Updated: Sep 17, 2008
The genitourinary tract is the most common site, after the lungs, for tuberculous infection. The infection almost always affects the kidneys during the primary exposure to infection but does not present clinically. The spread to the kidneys from the lungs, bone, or a GI tract focus usually is hematogenous. The true incidence of renal tuberculosis may be underestimated, because radiologic findings may be absent and diagnosis is made by urine culture. Genital tuberculosis is usually secondary to renal tuberculous infection.
Renal involvement may be indolent, with a latency period of more than 20 years after the primary infection to the appearance of urinary tract symptoms of hematuria and stone disease. In patients with renal tuberculosis, treatment involves antitubercular drugs, with surgical excision as an adjunct to antitubercular therapy. The urine can be free of bacteria in less than 72 hours, but anatomic changes can progress as part of the healing process. Females with genital tuberculosis may present with infertility, menstrual disorders, and pain. Pregnancy is unusual in the presence of genital tuberculosis. When pregnancy occurs, spontaneous abortion or ectopic pregnancy usually result. As a result of the lack of clinical features, diagnosis of genital tuberculosis may be difficult.
Tuberculosis of the kidneys usually spreads by a hematogenous route from pulmonary disease, although it occasionally may be secondary to tuberculosis of the GI tract or bone. By the time of diagnosis of renal tuberculosis, the primary source of pulmonary infection may be inactive or calcified. True prevalence of renal tuberculosis is underestimated, because radiologic signs may be absent. Moreover, tubercle bacilli are found in 7-29% of urine samples in patients with extrarenal tuberculosis.
The initial renal focus is usually a small tubercle in the glandular and cortical arterioles. With the passage of time, these lesions progress to form necrotizing lesions. The disease spreads to the renal tubules and renal medulla, in which further tubercles develop, usually at the turn of the loop of Henle, coalescing into larger, necrotic, irregular cavities. The cavities usually communicate with the renal collecting system, generally a calyx, with formation of fistulae and stricturing. Eventually, the kidney may become fibrotic and scarred.
The course of renal tuberculosis may be indolent, with the appearance of few, if any, symptoms. Presentation is usually late, and symptoms usually occur as a result of nonspecific urinary tract infection. Constitutional symptoms usually do not occur or are sparse. Renal tuberculosis is bilateral, although radiologic findings are asymmetric and unilateral in 25% of patients. Ultimately, the kidney becomes atrophic, scarred, densely calcified, and nonfunctioning (autonephrectomy) if not appropriately treated.1
Ureteric involvement occurs as a descending infection secondary to kidney infection. Tubercles may involve the transitional epithelium, causing mucosal granulomas that project into the ureteric lumen. Eventually, fibrosis occurs in the ureter. These pathologic processes can be demonstrated radiologically by the appearance of a beaded, saw-toothed, corkscrew, or pipestem ureter, depending on the stage of disease. Usually, the upper and/or lower third of the ureters are involved. The vesico-ureteric junction may become fixed and patulous, allowing vesico-ureteric reflux. The kidneys are always involved when ureteric tuberculosis is present.
Bladder tuberculous infection is almost always secondary to renal involvement. Initially, interstitial cystitis occurs, eventually causing bladder mucosal ulceration and thickening of the bladder wall. End-stage disease causes scarring and bladder fibrosis, resulting in diminished capacity of the urinary bladder. Bladder wall calcification is uncommon. Bladder tuberculosis may be complicated by fistulae or sinus tract formation, although these complications are rare.
Tuberculosis of the seminal vesicles usually occurs as a result of hematogenous spread. Descending infection is unusual. The same pathologic processes occur as within the bladder (ie, mucosal tuberculomas, ulceration, fibrosis). Calcification is present in only 10% of patients.
Unlike seminal vesicle tuberculosis, tuberculosis of the prostate is usually secondary to descending infection from the kidney. However, the kidneys may occasionally appear normal, suggesting subclinical infection or a hematogenous prostatic infection. The tuberculous cavities or abscesses may discharge into the surrounding tissues, forming sinuses or fistulae to the perineum or rectum (eventually resulting in a watering-can perineum). The scrotum and urethra may be involved, although rarely. Urethral involvement may be complicated by urethral strictures.
