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RESEARCH ARTICLE
Year : 2004  |  Volume : 20  |  Issue : 2  |  Page : 19-23
 

Is contralateral renal involvement in genitourinary tuberculosis primary?


SGPGIMS, Lucknow, India

Correspondence Address:
A Mandhani
Department of Urology and Renal Transplantation, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow 226014
India
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Source of Support: None, Conflict of Interest: None


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   Abstract 

Objective: To know whether contralateral involvement in genitourinary tuberculosis is primary or sequential to the involvement of the bladder.
Methods: Retrospectively from June 1989 to Jan 1998 and then prospectively till Dec 2002, patients of genitourinary tuberculosis were reviewed. Of 147 patients complete record with follow up was available in 117. Diagnosis was considered proven only on the presence of one major and or two minor criteria. Major criteria were granulomatous lesion on histopathology, AFB positivity in urine or histopathology and a positive PCR. Minor criteria were changes suggestive of tuberculosis on intravenous urography, hematuria, raised ESR and or pulmonary changes of old Koch's lesion. Patients were grouped as group 1 (N=64) with renal involvement only, Group 2 (N=20) with renal and reversible bladder involvement and group 3 (N=33) with tubercular contracted bladder (capacity <250m1). Laterality and degree of involvement (grade I, single calyceal involvement, grade II more than one and grade 3, involvement of the ureter on intravenous urogram or Nephrostogram) were recorded.
Results: There was no difference in patient age, symptoms, positive urine culture for Acid fast bacilli in all 3 groups. Bilateral involvement was present in 23 (19.6%) patients and all the cases were in group 3. Of these, contra lateral lower ureteric stricture was present in 12 and vesico­ureteric reflux in 11 patients. None of these 23 patients on imaging showed calyceal changes in contra lateral kidney suggestive of primary hematogenous involvement. The only finding was pelvicalyceal dilatation, which was a consequence of reflux or backpressure changes. At a mean follow up 46.8±34.2 months no patient developed complication in the contra lateral kidney in terms of calyceal deformity and ureteric stricture.
Conclusions: As the involvement of the contralateral ureter is through the bladder, diagnosis of bilateral lower ureteric tubercular stricture in absence of contracted bladder should be made with caution. This fact would help in minimizing intervention on the contra lateral low grade reflux and prognosticating the reversibility of function in patients with renal impairment.


Keywords: Tuberculosis, genitourinary tuberculosis, intravenous urography.


How to cite this article:
Chaudhary H, Mandhani A, Dubey D, Jain M, Srivastava A, Kapoor R, Kumar A, Bhandari M. Is contralateral renal involvement in genitourinary tuberculosis primary?. Indian J Urol 2004;20:19-23

How to cite this URL:
Chaudhary H, Mandhani A, Dubey D, Jain M, Srivastava A, Kapoor R, Kumar A, Bhandari M. Is contralateral renal involvement in genitourinary tuberculosis primary?. Indian J Urol [serial online] 2004 [cited 2019 Nov 14];20:19-23. Available from: http://www.indianjurol.com/text.asp?2004/20/2/19/37162



   Introduction Top


Genitourinary tuberculosis (GUTB), which constitutes the second most common extra pulmonary site for tuberculosis, is a consequence of hematogenous spread [1],[2]. Disease usually occurs unilaterally and asymmetrically within the involved kidney [2],[3] . Bilateral involvement in GUTB is not uncommon but whether this is a primary phenomenon or a progressive spread from one kidney to other via bladder is not well defined. As lower urinary tract involvement occurs in 1/3rd of cases and is always secondary to upper tract involvement, the cause of bilateral ureteric stricture is attributed to tuberculosis even in the presence of normal bladder [2] . We hypothesized that the spread of tuberculosis is in a stepladd1er pattern to contra lateral side via bladder so the bilateral ureteric stricture in presence of a normal bladder is an unlikely event. In other words the primary bilateral involvement is very rare. [Figure - 1] This information is important as it helps in prognosticating the outcome of bilateral involvement in presence of impaired renal function and helps in deciding the need for contralateral ureteric re-implantation at the time of augmentation of contracted tubercular bladder.

