Imaging
Imaging Findings in Renal Tuberculosis on Computed Tomography Urography Emilio Quaia, MD1
and Fulvio Stacul, MD2 1. Assistant Professor; 2. Consultant Radiologist, Department of Radiology, Cattinara Hospital, University of Trieste
Abstract
Genito-urinary tuberculosis is the most common manifestation of extrapulmonary tuberculosis. Classic findings of renal tuberculosis on computed tomography (CT) urography include calcifications, deformation of calyces, obstructive hydronephrosis or hydrocalyx, and medullary and papillary necrosis. The different macroscopic patterns of renal tuberculosis on CT urography include: the open form, with extension of the caseified necrosis to the intra-renal excretory tract; the closed form, with extension of necrosis toward the renal parenchyma with progressive tissue scarring; and putty kidney.
Keywords Renal tuberculosis, kidney, computed tomography urography, chronic infection
Disclosure: The authors have no conflicts of interest to declare. Received: June 14, 2010 Accepted: September 9, 2010 Citation: US Nephrology, 2011;6(2):138–41 Correspondence: Emilio Quaia, MD, Assistant Professor, Department of Radiology, Cattinara Hospital, University of Trieste, Strada di Fiume 447, Trieste, 34149, Italy. E:
quaia@univ.trieste.itv
Genito-urinary tuberculosis is the most common manifestation of extra-pulmonary tuberculosis,1,2 outside the lungs.3
accounting for 15–20 % of infections
Approximately 4–8 % of patients with pulmonary tuberculosis will develop a clinically significant genito-urinary infection.3 Mycobacterium tuberculosis reaches the genito-urinary organs, particularly the kidneys, through haematogenous seeding from disease in the lungs. The seeding occurs at the time of the initial lung infection, with seeding of M. tuberculosis in the peri-glomerular and peri-tubular capillary beds. Small granulomas form in the renal cortex bilaterally, adjacent to the glomeruli, and remain stable for many years.4
A high rate of perfusion and
In patients with intact cellular immunity, the disease remains confined to the renal cortex; however, in some patients the breakdown of host defense mechanisms leads to reactivation of the cortical granulomas with enlargement and coalescence, and organisms spread into the renal medulla, causing a papillitis that can extend into the collecting system.4 After capillary rupture, the organisms migrate to the proximal tubule and loop of Henle, with eventual development of enlarging, caseating granulomas and papillary necrosis. Granuloma formation, caseous necrosis, and cavitation are the stages of progressive infection that will ultimately determine the loss of renal function and calcification of the entire kidney (autonephrectomy).
favorable oxygen tension increase the likelihood of bacilli proliferating in this location.3
The renal disease remains quiescent until there is an insult to the host’s immunity, at which point reactivation occurs. Patients with genito-urinary tuberculosis typically have local symptoms including frequent voiding and dysuria. Hematuria can be either microscopic or macroscopic. Symptoms may also include back, flank, or abdominal pain.3,5
Constitutional symptoms such as fever, weight loss, fatigue, 138
It must be emphasized that each finding of renal tuberculosis can be caused by other diseases, but multiple abnormalities are usually present and allow a correct diagnosis. It is for this reason that renal tuberculosis is called ‘the great imitator.’ On plain film and unenhanced computed tomography (CT), the kidney may appear large, normal-sized, or small. Despite hematogenous seeding of both kidneys, clinically significant disease is usually limited to one side: approximately 75 % of renal tuberculous involvement is unilateral. The grayscale ultrasound (US) appearance of renal tuberculosis is not specific. US is advisable to evaluate the non-functioning kidney after iodinated contrast agent injection and for follow-up during antitubercular therapy. The kidney may appear large, normal-sized, or small, and calcifications are common. Hydronephrosis or hypoechoic parenchymal lesions, which correspond to parenchymal abscesses resulting from caseating necrosis, may be observed.
Computed Tomography Urography
CT urography, as was previously the case for intravenous excretory urography, is today considered the correct imaging technique to assess
© TOUCH BRIEFINGS 2011
and anorexia are less common.3,5
Laboratory abnormalities include
pyuria, proteinuria, and hematuria. Standard urine cultures can be normal. Furthermore, the presence of routine urinary tract pathogens can delay the diagnosis of coexistent tuberculosis.3
isolated from the urine in 80–95 % of patients with genito-urinary tuberculosis. In adults, renal tuberculosis is the most common etiology of infundibolar strictures with consequent hydrocalyx. Obstruction may develop early or during the healing phase, even while the patient is receiving antituberculous therapy.
M. tuberculosis is
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80 |
Page 81 |
Page 82 |
Page 83 |
Page 84