Etiology and pathology
Urinary tuberculosis is part of systemic tuberculosis, mostly secondary to pulmonary tuberculosis, and rarely secondary to intestinal or osteoarticular tuberculosis. It can involve the kidney, ureter, bladder, urethra, prostate, seminal vesicles, testes, vas deferens, and fallopian tubes.
The pathological basis for radiological diagnosis of genitourinary tuberculosis is as follows: When Mycobacterium tuberculosis spreads to the genitourinary tract via blood or lymph, it often involves the renal cortex first. Under suitable conditions for growth, foci of caseous necrosis are formed, followed by the development of the renal medulla, which develops into foci of caseous necrosis in the renal papillae and subsequently spreads to the renal calyces to form tuberculous cavities, i.e., typical symptoms of renal tuberculosis appear, and the tuberculous lesions can spread to all parts of the genitourinary system with the urinary tract.
Clinical manifestations
I. Medical history
Frequent urination, urgent urination, painful urination and pus urination are common symptoms in the early stage, and hematuria in the naked eye is not uncommon.
2, the development of the disease may have fever, night sweats, wasting, weakness and other symptoms of tuberculosis poisoning, and often accompanied by other organs of tuberculosis corresponding symptoms.
3, long-term persistent chronic cystitis, and the general urine culture negative, and the general antibacterial drug treatment after the symptoms do not reduce but aggravate, even if the urine culture for general bacteria can not exclude the possibility of renal tuberculosis and secondary bacterial infection.
Physical examination: There are no positive signs in the early stage, but in the late stage, there are signs of tuberculosis systemic toxicity, such as fever, facial flushing and emaciation. Sometimes enlarged kidneys are palpable in the kidney area, with local pressure pain and percussion pain.
Auxiliary examination
The urine is often cloudy and washed, with a little urine protein, acidic reaction of fresh urine, leukocytes, pus cells and red blood cells on microscopic examination of the sediment, and a positive rate of more than 70% on direct smear antacid staining for Mycobacterium tuberculosis, and a positive rate of about 90% on culture or animal inoculation for Mycobacterium tuberculosis.
2, erythrocyte sedimentation rate is often increased. In advanced renal decompensation, there may be anemia and increased plasma urea nitrogen and myophenol values.
3.Urological X-ray plain film
4.Intravenous pyelogram
[Imaging performance]
1.Flat film
(1) Calcification of the renal parenchyma is the main finding. The low density of the calcification foci is not very clear, which is due to the small amount of calcium salt deposition within the caseous necrotic material. The calcification foci can be small and single, or scattered and multiple. When whole kidney calcification appears, the kidney may atrophy and become small, and the kidney function is very poor or non-functional. This kind of whole kidney diffuse calcification is called “self-truncated kidney”, which is common in advanced renal tuberculosis.
(2) Ureteral calcification: Sporadic calcium salt deposits along the ureter with tuberculosis.
(3) Calcification of the bladder: there are mostly dense shadows on the bladder wall.
(4) The prostate, seminal vesicles, and vas deferens also have scattered or curved dense linear dot-like shadows.
2.Urographic and CT findings
(1) The urography begins to show early changes after the tip of the renal cone is involved in renal tuberculosis, showing a mildly blurred irregular shape in a certain calcium. If the lesion continues to expand, the renal calyx also expands and is accompanied by irregular destruction, indicating that the renal cone and cortex have undergone erosion and necrosis, and further development of the lesion, the appearance of the renal calyx is like feathery or worm-like necrosis, and the contrast agent can be seen outside the calyx, and even the fistula between the involved renal calyx and the cavity can be seen.
(2) Extensive caseous necrotic cavities in the kidney with large irregular foci of contrast-fillable destruction are seen in the advanced stage of renal tuberculosis, and such cavities are more clearly shown in the enhanced CT images with pus accumulation in the cavity, watery density, and no enhancement. Extensive renal tuberculosis destruction is accompanied by repair, and large amounts of calcium salts are deposited in the foci of renal caseous necrosis, which can become non-functional kidneys, called “self-cutting kidneys”.
(3) The early manifestation of ureteral tuberculosis is dilatation of ureter with worm-like edges, which is caused by the invasion of the ureteral muscle layer by the nodal pattern, resulting in dystonia and multiple ulcers. Subsequently, the ureteral wall thickens and thickens, loses elasticity, and peristalsis disappears. When there is a large amount of fibrotic scar deformation, the ureteral lumen is narrowed or the narrowing and dilatation alternate, manifesting as bead-like, spiral, and finally may become a short and rigid thin tube, or even completely atretic, all accompanied by hydronephrosis on the affected side.
(4) Tuberculosis of the bladder is mostly caused by the downstream spread of tuberculosis in the upper urinary tract. There is blurring and marginal irregularity at the junction of the vesicoureter, volume reduction, spasm and fibrosis, and the “small bladder sign”. Sometimes lamellar foci of calcification are seen in the bladder wall. If the bladder tuberculosis involves the ureteral orifice of the healthy bladder, the sphincter atresia is incomplete and urinary reflux occurs, which leads to the phenomenon of hydronephrosis on the healthy side.
(5) Urological tuberculosis can spread to reproductive organs, including prostate, seminal vesicles, epididymis and vas deferens in men, mainly through the tuberculosis bacilli in the urine of the kidney entering the prostate and seminal vesicles through the prostatic tubules and ejaculatory ducts of the posterior urethra, and then from the vas deferens to the epididymis and testes, and also through hematogenous dissemination to these organs.