This study analyzed the pattern of spread of tuberculosis in context to laterality of involvement of the genitourinary system.


   Patients and Methods Top


Retrospectively from June 1989 to Jan 1998 and then prospectively till Dec 2002, patients of GUTB were reviewed. Of 147 patients of GUTB, complete record with follow up was available in 117.

Diagnosis was considered proven only on the presence of one major and or two minor criteria [Table - 1]. Approach towards diagnosis included clinical history, previous history of tuberculosis, X-ray chest, ultrasonography (US) and intravenous urography (IVU). Patients with lower tract symptoms had micturating cystourethrogram. Tissue biopsy was taken from the bladder; cystoscopically in cases where urine Acid Fast Bacilli (AFB) was negative and at the time of augmentation.

Patients were divided into three groups based on the involvement of the bladder, documented clinically and histopathologically. Group 1 (n=64) had renal involvement only, Group 2 (n=20) had renal and bladder involvement with normal bladder capacity and group 3 (n=33) had tubercular contracted bladder. Only those patients with biopsy proven granulomatous cystitis were taken in Groups 2 & 3. Tubercular contracted bladder was defined as maximum capacity (functional, cystometric or capacity under anesthesia) of less than 250 ml that is incapacitating for the patients.

Variables like laterality, degree of involvement, haematuria, fever, lower tract symptoms, duration of the symptoms, hemoglobin, serum creatinine at the time of presentation, urine for AFB and radiological features on intravenous urography (IVU) were noted in all the patients. In patients with poorly visualized or non-visualized renal units, ultrasonography and CT scan when required and retrograde pyelography (RGP) was performed.

Upper tract involvement in these patients was graded based on the degree of involvement of pelvicalyceaI system and ureter on IVU and on RGP in non visualized kidneys. [Table - 2], [Figure - 2]. Depending on the presence or absence of ureteric abnormality radiological grade 3 or 2 was assigned to these patients respectively.

All the patients were given anti-tubercular treatment, consisting of an initial intensive 4 drugs for 2 months (Isoniazid, Streptomycin, Rifampicin and Pyrazinamide) followed by a maintenance phase of 7-16months of 2 drugs (Isoniazid and Rifampicin) depending on the severity of the disease. All cases had a minimum of 2 months of ATT prior to surgery and total duration of ATT ranged from 9 to 20 months.

Of 23 cases with bilateral involvement ureteric reimplantation was done in 16 at the time of augmentation ileocystoplasty. Twelve of these patients had lower ureteric stricture and 4 had grade III and IV reflux. 7 patients with grade I and II reflux were followed without reimplantation.

Patients were followed up on outpatient basis clinically and with serial serum creatinine, ultrasound and serial renal scans. Data were analyzed using ANOVA (analysis of variants) with a p<0.05 taken as significant.


   Results Top


Mean age of the patients was 33 (range 12-61) years. There were 52 males and 65 females. There were no difference in age of the patient, symptoms and renal function at the time of presentation in all 3 groups. Duration of symptoms was significantly more in group 3 patients [Table - 3]. AFB positivity was 40.6%, 65% and 81% and gross haematuria was present in 92.2%, 70% and 72.7% patients in groups 1-3 respectively [Table - 3].

All patients had some degree of involvement of upper tracts on intravenous pyelogram on one side and only 23 in group 3 had contra lateral involvement. Rest 94 patients did not show any evidence of GUTB on IVU.[Table - 4]. Grade 3 involvement was significantly higher in group 3 patients (94%).

