(See also Gram-Negative Bacilli; see Benign Prostate Disease: Prostatitis; see Miscellaneous Infections in Infants and Children: Urinary Tract Infection in Children (UTI).)
Bacterial UTIs can involve the urethra, prostate, bladder, or kidneys. Symptoms may be absent or include urinary frequency and urgency, dysuria, lower abdominal pain, and flank pain. Systemic symptoms and even sepsis may occur with kidney infection. Diagnosis is based on analysis and culture of urine. Treatment is with antibiotics.
Among adults aged 20 to 50 yr, UTIs are about 50-fold more common in women. The incidence increases in patients > 50 yr, but the female:male ratio decreases because of the increasing frequency of prostate disease.
The urinary tract, from the kidneys to the urethral meatus, is normally sterile and resistant to bacterial colonization despite frequent contamination of the distal urethra with colonic bacteria. Mechanisms that maintain the tract's sterility include urine acidity, emptying of the bladder at micturition, ureterovesical and urethral sphincters, and various immunologic and mucosal barriers.
About 95% of UTIs occur when bacteria ascend the urethra to the bladder and, in the case of acute uncomplicated pyelonephritis, ascend the ureter to the kidney. The remainder of UTIs are hematogenous. Systemic infection can result from UTI, particularly in the elderly. About 6.5% of cases of hospital-acquired bacteremia are attributable to UTI.
Complicated UTI is considered to be present when there are underlying factors that predispose to ascending bacterial infection. Predisposing factors include urinary instrumentation (eg, catheterization, cystoscopy), anatomic abnormalities, and obstruction of urine flow or poor bladder emptying. A common consequence of anatomic abnormality is vesicoureteral reflux (VUR), which is present in 30 to 45% of young children with symptomatic UTI (see Miscellaneous Infections in Infants and Children: Urinary Tract Infection in Children (UTI)). VUR is usually caused by a congenital defect that results in incompetence of the ureterovesical valve. It is most often due to a short intramural segment (the ureter normally transits the bladder wall at an angle; the resultant lengthy segment is more readily closed by muscular contraction than the shorter segment that occurs when the ureter passes straight through the wall). VUR can also be acquired in patients with a flaccid bladder due to spinal cord injury. Other anatomic abnormalities predisposing to UTI include urethral valves (a congenital obstructive abnormality), delayed bladder neck maturation, bladder diverticulum, and urethral duplications. Urine flow can be compromised by calculi and tumors. Bladder emptying can be impaired by neurogenic dysfunction (see Voiding Disorders: Neurogenic Bladder), pregnancy, uterine prolapse, cystocele, and prostatic enlargement. UTI caused by congenital factors presents most commonly in childhood. Most other factors are more common in the elderly.
Uncomplicated UTI occurs without underlying abnormality or impairment of urine flow. It is most common in young women but also somewhat common in younger men who have unprotected anal intercourse, an uncircumcised penis, unprotected intercourse with a woman whose vagina is colonized with urinary pathogens, or AIDS. Risk factors in women include sexual intercourse, diaphragm and spermicide use, antibiotic use, and a history of recurrent UTIs. Even use of spermicide-coated condoms increases risk of UTI in women. The increased risk of UTI in women using antibiotics or spermicides probably occurs because of alterations in vaginal flora that allow overgrowth of Escherichia coli. In elderly women, soiling of the perineum due to fecal incontinence increases risk. Patients of both sexes with diabetes have an increased incidence and severity of infections.
Commensal colonic gram-negative aerobic bacteria cause most bacterial UTIs. In relatively normal tracts, strains of E. coli with specific attachment factors for transitional epithelium of the bladder and ureters are the most frequent causes. The remaining gram-negative urinary pathogens are other enterobacteria, especially Klebsiella
Proteus mirabilis, and Pseudomonas aeruginosa. Enterococci (group D streptococci) and coagulase-negative staphylococci (eg, Staphylococcus saprophyticus) are the most frequently implicated gram-positive organisms.
