. 20-35 ). Although the

hematogenous route is the less common of the two, acute pyelonephritis does result from seeding of the kidneys by bacteria from distant foci in the course of septicemia or infective

endocarditis. Hematogenous infection is more likely to occur in the presence of ureteral obstruction, in debilitated patients, in patients receiving immunosuppressive therapy, and with

nonenteric organisms, such as staphylococci and certain fungi and viruses.

Ascending infection is the most common cause of clinical pyelonephritis. Normal human bladder and bladder urine are sterile; therefore, a number of steps must occur for renal infection to

occur:

• The first step in the pathogenesis of ascending infection appears to be the colonization of the distal urethra and introitus (in the female) by coliform bacteria. This colonization is

influenced by the ability of bacteria to adhere to urethral mucosal cells. Such bacterial adherence, as discussed in Chapter 8 , involves adhesive molecules (adhesins) on the Pfimbriae

(pili) of bacteria that interact with receptors on the surface of uroepithelial cells. Specific adhesins (e.g., the pap variant) are associated with infection. In addition, certain

types of fimbriae promote renal tropism, or persistence of infection, or an enhanced inflammatory response to bacteria.[87]

From the urethra to the bladder, organisms gain entrance during urethral catheterization or other instrumentation. Long-term catheterization, in particular, carries a risk of

infection. In the absence of instrumentation, urinary infections are much more common in females, and this has been variously ascribed to the shorter urethra in females, the

absence of antibacterial properties such as are found in prostatic fluid, hormonal changes affecting adherence of bacteria to the mucosa, and urethral trauma during sexual

intercourse or a combination of these factors.

Multiplication in the bladder. Ordinarily, organisms introduced into the bladder are cleared by the continual flushing of voiding and by antibacterial mechanisms. However,



outflow obstruction or bladder dysfunction results in incomplete emptying and increased residual volume of urine. In the presence of stasis, bacteria introduced into the bladder can

multiply unhindered without being flushed out or destroyed in the bladder wall. Accordingly, urinary tract infection is particularly frequent among patients with lower urinary tract

obstruction, such as may occur with benign prostatic hypertrophy, tumors, or calculi or with neurogenic bladder dysfunction caused by diabetes or spinal cord injury.

Vesicoureteral reflux. Although obstruction is an important predisposing factor in the pathogenesis of ascending infection, it is incompetence of the vesicoureteral valve that

allows bacteria to ascend the ureter into the renal pelvis. The normal ureteral insertion into the bladder is a competent one-way valve that prevents retrograde flow of urine,

especially during micturition, when the intravesical pressure rises. An incompetent vesicoureteral orifice allows the reflux of bladder urine into the ureters (vesicoureteral reflux)

( Fig. 20-36 ). Reflux is most often due to a congenital absence or shortening of the intravesical portion of the ureter ( Fig. 20-37 ), such that the ureter is not compressed during

micturition. In addition, bladder infection itself, probably as a result of the action of bacterial or inflammatory products on ureteral contractility, can cause or accentuate

vesicoureteral reflux, particularly in children. Acquired vesicoureteral reflux in adults can result from persistent bladder atony caused by spinal cord injury. The effect of

vesicoureteral reflux is similar to that of an obstruction in that after voiding, there is residual urine in the urinary tract, which favors bacterial growth.

Intrarenal reflux. Vesicoureteral reflux also affords a ready mechanism by which the infected bladder urine can be propelled up to the renal pelvis and deep into the renal

parenchyma through open ducts at the tips of the papillae (intrarenal reflux). Intrarenal reflux is most common in the upper and lower poles of the kidney, where papillae tend to

have flattened or concave tips rather than the convex pointed type present in the midzones of the kidney (and depicted in most textbooks). Reflux can be demonstrated

radiographically by a voiding cystourethrogram: The bladder is filled with a radio-opaque dye, and films are taken during micturition. Vesicoureteral reflux can be demonstrated in

about 30% of infants and children with urinary tract infection (see Fig. 20-36 ).

Figure 20-35Schematic representation of pathways of renal infection. Hematogenous infection results from bacteremic spread. More common is ascending infection, which results from a

combination of urinary bladder infection, vesicoureteral reflux, and intrarenal reflux.

Figure 20-36Vesicoureteral reflux demonstrated by a voiding cystourethrogram. Dye injected into the bladder refluxes into both dilated ureters, filling the pelvis and calyces.

Figure 20-37The vesicoureteral junction. In normal individuals (A), the intravesical portion of the ureter is oblique, such that the ureter is closed by muscle contraction during micturition.

The most common cause of reflux is congenital complete or partial absence of the intravesical ureter (B).

Figure 20-38Acute pyelonephritis. Cortical surface exhibits grayish white areas of inflammation and abscess formation.

Figure 20-39Acute pyelonephritis marked by an acute neutrophilic exudate within tubules and the renal substance.

Figure 20-40Papillary necrosis. Areas of pale gray necrosis are limited to the papillae.

Figure 20-41Polyoma virus nephropathy. A, The kidney shows enlarged tubular epithelial cells with nuclear inclusions (arrow) and interstitial inflammation (arrowheads). B, Intranuclear

viral inclusions visualized by electron microscopy. (Courtesy of Dr. Jean Olson, Department of Pathology, University of California San Francisco, San Francisco, CA.)

Figure 20-42Typical coarse scars of chronic pyelonephritis associated with vesicoureteral reflux. The scars are usually polar and are associated with underlying blunted calyces.

Figure 20-43 A, Chronic pyelonephritis. The surface (left) is irregularly scarred. The cut section (right) reveals characteristic dilation and blunting of calyces. The ureter is dilated and

thickened, a finding that is consistent with chronic vesicoureteral reflux. B, Low-power view showing a corticomedullary renal scar with an underlying dilated deformed calyx. Note the

thyroidization of tubules in the cortex.

Figure 20-44Drug-induced interstitial nephritis, with prominent eosinophilic and mononuclear cell infiltrate. (Courtesy of Dr. H. Rennke, Brigham and Women's Hospital, Boston, MA.)

Figure 20-45Analgesic nephropathy. A, The brownish necrotic papilla, transformed to a necrotic, structureless mass, fills the pelvis. B, Microscopic view. Note the fibrosis in the medulla.

(Courtesy of Dr. F.J. Gloor, Institut für Pathologie, Kantonsspital, St. Gallen, Switzerland.)

TABLE 20-10-- Causes of Papillary Necrosis


Date: 2016-04-22; view: 941


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