Indian Journal of Urology
: 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

Correspondence Address:
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 Jan 29 ];16:111-115
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Of all the patients affected with tuberculosis, approxi­mately 15-20% have extra pulmonary infection in the form of urogenital tuberculosis. [1] 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. [2]

The reported incidence of calcification in urinary tract tuberculosis varies from 7.1% to 24% [3],[4],[5],[6],[7],[8] 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. [9]

 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. [10]

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. [11]

Cappel [12] 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. [13]

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. [13] 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. [14]

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. [14]

 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, [15] 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. [6]

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. [11]

As calcification is not pathognomic of tuberculosis un­less advanced, we need to consider a number of differen­tial diagnostic possibilities that show different character­istics. [16] 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. [1]

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. [10] 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 [10] 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. [3] 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.


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