What Is Kidney Tuberculosis?
Tuberculosis of the urinary tract and kidney is caused by bacteria of the Mycobacterium tuberculosis complex. The members of the M. tuberculosis complex are obligate bacteria and are free-living environmental saprophytes commonly found in water, involving piped water supplies. These environmental Mycobacteria sometimes cause human infection, especially in immunosuppressed patients, affecting recipients of renal transplants. The kidney gets involved in the infection when mycobacteria cause disseminated disease. Kidney disease caused by Mycobacteria in nonimmunosuppressed people is extremely rare. However, as they are present in water, Mycobacteria easily contaminate the lower urethra and external genitalia and, thus, can be isolated from urine samples.
Renal involvement in tuberculosis can be a component of a disseminated infection or a localized genitourinary disease. Pulmonary infection is the major center in most patients. After the presentation, the bacilli remain reserved in macrophages, where they multiply slowly. In most patients, the primary infection is self-limited. The kidneys are generally involved in miliary tuberculosis, where miliary lesions are seen in renal tissue as an outcome of hematogenous dissemination, especially in the cortical region. In some cases with pulmonary or disseminated tuberculosis, there is proof of renal failure without evidence of commonly localized lesions in the renal parenchyma. In these patients, interstitial nephritis is generally found, and in some cases, acid-fast bacilli can be detected by Ziehl-Neelsen staining.
What Causes Kidney Tuberculosis?
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The hematogenous spread occurs after a vessel erosion, mainly a vein in the lung, with emboli-containing microorganisms, which drop into the systemic circulation.
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Mycobacterium tuberculosis requires determinate environmental situations to grow, which causes its predisposition to other organs, that include the kidney, uterine tube, bone marrow, epididymis, and encephalus.
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In the kidneys, the best place for colonization by M. tuberculosis bacteria is the medullary region, where granulomatous lesions occur, with caseous necrosis, resulting in local tissue destruction.
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The renal lesion starts at the cortex, which grows to heal when the individual is resistant to this organism. Thereafter, the bacilli migrate to the cortico-medullary junction and form cortical granulomas.
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These granulomas remain dormant for years, and during reactivation, the bacterias occupy the renal medulla and result in papillitis.
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With disease advancement, large areas of papillary necrosis stimulate the formation of cavities that erode the renal parenchyma and migrate into the collecting system. The infection can result in papillary necrosis due to vascular insufficiency in renal papillae.
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The transmission of infection to the renal pelvis causes tuberculous pyelonephritis, which evolves into pyonephrosis.
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The infection typically transmits from the ureter to the bladder, affecting granulomatous lesions related to fibrosis. These procedures occur slowly for several years.
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In the ureter, the lesions induce a sequel of dilations intercalated with strictures, which comprises one of the most significant tuberculosis signs that can be seen in the pyelogram.
What Are the Symptoms of Kidney Tuberculosis?
Renal tuberculosis has an insidious onset, no particular symptoms, and atypical presentations, which bring difficulty and delay in diagnosis.
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Most patients present with local symptoms such as dysuria, pyuria, periodic voiding, back and flank pain, abdominal pain, and microscopic or macroscopic hematuria.
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Systemic signs of weight loss, fever, and anorexia are less common.
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Hematuria and culture-negative pyuria is detected in urine analysis.
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Many patients suffer from lower urinary tract infection symptoms, particularly bacterial cystitis, and doubts about tuberculosis are awakened only when there is no reaction to the antibacterial regimen or when urine examination indicates pyuria in the absence of a positive culture on routine media.
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Other symptoms include suprapubic pain and flank pain, increased frequency of urination, hematuria, and nocturnal pain. These symptoms are also suggestive of bacterial urinary tract infections.
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Renal colic is unusual, with symptoms such as weight loss, fever, and night sweats also being unusual.
How Is Kidney Tuberculosis Diagnosed?
The diagnosis can be done through the following methods:
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Culture Media - The diagnosis of tuberculosis of the kidney is based on the finding of pyuria in the absence of infection as assessed by culture on routine media.
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Intravenous Urography - In initial disease, it is often possible on intravenous urography to detect changes in a single calyx of the kidney with an indication of parenchymal necrosis, and generally there is calcification on the plain film. In advanced cases, urography shows calyceal distortion and bladder fibrosis.
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Kidney Ultrasound - An Ultrasound examination of the kidney and urinary tract can detect renal calyceal dilation and more overturned evidence of obstruction.
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Urinalysis - Urine analysis of residue from a 24-hour specimen for acid-fast bacilli (AFB) is positive in 80 to 90 percent of cases of tuberculosis. Urine culture requires six to eight weeks for diagnosis and there is a 10 to 20 percent false-negative rate. Laboratory results do not disclose the site or extent of the disease, understanding which is imperative for further management.
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Chest X-ray - Imaging plays a major role, both in the initial workup and during follow-up. A negative chest radiograph and tuberculin test cannot exclude the diagnosis of extrapulmonary tuberculosis. Evidence of active tuberculosis or an abnormal chest radiograph is present in less than 50 percent of cases.
How Is Kidney Tuberculosis Treated?
The treatment of kidney tuberculosis includes:
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All cases of active or latent tuberculosis require comprehensive treatment.
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The first-choice drugs are Rifampicin, Isoniazid, Pyrazinamide, Ethambutol, and Streptomycin. After diagnosis, chemotherapy with three or four drugs needs to be started immediately and concluded at least six months.
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Two regimens can be used. The first-line regimen used for six months is Isoniazid, Rifampicin, and Ethambutol or Pyrazinamide daily for two or three months; and Rifampicin and isoniazid twice a week for three or four months. The second-line regimen used for nine months includes Rifampicin, Isoniazid, Ethambutol, or Pyrazinamide daily for two or three months, followed by Isoniazid and Rifampicin, twice a week, for six to seven months.
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Rifabutin can replace Rifampicin to decrease drug interactions with drugs used in the treatment of human immunodeficiency virus (HIV)
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Patients with loss of renal function must receive doses of Isoniazid, Pyrazinamide, Rifampicin, and Ethionamide because these drugs have biliary excretion properties and are metabolized into compounds that are not excreted by the kidneys. However, precaution needs to be taken when administering Streptomycin, other aminoglycosides, and Ethambutol because these drugs have renal excretion properties. Ethambutol can lead to optic nerve neuritis, which is reversible if the dose is reduced based on the glomerular filtration rate (GFR). Streptomycin and other aminoglycosides can result in ototoxicity and nephrotoxicity and should not be used in patients with reduced renal function.
Conclusion
Renal tuberculosis is a slow and uncommon complication of pulmonary disease. It generally occurs after four or five years of primary infection and thus it is likely to be diagnosed during adolescence. The tubercle bacilli can be isolated from the urine in many cases of miliary tuberculosis. Infection can be unilateral or bilateral and can spread downward to involve the bladder. Hematuria, dysuria, and sterile pyuria are the initial findings in the urine. The surgical treatment is generally delayed to allow the completion of five to five weeks of anti-tuberculosis chemotherapy before surgery. Partial or complete nephrectomy may be needed to remove destructed kidneys or treat cases of recurrent cystitis.