Tuberculosis may cause chronic epididymitis and epididymo-orchitis.2 Tuberculous granulomas may develop within the testes and epididymis and rarely may be complicated by abscesses and discharging sinuses. Thickening of the scrotal wall and tunica albuginea, as well as moderate hydrocele, also may occasionally be observed.
Female genital tuberculosis is invariably secondary to tuberculosis elsewhere, and spread may be hematogenous, via the lymphatic system, or by direct spread from adjacent organs. Patients usually present with infertility, menstrual irregularity, and pain. Pregnancy is rare in the presence of genital tuberculosis and is often complicated by ectopic pregnancy or spontaneous abortion.
Clinical features of female genital tuberculosis, if any, are nonspecific, and diagnosis may be difficult. A definitive diagnosis of endometrial involvement can be made using endometrial biopsy. The endometrial cavity may be obliterated by adhesions and thick synechia. In end-stage disease, the endometrial cavity may be completely obliterated. Tubal obstruction is common, as are hydrosalpinx and pyosalpinx. Dilatation of the terminal segment can be moderate or marked.3
In end-stage disease, the tubes become rigid and pipelike because of fibrosis, and they lack peristalsis. A wet or dry peritonitis may accompany genital tuberculosis. Surprisingly, tuberculous endometritis is not a significant cause of sterility (<2% of patients).
The genitourinary tract is the second most common site of tuberculosis, the most common site being the lung. Renal tuberculosis is associated with active pulmonary tuberculosis in 4-8% of patients. Tuberculous salpingitis is uncommon in the United States and probably accounts for no more than 1-2% of cases. Before the human immunodeficiency virus (HIV) epidemic, approximately 15% of newly reported cases of tuberculosis had extrapulmonary involvement. In the years since, reported cases of extrapulmonary tuberculosis infection have increased.4
Exact worldwide incidence of genitourinary tuberculosis is unknown. Genitourinary tuberculosis appears to be fairly common in developing countries.
Although no specific figures for genitourinary tuberculosis are released, the World Health Organization (WHO) estimates that about one third of the world's population is infected with Mycobacterium, that about 9 million new cases of tuberculosis disease occur each year, and that tuberculosis causes nearly 2 million deaths each year.5
Untreated, the end result of renal tuberculosis is autonephrectomy.1 The exact incidence of infertility in patients with genital tuberculosis is unknown, but in parts of the world where tuberculosis is common, genital tuberculosis is an important cause of infertility.
Incidence of renal tuberculosis varies throughout the developing world, where the infection is common. The disease is more common in higher socio-economic groups, similar to the pattern found in Europe. Renal tuberculosis is uncommon in tropical Africa despite the fact that other forms of tuberculosis are common. High prevalence is observed in Eastern Europe, Asia, and (particularly) Bangladesh, India, and Pakistan. On the Indian subcontinent, renal tuberculosis is associated with diabetes.
Males are affected more often than are females.
Individuals of any age can be affected, but most patients who present are younger than 50 years.
Renal tuberculosis may remain dormant for many years after the kidneys become seeded during the primary tuberculous infection. With reactivation, 1 or more renal abscesses are produced. Patients usually become symptomatic, with extension of the disease to the renal pelvis and ureters causing hydronephrosis. Specific symptoms may be lacking until the hydronephrotic kidney becomes secondarily infected.
Symptoms of frequency and urgency of urination and dysuria may ensue, with development of tuberculous cystitis. However, long before patients become symptomatic, sterile pyuria, albuminuria, and hematuria are present, although cultures for pyogens demonstrate negative results. Diagnosis usually is achieved using imaging, cystoscopy, and culture of acid-fast bacilli from early morning urine specimens. Needle aspiration biopsy is a last resort when urine cultures are negative.
Male genital tuberculosis may present with epididymitis, hydrocele or a palpable testicular mass, and discharging scrotal or perineal sinuses. Tuberculous prostatitis may present with rectal/pelvic pain and dysuria. Acute prostatic inflammation later is replaced by induration and hard nodules, occasionally followed by abscesses. The abscesses may discharge into the surrounding tissues, forming sinuses or fistulae to the perineum or rectum and eventually resulting in a watering-can perineum.
