Basic methods: Ultrasound and intravenous urography
Ultrasound (US) and intravenous urography (IVU) remain essential primary tools in evaluating specific lesions of the renal parenchyma.
On echograms (US), changes depend on the stage of the process. Focal lesions—both hyperechoic and hypoechoic—may be identified within the parenchyma. As the disease progresses and calcifications form, a diffuse increase in echogenicity (hyperechoic renal tissue) is observed. In severe cases, a localized abscess may form.
Intravenous urography (IVU) allows detailed evaluation of the pelvicalyceal system and identification of classic signs of tuberculosis involvement:
- Parenchymal calcification.
- Presence of cavitary destructive changes.
- Stenosis of the calyx neck (infundibulum), leading to the characteristic radiological pattern of "amputated" calyces.
- Renal pelvis stenosis, inevitably causing secondary hydronephrosis.
Computed tomography and magnetic resonance imaging
Tomographic methods provide the most accurate spatial depiction of pathological changes, particularly when assessing contrast agent enhancement.
CT semiotics:
- On unenhanced CT scans, a tuberculosis focus (e.g., in the upper pole of the kidney) is usually visualized as a hypodense area.
- Upon contrast administration (on axial slices), marginal (peripheral) contrast enhancement is noted.
MRI semiotics: Tuberculosis granulomas present as soft-tissue formations that generally demonstrate rather weak contrast enhancement.
- T2-weighted images (T2WI): lesions demonstrate high signal intensity.
- T1-weighted images (T1WI): the lesion area is generally isointense relative to the unaffected renal parenchyma.
- T1-weighted GRE with contrast enhancement: clearly demonstrates ring-like enhancement (rim sign) at the edges of the lesion, as well as weak enhancement of internal septa.
Terminal stage: "Putty kidney"
A specific outcome of long-standing untreated tuberculosis is the "putty kidney" (Putty kidney) phenomenon. This is the terminal stage of the disease characterized by complete loss of organ function (autonephrectomy).
The entire organ undergoes total dystrophic calcification. On imaging, this appears as follows:
- Plain radiograph: a massive radiopaque (calcified) bean-shaped formation is visualized, completely repeating the contours of the affected kidney.
- Unenhanced CT (coronal projection): dense hyperdense calcified material is determined. It not only replaces the parenchyma but also densely fills the lumens of the dilated renal calyces and even the upper third of the ureter.
Complex clinical cases and associated pathologies
Tuberculosis can affect kidneys with developmental anomalies, significantly complicating the imaging picture. A striking example is bilateral tuberculosis in a horseshoe kidney.
In such cases, asymmetric involvement can be observed on CT reconstructions:
- One half (e.g., the right kidney) may be small, atrophic, and completely calcified (a state of autonephrectomy).
- The other half (in the lower pole of the left kidney) may show a large cystic formation with marginal calcification that does not enhance with contrast.
- The fibrous isthmus connecting the lower poles of the anomalous kidney is clearly visualized on contrast-enhanced axial CT scans, located anterior to the abdominal aorta and inferior vena cava.
It is also important to remember that tuberculous infection can spread along the urinary tract, becoming a specific etiological cause of cystitis (inflammation of the urinary bladder).
Briefly: answers to topical questions
What diseases require differential diagnosis with renal tuberculosis based on imaging data?
Differential diagnosis of renal tuberculosis using imaging methods must be carried out with complicated urinary tract infections and various tumor lesions.
- Xanthogranulomatous pyelonephritis (XPN) and renal abscess — differentiated in the context of diagnosing complicated infections.
- Tumor lesion — must be excluded when volumetric destructive formations are identified in the parenchyma.
What clinical and radiological stages of the destructive process are distinguished in renal tuberculosis?
Several stages of the destructive caseous-necrotic process are distinguished in renal tuberculosis.
- Initial destructive form — tuberculous papillitis with involvement and ulceration of the renal papilla.
- Cavernous tuberculosis — formation of one or more cavities in the parenchyma.
- Widespread destruction — polycavernous (fibrocavernous) tuberculosis with involvement of the pelvicalyceal system.
- Total purulent-destructive lesion — tuberculous pyonephrosis with impaired urine outflow.
- Outcome of the process — renal shrinkage or calcification (autonephrectomy) with mineralization ("tuberculous putty").
What are the main pathways of Mycobacterium tuberculosis penetration into the renal tissue?
The main pathway of mycobacterial penetration into the renal tissue is hematogenous.
- Hematogenous pathway — is the main one, occurring during primary dissemination of mycobacteria from a pulmonary or intestinal focus.
- Lymphogenous pathway — is possible in case of tuberculous involvement of the peritoneum.
- Contact pathway — is realized when the specific process spreads from the peritoneum to adjacent organs.
What specific complications from the ureter and urinary bladder does descending tuberculous infection cause?
Descending (urinogenic) tuberculous infection causes a number of specific complications of the urinary tract.
- Ureter — formation of scar strictures and obliterations, and with total involvement, urinary obstruction and reflux develop.
- Urinary bladder — contracture and persistent decrease in organ capacity with the development of microcystitis (shrunken small bladder).
For memorizing the IVU pattern: "Amputated calyces" — the infection "cuts off" the outflow pathways due to infundibular stenosis.
Class and exam questions
What is a «putty kidney»?
This is the terminal stage of renal tuberculosis, characterized by a non-functional organ (autonephrectomy) and massive dystrophic calcification of the entire parenchyma and pelvicalyceal system.
What do tuberculous lesions look like on MRI?
On T2WI they have high signal intensity, on T1WI they are isointense to the parenchyma. Upon contrast administration (T1 GRE), typical ring-like enhancement at the periphery of the lesion and weak enhancement of the septa are noted.
What is the classic sign of renal tuberculosis detected on intravenous urography?
Stenosis of the calyx neck (infundibulum), which forms the characteristic radiological pattern of "amputated" calyces.
What changes does unenhanced CT detect in a «putty kidney»?
Hyperdense calcified material densely filling dilated calyces and the upper third of the ureter.
What else to study on this topic
- Encrusted pyelitis as a differential diagnosis in pelvic calcification
- Specific tuberculous cystitis and its radiation differentiation
- Emphysematous cystitis in immunocompromised patients
- Diagnostic imaging of prostatic abscess on TRUS and MRI
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