3.B ultrasound: early stage cannot be detected. The middle and late stages can show.
①Nodular cavity: single or multiple liquid dark areas with unsmooth edges and scattered light spots inside .
(2) Calcification of renal parenchyma: in small cases, small light clusters with acoustic shadow, in large cases, whole kidney calcification, showing dense arc-shaped light clusters with posterior acoustic shadow.
③When the lesion is extensive and becomes a septic kidney, the hydronephrosis sound image appears.
④The renal envelope is blurred or the kidney is shrunken and deformed.
Calcification of left renal tuberculosis: Plain film shows encapsulated calcification in the left kidney area, and there are also patches of calcification within it, which is a “self-cut kidney”. Calcification of the left ureter is also seen.
The kidney and ureter were found to be tuberculous. Retrograde imaging shows enlarged hydronephrosis in the left upper and middle calyces, partial destruction of the lower calyces, partial calcification in the renal parenchyma, and irregular destruction and dilatation of the upper left ureter. The bladder volume is small with irregular margins
[Differential diagnosis]
Differential diagnosis of urinary tract tuberculosis.
(1) Calcification caused by renal and ureteral tuberculosis should be differentiated from calculi. The latter are dense, mobile and located in the lumen.
(2) Calcification of seminal vesicles is mostly tuberculous, and calcification of prostatic tuberculosis should be distinguished from stones.
(3) Tuberculous hydronephrosis should be distinguished from non-tuberculous hydronephrosis.
Treatment of [renal tuberculosis]
Since renal tuberculosis is part of systemic tuberculosis, treatment must pay attention to both systemic and local treatment in order to achieve satisfactory results. Specifically, on the one hand, anti-tuberculosis drugs, proper rest, sunlight and adequate nutrition are given, and on the other hand, diseased kidney or diseased tissues are surgically removed as needed to shorten the course of treatment and improve the efficacy.
The indications for drug therapy are:
(1) preclinical renal tuberculosis.
(2) renal tuberculosis with small lesions.
(3) Bilateral or solitary renal tuberculosis that is in advanced stage and not suitable for surgery.
(4) Active tuberculosis in other parts of the body, which is not suitable for surgery for the time being.
(5) Patients with other serious diseases that are temporarily unfit for surgery.
There are many kinds of anti-tuberculosis drugs, such as isoniazid, streptomycin, para-aminosalicylic acid, rifampin, kanamycin, cycloserine, ethambutol, ethanethionamide, pyrazinamide, tendragynine, etc. Generally, a combination of 3 drugs is used: isoniazid 100 mg orally 3 times a day; streptomycin l g daily in two intramuscular injections, changing to 2 g weekly after l-3 months; and sodium para-aminosalicylate 2-4 g 4 times a day. To reduce the gastric irritation of sodium para-aminosalicylate, sodium bicarbonate can be added at l gram 3 times a day. Of course, it can be combined with other drugs listed above. The medication course is 2 years, with a minimum of l-1.5 years. It is also possible to combine rifampin 600 mg, isoniazid 300 mg and pyrazinamide 1.0 g with the application of vitamin C 1.0 g orally once a day. After two months, the treatment was changed to rifampicin and pyrazinamide and continued for 4 months.
(ii) Surgical treatment.
Surgical treatment of renal tuberculosis includes nephrectomy, partial nephrectomy and nephrogenic lesion removal. The choice of surgical method depends on the extent of the lesion, its degree and its response to drug therapy.
1, nephrectomy: unilateral nephrotuberculosis with a large extent of destruction, unilateral tuberculous septic kidney, calcified kidney, if the contralateral kidney function is good, all adapt to nephrectomy. In case of bilateral renal tuberculosis, if one side is severely damaged and the renal function is lost while the other side is mild enough to compensate, the kidney on the heavy side should be removed with the cooperation of anti-tuberculosis drugs.
2.Partial nephrectomy: If the lesion is confined to one pole of the kidney and does not improve after long-term drug treatment, or if it is complicated by poor drainage of urine due to narrowing of the funnel of the kidney, partial nephrectomy is indicated.
If the tuberculosis cavity formed near the surface of the renal parenchyma is not accessible to the renal calyx and drug treatment is ineffective, nephrectomy is feasible.
(C) Principles of management of late complications of renal tuberculosis.
The late complications of renal tuberculosis mainly include contralateral hydronephrosis and bladder contracture.
1, the principle of management of contralateral hydronephrosis is to remove the tuberculous kidney first if the kidney function on the hydronephrosis side is sufficient to compensate and the blood urea nitrogen and creatinine are normal, and then deal with hydronephrosis; if the kidney function on the hydronephrosis side is not compensated and the blood urea nitrogen and creatinine are elevated, nephrostomy on the hydronephrosis side should be performed first, and then remove the tuberculous kidney and deal with hydronephrosis after the kidney function improves. When dealing with hydronephrosis on the opposite side, if there is no bladder contracture, ureteral bladder reimplantation is feasible.
2, bladder contracture, then bladder enlargement should be performed along with ureteral intestinal transplantation. The principle of management of bladder contracture is that if there is no urethral stricture or vesicovaginal fistula, sigmoid cyst enlargement is often used. In case of urethral stricture or vesicovaginal fistula, ileal cystectomy or rectal cystectomy is used.