Female genital tuberculosis may present with pelvic pain, menstrual irregularity, and sterility. Diagnosis is based on analysis of biopsy specimens obtained from the endometrium, laparoscopic biopsy specimens, or culture of menstrual fluid or vaginal discharge.6
The incidence of pulmonary and extrapulmonary tuberculosis has shown an increase since the late 20th century, due mainly to the rising number of people with acquired immunodeficiency syndrome (AIDS) and the development of drug-resistant strains of Mycobacterium tuberculosis. Diagnosis of extrapulmonary tuberculosis may be challenging because of its clinical and radiological spectra, and because it can mimic many other disease entities.6 Therefore, to allow early diagnosis and timely management, a high index of clinical suspicion is required, as is familiarity with the spectra of imaging findings .
All imaging findings may be normal in patients with early genitourinary tuberculosis. Genitourinary calcification may occur in patients with diabetes mellitus and schistosomiasis. Brucellosis also may mimic tuberculosis. The differential diagnosis of an adnexal mass is wide. A congenital megacalyx and focal papillary necrosis may mimic renal tuberculosis radiologically. Papillary necrosis can result from tuberculosis. A tuberculous testicular granuloma may mimic a testicular neoplasm on ultrasonographic images.
Small areas of calcification are difficult to detect on MRI scans, although they are pivotal to the diagnosis of tuberculosis. Hysterosalpingographic findings are also nonspecific; blockage of the fallopian tubes is not pathognomonic for tuberculous salpingitis and may occur as a result of other forms of infective processes of the genital tract.
Findings in all imaging modalities used in the diagnosis of genitourinary tuberculosis are essentially nonspecific, because the diagnosis is based on the presence of calcification, cavities, and strictures, which are associated with a long list of differential diagnoses. However, a fairly confident diagnosis can be made in most instances with clinical correlation. In summary, (1) imaging changes are observed late in the disease; (2) in many instances, there is a significant group of differential diagnoses; and (3) the diagnosis is determined by culture, not by imaging.
Brucellosis
Papillary Necrosis
Pelvic Inflammatory Disease/Tubo-ovarian
Abscess
Schistosomiasis, Bladder
Diabetes mellitus
Fungal infections
Causes of fallopian tube obstruction
Congenital megacalyx
Focal papillary necrosis
Scrotal sarcoidosis may mimic tuberculosis. Datta and colleagues described a case in which a scrotal ultrasonogram revealed the presence of multiple, intratesticular, hypo-echoic lesions (even though the findings on a chest radiograph and abdominal ultrasonogram were normal).8 A CT scan revealed extensive lymphadenopathy. The patient’s clinical status deteriorated following a 3-month trial of antitubercular treatment. A diagnosis of sarcoidosis was entertained, because the blood results revealed hypercalcemia, elevated serum angiotensin-converting enzyme, and an elevated erythrocyte sedimentation rate. The patient showed rapid recovery following corticosteroid therapy.
Findings in the kidneys
Findings in the ureters
Findings in the bladder
Findings in the prostate
Findings in the seminal vesicles
Findings in the epididymis and vas deferens
Calcification of the epididymis and vas deferens may be visualized on plain radiographs of the male pelvis and must be differentiated from diabetes and schistosomiasis.
Findings in female genital tuberculosis
Early features of renal tuberculosis may be difficult to detect, and the kidneys may appear entirely normal. With the development of a caseating cavity and calcification at the stage of autonephrectomy, a fairly reliable diagnosis can be achieved. Diagnosis of renal tuberculosis can be confirmed by examination of an early morning urine specimen using microscopy, but diagnosis depends on urine culture for tuberculosis. Certain features are highly suggestive of a tuberculous female genital tract, such as an irregular distribution of contrast on HSG, termed the cotton-wool plug appearance.
Ureteric calcification more commonly occurs in patients with schistosomiasis, but differentiation from ureteric, tuberculous calcification is fairly reliable. In schistosomiasis, calcification is first observed in the bladder and then extends up the ureter. Ureteric calcification without bladder calcification is most unusual. In tuberculosis, calcification is more amorphous and patchy, and it extends down the ureter; moreover, the bladder is seldom calcified. Multiple strictures and nodules of ureteritis cystica are fairly rare in ureteric tuberculosis.
Calcification may occur within bladder tumors, or calcium may be encrusted on the surface of bladder tumors, which need to be differentiated from bladder tuberculosis. A shrunken bladder may be neurogenic, but the clinical presentation is not that of urinary tuberculosis.