E. coli causes > 75% of community-acquired UTIs in all age groups; S. saprophyticus accounts for about 10%. In hospitalized patients, E. coli accounts for about 50% of cases. The gram-negative species Klebsiella, Proteus, Enterobacter, and Serratia account for about 40%, and the gram-positive bacterial cocci Enterococcus faecalis and S. saprophyticus and S. aureus account for the remainder.
Infection of the urethra with bacteria (or with protozoa, viruses, or fungi) occurs when organisms that gain access to it acutely or chronically colonize the numerous periurethral glands in the bulbous and pendulous portions of the male urethra and in the entire female urethra. The sexually transmitted pathogens Chlamydia trachomatis (see Sexually Transmitted Diseases (STDs): Chlamydial, Mycoplasmal, and Ureaplasmal Infections), Neisseria gonorrhoeae (see Sexually Transmitted Diseases (STDs): Gonorrhea), Trichomonas vaginalis (see Sexually Transmitted Diseases (STDs): Trichomoniasis), and herpes simplex virus (see Herpesviruses: Herpes Simplex Virus (HSV) Infections) are common causes in both sexes.
In women, sexual intercourse usually precedes uncomplicated cystitis (honeymoon cystitis). In men, bacterial infection of the bladder is usually complicated and generally results from ascending infection from the urethra or prostate or is secondary to urethral instrumentation. The most common cause of recurrent cystitis in men is chronic bacterial prostatitis.
Acute urethral syndrome
Acute urethral syndrome, which occurs in women, causes dysuria and pyuria (dysuria-pyuria syndrome) due to bacterial urinary pathogens. Occasionally, it is caused by N. gonorrhoeae, TB, or fungal disease or by trauma or inflammation of the urethra. Patients with acute urethral syndrome have dysuria, frequency, and pyuria, but urine cultures are either negative or show colony counts that are < 105/mL, which is less than the traditional criterion for bacterial UTI.
Certain patients, primarily elderly women and patients with diabetes or those who require long-term use of indwelling catheters, have persistent bacteriuria with changing flora that is both asymptomatic and refractory to treatment. WBC count in urine may be modestly elevated. Most of these patients are best left untreated because the usual result of treatment is the establishment of highly resistant organisms. Asymptomatic bacteriuria can also occur in pregnant women and may cause infection of the urinary tract, sepsis, low birth weight, spontaneous abortion, premature delivery (see Pregnancy Complicated by Disease: Urinary Tract Infection in Pregnancy), and stillbirth, so treatment is indicated.
Pyelonephritis is bacterial infection of the kidney parenchyma. The term should not be used to describe tubulointerstitial nephropathy unless infection is documented. In women, about 20% of community-acquired bacteremias are due to pyelonephritis. Pyelonephritis is uncommon in men with a normal urinary tract.
Although obstruction (eg, strictures, calculi, tumors, neurogenic bladder, VUR) predisposes to pyelonephritis, most women with pyelonephritis have no demonstrable functional or anatomic defects. Cystitis alone or anatomic defects may cause reflux. This tendency is greatly enhanced when ureteral peristalsis is inhibited (eg, during pregnancy, by obstruction, by endotoxins of gram-negative bacteria). Pyelonephritis or focal abscess may be due to hematogenous spread, which is infrequent and usually results from bacteremia with virulent bacilli (eg, Salmonella sp, S. aureus). Pyelonephritis is common in young girls and in pregnant women after instrumentation or bladder catheterization.
The kidney usually is enlarged because of inflammatory PMNs and edema. Infection is focal and patchy, beginning in the pelvis and medulla and extending into the cortex as an enlarging wedge. Chronic inflammatory cells appear within a few days, and medullary and subcortical abscesses may develop. Normal parenchymal tissue between foci of infection is common. Papillary necrosis may be evident in acute pyelonephritis associated with diabetes, obstruction, sickle cell disease, pyelonephritis in renal transplants, pyelonephritis due to candidiasis, or analgesic nephropathy. Although acute pyelonephritis is frequently associated with renal scarring in children, similar scarring in adults is not detectable in the absence of reflux or obstruction.
