Pyelonephritis is a renal disorder affecting tubules, interstitium, and renal pelvis and is one of the most common disease of the kidney. It occurs in two forms. Acute pyleonephritis is caused by bacterial infection and is the renal lesion associated with urinary tract infection. Chronic pyelonephritis is a more complex disorder: bacterial infection plays a dominant role, but other factors (vesicoureteral reflux, obstruction) are involved in its pathogenesis. Pyelonephritis is a serious complication of an extremely common clinical spectrum of urinary tract infections that affect the urinary bladder (cystitis) or both. Bacterial infection of the urinary tract may be completely asymptomatic (asymptomatic bacteriuria) and most often remains localized to the bladder without the development of renal infection. However urinary tract infection always carries the potential of spread to the kidney.

Etiology and pathogeneisis

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. 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 most patients with urinary tract infection the infecting organisms are derived from thepatients 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 bloodstream (hematogenous infection) and (2)from the lower urinary tract (ascending infection).

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. Hematogeneous infection is more likely to occur in the presence of ureteral obstruction, in debiliated patients in patients receiving immunosuppressive therapy and with nonenteric organisms such as staphylococci and certain fungi.

Ascending infection is the most common cause of clinical pyelonephritis. Normal human bladder and bladder urine are sterila, and thus 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 by coliform bacteria. This colonization is influenced by the ability of bacteria to adhere to urethral mucosal cells. Such bacterial adherence, involves adhesive molecules on the P-fimbraie of bacteria that interact with receptors on the surfact of uroepithelial cells. Specific adhesins are associated with infection. In addition certain types of fimbriae promote renal tropism or persistence of infection or an enhanced inflammatory response to bacteria.

From the urethra to the bladder, organisms gain entrance during urethral catheterization or other instrumentation. Long term catheterization, in perticular carries a risk of infection. In the absence of instrumentaion urinary infections are much more common in females and tthis 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 dnd urethral trauma.

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 unceremoniously flushed or destroyed by 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.

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 ascent the ureter into the pelvis. The normal ureteral insertion into the bladder is a competent one way valve that prevents retrograde flow of uring especially during micturition, when the intravesical pressure rises. An incompetent vesicoureteral orifice allows the reflux of bladder urine into the ureters. Reflux is most often due to a congenital inherited absence or shortening of the intravesical portion of the ureter such that the ureter is nor compressed during micturition. In addition bladder infection itself , probably as a result of the action of bacterial or inflammatory products on ureteral contracility can cause or acentuate vesicoureteral reflux particularly in children. Acquired vesicoureteral reflux in elders 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.

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