Calcification of the epididymis and vas deferens may occur in patients with diabetes and schistosomiasis, as well as in patients with tuberculosis. Prostatic calcification may be the aftermath of chronic prostatitis, prostatic carcinoma, or diabetes mellitus.
Blockage of the fallopian tubes is not pathognomonic for tuberculous salpingitis and may occur as a result of previous ectopic pregnancy, iatrogenic or developmental causes, pelvic inflammatory disease, or other forms of infective processes of the genital tract.
Although intravenous urography is the primary modality for imaging renal tuberculosis, CT scans clearly reveal changes of renal tuberculosis, particularly in advanced disease. Changes such as calcification, calyceal dilatation without a hydropelvis, parenchymal loss, and extrarenal spread are well depicted.
CT scans may demonstrate dense prostatic calcification in tuberculous prostatitis, sloughing, and irregular cavitation of the prostate, eventually resulting in a smooth-walled cavity that replaces the prostate.
In a series of 42 patients with renal tuberculosis, Lu and associates described the following typical CT scan features, listed in order of decreasing frequency9 :
According to the study, atypical features included the following:
In just over 70% of patients with renal tuberculosis, contrast enhanced CT scanning showed intensified HU (by 20 to approximately 120 HU) in the affected kidney.
Wang and associates reviewed the intravenous urograms and CT scans of 53 patients with urinary tuberculosis.10 The most common findings on the intravenous urography were hydrocalycosis, hydronephrosis, or hydro-ureter subsequent to strictures. Renal parenchymal scarring was the most common finding on CT scans. The findings of renal parenchymal masses and scarring, thick urinary tract walls, and extra-urinary tubercular manifestations were better depicted and were significantly more common on CT scans than they were on intravenous urograms.
Because the type and distribution of calcification features may be suggestive of tuberculosis, CT scans (with the ability to depict calcification) may show relatively specific findings. Although CT scans clearly demonstrate changes of advanced disease, sensitivity in early disease may be low, because scans do not demonstrate the detailed calyceal anatomy.
Early disease may be missed on CT scans. Mimics of renal tuberculosis include schistosomiasis, diabetes mellitus, fungal infections, brucellosis, and focal papillary necrosis from other causes.
MRI is good at depicting tuberculous cavities, sinuses tracts, fistulous communications, and extrarenal and extraprostatic spread. Multiplanar MRI allows evaluation of the disease extent in the prostatic bed and the presence of sinuses and fistulae. MRI contrast agents facilitate evaluation. MRI is also useful in the evaluation of peritonitis and adnexal masses.
Renal parenchymal changes not dissimilar to acute pyelonephritis occur in renal involvement with tuberculosis. Active inflammation may cause focal tissue edema and vasoconstriction resulting in focal hypoperfusion well depicted on contrast-enhanced CT or MRI scans. Rarely renal, tuberculosis may manifest as single or multiple parenchymal nodules, without other urinary tract involvement.
In cases of the so-called pseudotumoral type, variably-sized, well-defined parenchymal nodules are seen on ultrasonographic, CT, or MRI scans. The pseudotumor may be difficult to differentiate from renal neoplasms, leading to unnecessary surgery. Renal pelvic and ureteric involvement presents as wall thickening and contrast enhancement of the effected segments on CT and MRI scans. Tuberculous involvement of the urinary bladder is depicted by bladder distortion associated with a ragged intraluminal wall; further damage results in a shrunken, small capacity urinary bladder. These changes are reflected on CT or MRI scans, appearing as wall thickening and shrinkage.
MRI features of a case of renal macronodular tuberculoma in an asymptomatic patient have been described. The lesion was hypo-intense on T1-weighted images, while a thick, irregular, hypo-intense peripheral wall and an intralesional fluid debris level were demonstrated on T2-weighted images. MRI contrast agents were not administered.11
MRI scans of tuberculous epididymitis show enlargement of the epididymis, with relatively low signal intensity on T2-weighted images, thereby indicating chronic inflammation or fibrosis. Features that demonstrate tuberculous involvement of the seminal vesicles and the vas deferens include wall thickening, contraction, and intraluminal or wall calcifications, which may be depicted on ultrasonograms or on CT or MRI scans.