Symptoms and Signs
In the elderly, UTIs are often asymptomatic. Elderly patients, and those with a neurogenic bladder or an indwelling catheter, may present with sepsis and delirium but without symptoms referable to the urinary tract.
When symptoms are present, they may not correlate with the location of the infection within the urinary tract because there is considerable overlap; however, some generalizations are useful.
In urethritis, the main symptoms are dysuria and, primarily in males, urethral discharge. Discharge tends to be purulent when due to N. gonorrhoeae and whitish and mucoid when not.
Cystitis onset is usually sudden, typically with frequency, urgency, and burning or painful voiding of small volumes of urine. Nocturia, with suprapubic and often low back pain, is common. The urine is often turbid, and gross hematuria occurs in about 30% of patients. A low-grade fever may develop. Pneumaturia (passage of air in the urine) can occur when infection results from a vesicoenteric or vesicovaginal fistula or from emphysematous cystitis.
In acute pyelonephritis, symptoms may be the same as those of cystitis; one third of patients have frequency and dysuria. However, with pyelonephritis, symptoms typically include chills, fever, flank pain, colicky abdominal pain, nausea, and vomiting. If abdominal rigidity is absent or slight, a tender, enlarged kidney is sometimes palpable. Costovertebral angle percussion tenderness is generally present on the infected side. In children, symptoms often are meager and less characteristic (see Miscellaneous Infections in Infants and Children: Symptoms and Signs).
Diagnosis by culture is not always necessary. If done, diagnosis by culture requires demonstration of significant bacteriuria in properly collected urine.
If a sexually transmitted disease (STD) is suspected, a urethral swab for STD testing is obtained prior to voiding. Urine collection is then by clean-catch or catheterization.
To obtain a clean-catch, midstream-voided specimen, the urethral opening is washed with a mild, nonfoaming disinfectant and air dried. Contact of the urinary stream with the mucosa should be minimized by spreading the labia in women and by pulling back the foreskin in uncircumcised men. The first 5 mL of urine is not captured; the next 5 to 10 mL is collected in a sterile container.
A specimen obtained by catheterization is preferable in older women (who typically have difficulty obtaining a clean-catch specimen) and in women with vaginal bleeding or discharge. Many clinicians also use catheterization to obtain a specimen if evaluation includes a pelvic examination. Diagnosis in patients with indwelling catheters is discussed elsewhere (see Urinary Tract Infections (UTI): Bacterial Urinary Tract Infections in Patients with Indwelling Bladder Catheters).
Microscopic examination of urine is useful but not definitive. Pyuria is defined as ≥ 8 WBCs/μL of uncentrifuged urine, which corresponds to 2 to 5 WBCs/high-power field in spun sediment. Most truly infected patients have > 10 WBCs/μL. The presence of bacteria in the absence of pyuria, especially when several strains are found, is usually due to contamination during sampling. Microscopic hematuria occurs in up to 50% of patients, but gross hematuria is uncommon. WBC casts, which require special stains to differentiate from renal tubular casts, indicate only an inflammatory reaction; they can be present in pyelonephritis, glomerulonephritis, and noninfective tubulointerstitial nephritis.
Dipstick tests also are commonly used. A positive nitrite test on a freshly voided specimen (bacterial replication in the container renders results unreliable if the specimen is not tested rapidly) is highly specific for UTI, but the test is not very sensitive. The leukocyte esterase test is very specific for the presence of > 10 WBCs/μL and is fairly sensitive. In adult women with uncomplicated UTI with typical symptoms, most clinicians consider positive microscopic and dipstick tests sufficient; in these cases, given the likely pathogens, cultures are unlikely to change treatment but add significant expense.
