Year : 2000 | Volume
: 16 | Issue : 2 | Page : 111--115
Calcification in urinary tract tuberculosis
Vatsala D Trivedi, Mukund G Andankar, Sujata Salve-Satwekar
Lokmanya Tilak Municipal Medical College and General Hospital, Mumbai, India
Vatsala D Trivedi
Lokmanya Tilak Municipal Medical College and General Hospital, Mumbai - 400 022
Objective: To review the incidence, nature and importance of calcification in urinary tract tuberculosis.
Method: The cases of urinary tract tuberculosis from Jan. 1995 to June 1998 were reviewed. 10 out of 32 patients showed evidence of calcification with the incidence of 31.2%. All the patients had renal parenchymal calcification with two cases associated with ureteral calcification.
Results: We performed nephroureterectomy in 4 cases who had putty kidney. 2 patients were subjected for polar nephrectomy, 1 for showing increase in size on follow-up and the other for associated destruction of polar parenchyma. One of these patients showed evidence of active tuberculosis on histopathology. 4 patients with small areas of calcification are being followed with yearly x-ray.
Conclusion: Calcification in urinary tract tuberculosis can increase in size leading to destruction of parenchyma even on treatment. It may also be associated with active tuberculosis. Hence patients should be treated with surgery or followed up intensely with the aim of retaining as much of parenchyma as possible.
|How to cite this article:|
Trivedi VD, Andankar MG, Salve-Satwekar S. Calcification in urinary tract tuberculosis.Indian J Urol 2000;16:111-115
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Trivedi VD, Andankar MG, Salve-Satwekar S. Calcification in urinary tract tuberculosis. Indian J Urol [serial online] 2000 [cited 2020 Sep 30 ];16:111-115
Available from: http://www.indianjurol.com/text.asp?2000/16/2/111/22207
Of all the patients affected with tuberculosis, approximately 15-20% have extra pulmonary infection in the form of urogenital tuberculosis.  The latent period between the original pulmonary infection and appearance of clinical renal disease is usually 5 to 20 years. Therefore renal involvement is predominant between 2nd and 4th decades and is distinctly low in children. Although the overall incidence of pulmonary tuberculosis is declining, calcification in urinary tract is a growing hazard and is assuming increasing importance. 
The reported incidence of calcification in urinary tract tuberculosis varies from 7.1% to 24% ,,,,, as depicted in [Table 1].
The importance of calcification is due to its capacity to increase in size, causing parenchymal destruction, inspite of the patient being on anti-tubercular drugs. The calcified matrix also harbours live mycobacteria as described by Wong & Lan in 28% of patients. 
Etiopathogenesis and Nature of Calcification
The cause of calcification in genitourinary tuberculosis remains obscure and there is no evidence to support different pathogenesis for tuberculous calcification.
Occasionally, precipitating factors that are known to be associated with calculus disease, such as prolonged recumbency, high calcium intake, recurrent urinary tract infection, obstructive uropathy and hypercalciuria are found but there is no common denominator. 
With regard to the actual process of calcification in tissues, Beattie and Dickson regard it as a retrogressive change characterised by the deposition of insoluble calcium salts, especially phosphate and carbonate, in cells or degenerative tissues. They regard this condition as an excessive development in the process of chronic inflammation. This deposition of calcium is of course due to local changes and unrelated to variations of blood calcium. 
Cappel  suggests that phosphate ions liberated by the disintegration of nucleoproteins and phospholipids in necrosed tissues may attract calcium and lead to the formation of lime salts containing carbonate and phosphate in the same proportions as bone. There seems to be a general agreement that calcification is usually preceded by a hyaline stage. Damage to the cell membranes causing increased permeability leads to disturbance of intracellular cations and accumulation of calcium in the damaged cells. This in turn impairs oxidation so that cellular respiration is impaired and the cell dies.
Although calcification is unusual in the early stages of the disease, nearly every end stage tuberculous kidney contains calcification. The calcification may take a variety of patterns, which in most cases is not specifically diagnostic of tuberculosis. 