Tuberculosis of the prostate takes the form of diffuse inflammation (prostatitis) or prostatic abscess. With a prostatic abscess, T2-weighted MRI shows a peripheral enhancing cystic mass with radiating, streaky areas of low signal intensity (so-called "watermelon skin"). Diffuse, dystrophic calcifications can be seen with chronic prostatic tuberculosis.Adrenal tuberculosis is the most common cause of adrenal insufficiency. Adrenal tuberculosis may be unilateral or bilateral; it may be seen as adrenal gland enlargement with central necrosis and calcifications. These changes reflected on cross-sectional imaging, including MRI. These imaging features should be interpreted in the prevailing clinical context, because radiologic differential diagnosis includes metastases, lymphoma, primary neoplasm, and hemorrhage.
MRI is an excellent modality for depicting extra-organ spread, as well as for demonstrating discharging sinuses and fistulae, but calcification is not readily seen.
Sensitivity of MRI in the diagnosis of early genitourinary tract tuberculosis is low, and changes resulting from more advanced disease, as demonstrated on MRI scans, are nonspecific.
Ultrasonographic findings may suggest genitourinary tuberculosis in the appropriate clinical setting, and, in the case of benign disease, findings may help clinicians to avoid the use of renal surgery or orchiectomy. In female patients with genital tract tuberculosis, awareness of ultrasonographic changes associated with the infection may improve diagnostic accuracy and allow clinical mismanagement and surgical explorations in genital infections associated with wet-type (peritonitis) tuberculosis to be avoided. Clinically, tuberculosis infection of the scrotum often cannot be distinguished from lesions such as tumor and infarction.13 High-resolution ultrasonography is currently the best technique for imaging the scrotum and its contents
Mimics of renal tuberculosis include such conditions as focal compensatory hypertrophy, focal nontuberculosis hydronephrosis, acute focal bacterial nephritis, focal or global xanthogranulomatous pyelonephritis, BCG granulomas, and chronic pyelonephritis. Tuberculous autonephrectomy may resemble renal hydatid disease. Bladder tuberculosis may mimic bladder papilloma/transitional cell tumors. Tuberculous epididymitis may mimic other forms of chronic epididymitis/orchitis, testicular granulomas, and tumors.
The role of radionuclides in imaging patients with renal tuberculosis is confined to assessment of relative renal function by renography when surgery or nephrectomy is contemplated. The agents used are technetium-99m (99m Tc) diethylenetriamine penta-acetic acid (DTPA),99m Tc mercaptotriglycylglycine (MAG-3), and iodine-123 (123 I) orthoiodohippurate (OIH).
Isotope renography is the most sensitive imaging modality available for the assessment of renal function.
Radionuclide imaging usually cannot differentiate between the various causes of depressed renal function.
Most women with genital tuberculosis present with infertility, because the fallopian tubes are affected in 94% of these patients.14 Selective salpingography and fallopian tube recanalization may be attempted after adequate treatment of genital tuberculosis, to diagnose and treat tubal infertility.
Patient Education: For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center, Men's Health Center, and Women's Health Center. Also, see eMedicine's patient education article Tuberculosis.
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GU TB, TB of the genitourinary tract, GU tract tuberculosis, GU tract TB, renal tuberculous infection, TB of the kidneys, genital TB, renal tuberculosis, lower urinary tract tuberculosis, renal TB, genital tuberculosis, ureteric tuberculosis, ureteral tuberculosis, bladder tuberculosis, seminal vesicle tuberculosis, prostate tuberculosis, urogenital tuberculosis
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP is a member of the following medical societies: American Institute of Ultrasound in Medicine, Radiological Society of North America, Royal College of Physicians, Royal College of Physicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons of England
Disclosure: Nothing to disclose.
Muthusamy Chandramohan, MBBS, DMRD, FRCR, Consultant Radiologist, Bradford Teaching Hospitals, UK
Disclosure: Nothing to disclose.
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR is a member of the following medical societies: British Medical Association, Royal College of Physicians, and Royal College of Radiologists
Disclosure: Nothing to disclose.
Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.
Joshua A Becker, MD, Professor, Department of Radiology, New York University School of Medicine
Joshua A Becker, MD is a member of the following medical societies: Society of Uroradiology
Disclosure: Nothing to disclose.
Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.
Eugene C Lin, MD, Consulting Radiologist, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.