Cultures are recommended when symptoms are suggestive but urinalysis is nondiagnostic; for complicated UTI, including UTI in patients with diabetes, immunosuppression, recent hospitalization or urethral instrumentation, or recurrent UTI; for patients > 65 yr; and perhaps for patients with symptoms of pyelonephritis. All prepubertal children should have a urine culture when a UTI is suspected. Urine should be cultured as soon as possible or stored at 4° C if a delay of > 10 min is expected. Samples contaminated with large numbers of epithelial cells are unlikely to be helpful. An uncontaminated specimen should be obtained for culture. Criteria, based on the guidelines of the Infectious Diseases Society of America, (see the Infectious Diseases Society of America's Guidelines for the Diagnosis and Treatment of Asymptomatic Bacteriuria in Adults) for bacteriuria are:
Occasionally, UTI is present despite lower colony counts, possibly because of prior antibiotic therapy, very dilute urine (specific gravity < 1.003), or obstruction to the flow of grossly infected urine. Repeating the culture improves the diagnostic accuracy of a positive result, ie, may differentiate between a contaminant and a true positive result.
Clinical differentiation between upper and lower UTI is impossible in many patients, and testing is not usually advisable. When the patient has high fever, costovertebral angle tenderness, and gross pyuria with casts, pyelonephritis is highly likely. The best noninvasive technique for differentiating bladder from kidney infection appears to be the response to a short course of antibiotic therapy. If the urine has not cleared after 3 days of treatment, pyelonephritis should be sought.
Symptoms similar to those of cystitis and urethritis can occur with vaginitis, which may cause dysuria from the passage of urine across inflamed labia. Vaginitis can often be distinguished by the presence of vaginal discharge, vaginal odor, and dyspareunia.
Seriously ill patients require evaluation for sepsis, typically with CBC, electrolytes, BUN, creatinine, and blood cultures. Patients with abdominal pain or tenderness are evaluated for other causes of an acute abdomen (see Acute Abdomen and Surgical Gastroenterology: Acute Abdominal Pain). Pyuria without bacteriuria can be present with appendicitis, inflammatory bowel disease, and other extrarenal disorders.
Most adults do not require assessment for structural abnormalities unless infections recur or are complicated, nephrolithiasis is suspected, there is painless hematuria or new renal insufficiency, or fever persists for ≥ 72 h. Imaging choices include ultrasonography, CT, and IVU. Occasionally, voiding cystourethrography, retrograde urethrography, or cystoscopy is warranted. Urologic investigation is not routinely needed in women with symptomatic or asymptomatic recurrent cystitis, because findings do not influence therapy. Children with UTI often require imaging (see Miscellaneous Infections in Infants and Children: Urinary tract imaging).
All forms of bacterial UTI require antibiotics. Obstructive uropathy, anatomic abnormalities, and neuropathic urinary tract lesions such as compression of the spinal cord usually require surgical correction. Catheter drainage of an obstructed urinary tract aids in prompt control of UTI. Occasionally, a renal cortical abscess or perinephric abscess requires surgical drainage. Instrumentation of the lower urinary tract in the presence of infected urine should be deferred if possible. Sterilization of the urine before instrumentation and antibiotic therapy for 3 to 7 days after instrumentation can prevent life-threatening urosepsis. For patients with troublesome dysuria, phenazopyridine may help control symptoms until the antibiotics do (usually within 48 h).
Sexually active patients with symptoms are usually treated presumptively for STDs pending test results. A typical regimen is ceftriaxone 125 mg IM plus either azithromycin 1 g po once or doxycycline 100 mg po bid for 7 days. For non-STD urethritis in men, trimethoprim/sulfamethoxazole (TMP/SMX) or a fluoroquinolone is given for 10 to 14 days; women are treated with a regimen for cystitis.
A 3-day oral course of TMP/SMX or a fluoroquinolone effectively treats acute cystitis and eradicates potential bacterial pathogens in vaginal and GI reservoirs. Single-dose therapy results in higher recurrence rates and is not recommended. Longer courses of therapy (7 to 14 days) are prescribed for patients with a history of recent UTI, diabetes mellitus, or symptoms lasting > 1 wk.
If pyuria but not bacteriuria is present in a sexually active woman, then C. trachomatis urethritis is diagnosed presumptively, and appropriate treatment is given to the patient and her sex partner. If symptoms recur and culture reveals an organism sensitive to the drugs used for 3-day antibiotic therapy or if pyelonephritis is suspected, a 14-day course of TMP/SMX or a fluoroquinolone is given as for pyelonephritis.