The calcification in renal tuberculosis can be either homogenous or heterogenous. Elken has described the radiological features in tuberculosis as smudgy i.e. a faintly calcified area with indistinct borders and speckled if it is sharply defined with calcific densities of varying size. If calcification occurs at the boundary between necrotic and viable tissue, its appearance is that of curvilinear calcification.  When the configuration of renal calcification defines a renal lobe, it is referred as lobar. The putty kidney is the one which is totally destroyed; it is caseated, densely calcified and is usually associated with obstruction. 
Tuberculosis of the ureter produces ulceration, fibrosis, stricture and calcification. Calcification of the kidney extending along the ureter is virtually diagnostic of tuberculosis. The prostate, seminal vesicles and vas deferens may calcify but this is not pathognomic of tuberculosis. 
Material and Methods
10 patients out of 32 cases of urinary tract tuberculosis who presented to us from Jan 1995 to June 1998 showed evidence of calcification with incidence of 31.2%. All were renal parenchymal with two cases associated with ureteral calcification. We had no case with bilateral renal involvement or urinary bladder involvement. We did not find any age or sex predilection. All patients presented with fever, pain or voiding symptoms and none was diagnosed incidentally. 50% had constitutional symptoms. 50% had past history of pulmonary tuberculosis with mean duration between pulmonary infection and clinical renal disease of 10 years.
All the calcifications were detected by plain x-ray [Figure 1],[Figure 3], IVU or ultrasound. The diagnosis of tuberculosis was made based on clinical features, urine AFB smear and culture, radiological features and cystoscopy if needed. Although CT scan has been described to detect calcification with greater accuracy, precision and sensitivity,  none of our cases warranted CT scan. We advice CT only if there is a doubt about diagnosis or a malignancy needs to be ruled out. None of our patients had obvious etiological contributing factors towards promoting calcification.
We performed nephroureterectomy in four out of ten cases of calcification [Figure 2]. They all had extensive calcification with a non-functioning kidney.
We subjected two patients for polar nephrectomy. One of the patients showed significant increase in size at one year of review. The area of calcification almost tripled in size in that duration, involving upper pole. The other patient had dense lower polar calcification with destruction of parenchyma. The histopathology report of resected specimen in this case showed evidence of active tuberculosis. The histologically active cases are those which show the presence of active epitheloid and round cell reaction with or without a fibroelastic proliferation around the periphery of a lesion. The histological inactivity is attributed to a specimen, which shows little or no epitheloid reaction and no ulcerocavernous lesions but shows evidence of granulomatous process. 
We are following 4 cases with small areas of calcification with yearly plain x-ray and limited IVU. None of these have shown increase in size in follow-up of 3 years.
The success attending the use of chemotherapy in the treatment of genitourinary tuberculosis has left a number of associated problems such as stricture formation, contracted bladder, pyelonephritis, calcification and others. Calcification in the kidney requires careful watching and merits treatment due to its potential to increase in size and parenchymal destruction in spite of antitubercular drugs. 
As calcification is not pathognomic of tuberculosis unless advanced, we need to consider a number of differential diagnostic possibilities that show different characteristics.  Renal neoplasms such as renal carcinoma may calcify. In these cases the calcification is rarely confluent and there is usually a mass that projects beyond the renal contour and displaces the adjacent calyx.
Shockwave lithotripsy when complicated by renal contusion or hematoma may calcify but is not associated withcalyceal changes or papillary necrosis.
Xanthogranulomatous pyelonephritis may be associated with segmental calcification. But in addition there is almost always an obstructing calyceal calculus, and a focal necrotic mass replacing the parenchyma and calyx. Confluent parenchymal calcification is never seen.
Calyceal blunting without an overlying parenchymal scar and without pelvic dilatation and calcification indicates papillary necrosis. The common causes of papillary necrosis include analgesic nephropathy, s-hemoglobinopathy, obstruction combined with infections like tuberculosis. Only tuberculosis is associated with calcification and calyceal truncation.
Transitional cell carcinoma originating with a calyx may amputate the underlying calyx. The calcification seen within the renal transitional cell carcinoma is more typically stippled within a luminal filling defect or is dystrophic within a mass. It does not exhibit confluent parenchymal calcification seen in tuberculosis.