Of the 23 cases with bilateral involvement, 17 patients had nonfunctioning kidney, 5 had grade 3 and one patient had grade 2 involvement on ipsilateral side. On contra lateral side lower ureteric stricture was present in 12 and vesico-ureteric reflux in 11 patients. None of these 23 patients on intravenous pyelography showed calyceal changes suggestive of primary hematogenous involvement of the contra lateral kidney. The only finding on the contralateral side was pelvicalyceal dilatation, which was possibly a consequence of backpressure changes due to lower ureteric stricture or vesico-ureteric reflux. [Figure - 3]

9 patients presented with raised serum creatinine 3.9±1.8mg% (range 2.5-8.4mg %). All these patients had one-sided non-functioning kidney and a contralateral lower ureteric stricture or vesico-ureteric reflux. Renal function improved in all but one case after putting contralateral nephrostomy or stent. Contralateral ureteric re­implantation was done in 8 patients where renal function improved. There was no deterioration of function on follow up. In 1 patient where renal function did not improve after contralateral diversion, definitive surgery was deferred due to high medical risks and was managed with antegrade ureteric dilatation and stenting.

At mean follow up of 46.8±34.2 months none of the 116 patients developed complication in the contra lateral kidney in terms of calyceal deformity and ureteric stricture [Table - 3].

22/23 patients with bilateral involvement are doing well and have not shown any evidence of calyceal involvement and renal impairment irrespective of their reimplantation status.


   Discussion Top


Genitourinary tuberculosis is one of the most common sites of extra pulmonary tuberculosis [2] . Renal tuberculosis is a secondary manifestation of hematogenous dissemination of tubercle bacilli from lungs and intestines, wherein, Mycobacteria settle in the periglomerular arterioles to form microscopic foci [4] . This leads to formation of granulomas with central Larigerhans giant cells surrounded with lymphocytes, fibroblasts and epitheloid cells. Later on depending on host resistance and virulence of the mycobacterium, tubercles either turn into fibrous tissues or coalesce to form typical casseating granulomas. Reactivation occurs between 5 to 15 years of initial infection [3],[5] . Lesions may slough into the collecting system or grow until they invade the papilla and become ulcerocavernous. This produces tuberculous bacilluria and subsequent involvement of the ureter and bladder [6].

Becker JA had observed that for unknown reasons the disease occurs unilaterally and asymmetrically within the involved kidney [3] . In literature it is not clear whether a bilateral renal involvement is due to simultaneous hematogenous spread of the tubercular bacilli or contra lateral renal involvement occurs through the lower urinary tract. This knowledge will help in deciding about the need for treatment on contra lateral side e.g. re-implantation and will also help in prognosticating recovery in the patients presenting with renal impairment.

Ureteric stricture constitute 10-20% of genitourinary tuberculosis [7] , this invariably results from tubercular bacilluria following rupture of renal focus into the calyx producing tubercular bacilluria. Other theoretical mechanisms described are through reflux of infected urine into the opposite ureter, primary hematogenous involvement and via passage of tubercular bacilli through communicating blood vessels and lymphatic between kidneys and ureter [8] . Had reflux of infected urine been the cause of contralateral involvement, this should have occurred in patients with normal bladder. In our series-none of the patients with normal bladder had contralateral involvement, thus we can assume that fibrosis of bladder occurs prior to the contralateral involvement in form of reflux or lower ureteric stricture.[Figure - 3]

Intravenous pyelography is a good modality for detecting early lesion of GUTB [2],[3] . Only 10-15% cases of macroscopic hematuria with positive urine AFB could present with normal IVU [4] . In all our patients some degree of involvement was present on intravenous pyelography. Bilateral involvement was present in 23 (19.6%) of the cases and all of these patients had tubercular contracted bladder. None of these 23 patients on intravenous pyelography showed calyceal changes suggestive of primary hematogenous involvement of the contra lateral kidney. The only finding on the contra lateral side was pelvicalyceal dilatation, secondary to reflux or backpressure changes.

Idea of assigning grade 3 to the ureteric involvement was that once ureteric stricture sets in, the backpressure effect on the kidney makes that unit resistant to salvage procedures [9] . Effect of ureteric stricture causing backpressure changes leading to atrophy and renal impairment is more pronounced than primary involvement of the renal parenchyma so prior knowledge in case of bilateral hydro-ureteronephrosis could foresee a long-term recovery.