Acute urethral syndrome
Acute urethral syndrome with pyuria is treated with doxycycline 100 mg po bid for 7 to 10 days or TMP/SMX 160/800 mg po bid for 3 days. If neither pyuria nor bacteriuria is present, antibiotics are not indicated. A course of urinary analgesics may be appropriate.
Ordinarily, asymptomatic bacteriuria in patients with diabetes, elderly patients, or patients with chronically indwelling bladder catheters should not be treated. However, asymptomatic bacteriuria in pregnant women is actively sought and treated as a symptomatic UTI, although many antibiotics cannot be safely used. Oral β-lactams, sulfonamides, and nitrofurantoin are considered safe in early pregnancy, but sulfonamides should be avoided near parturition because of a possible role in the development of kernicterus.
Treatment may also be indicated in asymptomatic UTI in patients with neutropenia, patients with recent renal transplantation, patients scheduled for instrumentation of the urinary tract (after removal of a bladder catheter that has been in place for > 1 wk), young children with gross VUR, and patients with frequent UTI symptoms from a struvite calculus that cannot be removed. Therapy typically consists of an appropriate antibiotic (based on culture results) for 3 to 14 days or long-term suppressive therapy for untreatable obstructive problems (eg, calculi, reflux).
Outpatient treatment with oral antibiotics is possible if the patient is reliable in following medical advice and is immunocompetent and has no nausea or vomiting, signs of volume depletion, or evidence of septicemia. Typical regimens are 14 days of TMP/SMX 160/800 mg po bid or ciprofloxacin 500 mg po bid. Otherwise, patients should be hospitalized and given parenteral therapy selected on the basis of local sensitivity patterns of the most common strains. Common regimens include ampicillin plus gentamicin, TMP/SMX and a fluoroquinolone, and broad-spectrum cephalosporins (eg, ceftriaxone). Aztreonam, β-lactam/β-lactam inhibitor combinations (ampicillin/sulbactam, ticarcillin/clavulanate, piperacillin/tazobactam), and imipenem/cilastatin are generally reserved for patients with more complicated pyelonephritis (eg, obstruction, calculi, resistant bacteria, hospital-acquired infection) or recent urinary tract instrumentation. If parenteral therapy is required, it is continued until defervescence and other signs of clinical improvement occur. In > 80% of patients, improvement occurs within 72 h. Oral therapy can then begin, and the patient can be discharged for the remainder of the 14-day treatment course. For complicated cases, prolonged antibiotic suppression may be needed as well as urologic correction of anatomic defects.
When pyelonephritis is diagnosed during pregnancy, hospitalization and parenteral therapy with a β-lactam with or without an aminoglycoside is appropriate.
In women who experience ≥ 3 UTIs/yr, voiding immediately after sexual intercourse and avoiding use of a diaphragm may be helpful. Drinking cranberry juice (50 mL of concentrate or about 300 mL of juice daily) reduces pyuria and bacteriuria. Increasing total fluid intake may also help.
If these techniques are unsuccessful, low-dose oral antibiotic prophylaxis greatly reduces the incidence of recurrent UTIs—eg, TMP/SMX 40/200 mg once/day or 3 times/wk, nitrofurantoin (macrocrystals) 50 or 100 mg once/day, or a fluoroquinolone (eg, ciprofloxacin, norfloxacin, ofloxacin, lomefloxacin, enoxacin). Long-term use of nitrofurantoin increases the risk of adverse effects and is contraindicated in patients with renal failure. Postcoital TMP/SMX or a fluoroquinolone may be effective. If UTI recurs after 6 mo of this therapy, prophylaxis may be reinstituted for 2 or 3 yr.
Because of potential injury to a fetus, users of fluoroquinolones should also use effective contraception. Some antibiotics (macrolides, tetracyclines, rifampin, metronidazole, penicillins, and TMP/SMX) interfere with the effectiveness of oral contraceptives by interrupting the enterohepatic recycling of estrogen or by inducing hepatic estrogen metabolism. Women who use oral contraceptives should use barrier contraceptives while they are taking these antibiotics.