Another feature of clinical interest is the association of calcification and free lying calculi with renal tuberculosis although we did not encounter such a case. It is often difficult to differentiate between calculi and calcification in the renal substance. Free lying calculi should not divert the focus of the clinician from carefully assessing for features of tuberculosis disease also. 
The aim of management of calcification in renal tuberculosis should be to retain as much functioning renal tissue as possible. The small lesions can be kept under review on an annual basis and managed conservatively provided there is no increase in size. This review should continue for ten years or longer because sudden increase in size may occur requiring surgical intervention. However most of the small calcified lesions remain unchanged for more than 20 years.  We have 4 cases with small areas of calcification being followed up with yearly plain x-ray. None of these have shown increase in size in follow up of three years.
J.G. Gow  has recommended removal of non-functioning kidneys with extensive calcification and excision of larger areas of calcification. We performed nephroureterectomy in four patients. They all had extensive calcification with non-functioning kidney. The opposite kidney was normal. The histopathology showed evidence of granulomatous process.
Partial nephrectomy is indicated if there is a localised polar lesion containing calcification that has failed to respond to 6 weeks of chemotherapy or an area of calcification slowly increasing in size. We have carried out polar nephrectomies in two such cases. Partial nephrectomy is also justified in such cases because of the fact that resected specimen may show histopathological evidence of tuberculosis even if the patient has received adequate chemotherapy as shown in 2 out of l l cases by J. G. Gow. The calcified matrix can also harbour live mycobacteria with a reported incidence of 28% by Wong and Lan.  In one of our cases, the histopathology of resected specimen showed evidence of active tuberculosis.
In view of significant possibility of active tuberculosis being associated with calcification, patients should be treated with surgery or followed up intensely with the aim of retaining as much of functioning parenchyma as possible. The calcification can increase in size and cause destruction of parenchyma even when patient is kept on antitubercular drugs. While the smaller lesion should be reviewed for prolonged periods, at least 10 years, larger areas need surgical management.
|1||Colabawalla BN. Reflections on urogenital tuberculosis. Indian J Urol. 1990; 6: 51-59.|
|2||Antonio D, Gow JG. Renal calcification in genitourinary tuberculosis. A clinical study Int Urol Nephrol 1975; 7: 289.|
|3||Crenshaw JL. Renal tuberculosis with calcification. J Urol. 1930; 23: 515.|
|4||Olsen S. Associated Renal Pathology in renal tuberculosis. J Urol 1930;23:81.|
|5||Mathe CP. Unilateral renal tuberculosis: management of the nephrectomised patient, review of ninety-eight cases. J Urol 1947; 57:451-458.|
|6||Cow JG. Renal calcification in genitourinary tuberculosis. Br J Surg 1965;52:283.|
|7||Cruz HMM, Cruz J, Penna DDO, Almeida SSA. Urolithiasis and parenchymal calcification in renal tuberculosis. Rev Hosp Clin Fac Med Sao Paulo 1966; 21: 133-141.|
|8||Marszalak WW, Dhai A. Genitourinary tuberculosis. S Afr Med J 1982;62:158.|
|9||Won- SH, Lau WY. The surgical management of non-functioning tuberculosis kidneys. J Urol 1980; 124: 187-191.|
|10||Gow JG. Genitourinary tuberculosis. In: Campbell's Urology, 7th ed. Philadelphia, Saunders, 1998: 807-836.|
|11||Cosbie Ross J. Calcification in genitourinary tuberculosis. Br J Urol. 1970; 42: 656-660.|
|12||Cappel DF. Disturbances of nutrition (calcification). In: Muir's textbook of pathology, 8th ed. ELBS and Edward Arnold publishers: 1964, 116-121.|
|13||Elkin M. Urogenital tuberculosis. In: Pollack HM ed. Clinical Urography. Philadelphia, Saunders, 1990: 1020-1052.|
|14||Suleman Merchant. Indian J Radiol Imag 1993: 3: 253-254.|
|15||Elkin M. Radiology of the urinary system. Boston, Little Brown and Co, 1980: 148-156.|
|16||Hartman AG, Stagg AS. Renal tuberculosis. Radiology 1998; 208: 69-72.|