Similarly bladder tuberculosis is due to tuberculous bacilluria from the kidney and starts usually at the ureteric orifice. Initially bladder tuberculosis manifests as superficial inflammation with bullous edema and granulations. Severe cases may involve entire bladder. Muscle layers may be eventually replaced by fibrous tissue producing thick fibrous contracted bladder. Edema and fibrosis in the region of the trigone may produce vesico-ureteral reflux and ureteral obstruction [7],[10]

In this series upper tract involvement was subtle in patients with normal capacity bladder as compared to patients with small capacity bladder (Grade 3 Involvement of upper tracts was present in 94% of Group 3 v/s 40% of Group 2 patients). Symptom duration in patients with contracted bladder is also significantly higher than the other group. This is consistent with literature that development of tubercular contracted bladder is directly proportional to the degree of upper tract involvement and the duration of disease [2] . None of the patients with normal bladder had contra lateral renal involvement as compared to 23(72%) patients who had contracted bladder. Thus the contra lateral renal changes were secondary to lower ureteric pathology, which occurred due to severe fibrosis of the bladder.

Therefore bilateral ureteral tuberculosis in a normal looking bladder is a rarity as none of the patients in the present series had this. Similarly patients with tubercular contracted bladder with nonfunctioning unit and contra lateral low-grade reflux did not show any deterioration in function and calyceal deformity in due course.

Though there is no clinical method to prove the direct involvement of contra lateral kidney in presence of ipsilateral non functioning unit with or without bladder involvement yet the supportive clinical evidence in the form of finding on intravenous pyelogram and remaining units faring well in long term follow up helps in proving the hypothesis of sequential bilateral involvement.


   Conclusions Top


A diagnosis of bilateral lower ureteric tubercular stricture in absence of contracted bladder should be made with caution as the involvement of the contralateral ureter is through the bladder.

This fact would help us minimizing intervention on the contra lateral side with low grade reflux and also prognosticating the reversibility in bilateral involvement with renal impairment. However this mechanism of sequential involvement of the contra lateral side needs a larger cohort of such patients to be verified and validated.

 
   References Top

1.Seung HK. Urogenital tuberculosis. In Pollack HM. Clinical Urography. 2nd ed. Philadelphia, WB Saunders, 2000. Pp. 1193-1228.  Back to cited text no. 1    
2.Bigongiari LR: Genitourinary tract tuberculosis. Radiologist 1994; 1: 19.  Back to cited text no. 2    
3.Becker JA. Renal tuberculosis. Urol Radiol. 1988; 10: 25-30.  Back to cited text no. 3    
4.Kenney PJ. Imaging of chronic renal infections. AJR Am J Roentgenol1990; 155: 485-494.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Cohen MS. Granulomatous nephritis. Urol Clin North Am 1986; 13: 647-659.  Back to cited text no. 5  [PUBMED]  
6.Tonkin AK, Witten DM. Genitourinary tuberculosis. Semin Roentgenol 1979; 14: 305-318.  Back to cited text no. 6  [PUBMED]  
7.Elkin M. Urogenital tuberculosis. In Pollack HM. Clinical Urography. 2nd ed. Philadelphia, WB Saunders, 1990: 1020-1052.  Back to cited text no. 7    
8.Friedenberg RM, Ney C, Stachenfeld RA. Roentgenographic manifestations of tuberculosis of ureter. J Urol 1968; 99: 25-29.  Back to cited text no. 8  [PUBMED]  
9.Carl P, Stark L. Indications for surgical management of genitourinary tuberculosis. World J Surg 1997; 21:505­510.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Pollack HM, Banner MP, Martinez LO, Hodson CJ. Diagnostic considerations in urinary bladder wall calcification. AJ RAm J Roentgenol 1981; 136:791-797.  Back to cited text no. 10    


    Figures

  [Figure - 1], [Figure - 2], [Figure - 3]
 
 
    Tables

  [Table - 1], [Table - 2], [Table - 3], [Table - 4]



 

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