In pregnant women, effective prophylaxis of UTI is similar to that in nonpregnant women. Appropriate patients include those with acute pyelonephritis during a pregnancy, patients with > 1 episode (despite treatment) of UTI or bacteriuria during pregnancy, and patients who required prophylaxis for recurrent UTI before pregnancy.
In postmenopausal women, antibiotic prophylaxis is similar to that described previously. Additionally, topical estrogen therapy markedly reduces the incidence of recurrent UTI in women with atrophic vaginitis or atrophic urethritis.
Bacterial Urinary Tract Infections in Patients with Indwelling Bladder Catheters
Patients with indwelling bladder catheters are predisposed to bacteriuria and UTIs. Symptoms may be vague or may suggest sepsis. Diagnosis depends on the presence of symptoms. Testing includes urinalysis and culture after the catheter has been removed and a new one inserted. The most effective preventive measures are avoiding unnecessary catheterization and removing catheters as soon as possible.
Bacteria can enter the bladder with the insertion of the catheter, through the catheter lumen, or from around the outside of the catheter. A biofilm develops around the outside of the catheter and on the uroepithelium. Bacteria enter this biofilm, which protects them from the mechanical flow of urine, host defenses, and antibiotics, making bacterial elimination difficult. Even with thoroughly aseptic catheter care, the chance of developing significant bacteriuria every day the catheter is indwelling is 3 to 10%. Of patients who develop bacteriuria, 10 to 25% develop symptoms of UTI. Fewer develop symptoms of sepsis. Risk factors for UTI include duration of catheterization, female sex, diabetes mellitus, opening a closed system, and suboptimal aseptic techniques. Indwelling bladder catheters can also predispose to fungal UTI (see Urinary Tract Infections (UTI): Fungal Urinary Tract Infections).
UTI can also develop in women during the days after a catheter has been removed.
Symptoms and Signs
Patients with UTI who have indwelling catheters may not have symptoms typical of UTIs. Symptoms of lower tract UTI in patients with indwelling catheters may be caused by obstruction of the catheter, development of bladder stones, and periurinary tract infections. Symptoms of acute or chronic pyelonephritis may also develop without the typical urinary tract symptoms. Patients may have nonspecific symptoms such as malaise, fever, flank pain, anorexia, and sepsis with fever, altered mental status, decreased BP, and tachypnea.
Testing is done only in patients who have symptoms, because treatment of asymptomatic bacteriuria is not recommended except for patients at high risk of developing sepsis, such as patients with granulocytopenia, organ transplant patients taking immunosuppressants, pregnant women, and patients undergoing urologic surgery. Diagnostic testing includes urinalysis and urine culture. If bacteremia is suspected, blood cultures are done. Urine cultures should be taken by a direct needle stick of the catheter with aseptic technique, so that contamination of the specimen is minimized. Pyuria tends to predict bacteriuria but not necessarily symptoms of UTI or bacteremia, so whether to treat is a clinical decision.
Women who have had a catheter removed should receive urine culture within 48 h regardless of whether symptoms occur.
Treatment includes antibiotics and supportive measures. A 14-day course of a fluoroquinolone is a reasonable empiric choice, depending on local resistance patterns. Antibiotic choice should be modified by the results of urine or blood culture and sensitivity testing. Asymptomatic women and men with recent catheter removal who have UTI diagnosed by urine culture should be treated based on the culture results.
The most effective preventive measures are avoiding catheterization and removing catheters as soon as possible. Optimizing aseptic technique and maintaining a closed drainage system also reduce risk. Routine, periodic catheter replacement is not recommended. Routine use of prophylactic antibiotics is controversial: Fluoroquinolones may slightly decrease bacteriuria and symptomatic UTIs, although this finding is not firmly established. A recent study has shown a decrease in UTI using catheters impregnated with nitrofurazone in trauma patients. However, most patients with bacteriuria do not develop symptoms, and bacteriuria develops almost inevitably when antibiotics are stopped.
(Chronic Infective Tubulointerstitial Nephritis)
Chronic pyelonephritis is chronic pyogenic infection of the kidney that occurs almost exclusively in patients with major anatomic abnormalities. Symptoms include fever, malaise, and flank pain. Diagnosis is with urinalysis, culture, and imaging tests. Treatment is with antibiotics and correction of any structural disorders.
Reflux of infected urine into the renal pelvis is the usual mechanism. Causes include obstructive uropathy, struvite calculi, and, most commonly, VUR.
Pathologically there is atrophy and calyceal deformity with overlying parenchymal scarring. The disease may progress to renal failure. Chronic pyelonephritis causes about 2 to 3% of end-stage renal disease. Patients with chronic pyelonephritis may have residual foci of infection that may predispose to bacteremia or, among kidney transplant patients, seed the urinary tract and transplanted kidney.
Xanthogranulomatous pyelonephritis (XPN) is an unusual variant that typically occurs in middle-aged women with a history of recurrent UTIs. It is a complication of obstruction due to renal calculi and is typically associated with Proteus infections. The kidney is enlarged, and perirenal fibrosis and adhesions to adjacent retroperitoneal structures are common. The disease is almost always unilateral and appears to represent an abnormal inflammatory response to infection. Giant cells, lipid-laden macrophages, and cholesterol clefts account for the yellow color of the infected tissue. The disease may also occur in children.
Symptoms and Signs
Symptoms and signs are often vague and inconsistent. Some patients have fever, flank or abdominal pain, malaise, or anorexia. In XPN, a unilateral renal mass can usually be palpated.
Chronic pyelonephritis is suspected in patients with a history of recurrent UTIs and acute pyelonephritis. However, most patients, except for children with VUR, do not have such a history. Sometimes the diagnosis is suspected because typical findings are incidentally noted on an imaging study. Symptoms, because they are vague and nonspecific, may not suggest the diagnosis.
Urinalysis and urine culture and usually imaging tests are done. On urinalysis, proteinuria is absent, minimal, or intermittent even when renal scarring is far advanced. Urinary sediment is usually scant, but renal epithelial cells, granular casts, and occasionally WBC casts are present. When both kidneys are involved, defects in concentrating ability and hyperchloremic acidosis may appear before significant azotemia occurs. Urine culture may be sterile or positive for gram-negative organisms.
Initial imaging is usually with ultrasonography or helical CT. The hallmark of chronic pyelonephritis (usually with reflux or obstruction) on imaging is classically a large, deep, segmental, coarse cortical scar usually extending to one or more of the renal calyces. The upper pole is the most common site. Initially, renal cortex is lost and the renal parenchyma thins. Uninvolved renal tissue may hypertrophy locally with segmental enlargement in patients with chronic pyelonephritis. Ureteral dilation may be present, reflecting the changes induced by chronic severe reflux. Similar changes can occur with urinary tract TB (see Mycobacteria: Genitourinary TB). Other studies are not done routinely.
In XPN, urinalysis and urine culture indicate the presence of infection, but diagnosis is confirmed by radiologic examination. CT can exclude renal carcinoma and other lesions and is preferred over IVU. Blood tests reveal nonspecific findings including anemia and mild liver dysfunction.
The course of chronic pyelonephritis is extremely variable, but the disease typically progresses very slowly. Most patients have adequate renal function for ≥ 20 yr after onset. Frequent exacerbations of acute pyelonephritis, although controlled, usually further deteriorate renal structure and function. Continued obstruction predisposes to or perpetuates pyelonephritis and increases intrapelvic pressure, which damages the kidney directly.
If obstruction cannot be eliminated and recurrent UTIs are common, long-term therapy with antibiotics (eg, TMP/SMX, trimethoprim, a fluoroquinolone, nitrofurantoin) is useful and may be required indefinitely. Complications of uremia or hypertension must be treated appropriately.
For XPN, an initial course of antibiotics should be given to control local infection, followed by en bloc nephrectomy with removal of all involved tissue and closure of any fistulas.
Patients undergoing renal transplantation who have chronic pyelonephritis may require nephrectomy before the transplant.
Last full review/revision September 2007 by Stewart Shankel, MD