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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2011  |  Volume : 22  |  Issue : 2  |  Page : 306-310
Tumoral calcinosis, calciphylaxis, hyperparathyroidism and tuberculosis in a dialysis patient


1 Department of Nephrology, Hedi Chaker Hospital, Sfax, Tunisia
2 Department of Histopathology, Habib Bourguiba Hospital, Sfax, Tunisia
3 Department of Radiology, Habib Bourguiba Hospital, Sfax, Tunisia

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Date of Web Publication18-Mar-2011
 

   Abstract 

Tumoral calcinosis and calciphylaxis are uncommon but severe complications in ure­mic patients. They occur generally after long-term hemodialysis (HD) treatment explained by ad­vanced secondary hyperparathyroidism and longstanding high calcium phosphorus product (Ca × P). Other factors such granulomatous diseases may worsen the calcium phosphate homeostasis alterations. We report a young male patient treated by HD for 6 years who developed tuberculosis in addition to tumoral calcinosis and calciphylaxis.

How to cite this article:
Kammoun K, Jarraya F, Hmida MB, Khebir A, Kharrat M, Boudawara T, Mnif J, Hachicha J. Tumoral calcinosis, calciphylaxis, hyperparathyroidism and tuberculosis in a dialysis patient. Saudi J Kidney Dis Transpl 2011;22:306-10

How to cite this URL:
Kammoun K, Jarraya F, Hmida MB, Khebir A, Kharrat M, Boudawara T, Mnif J, Hachicha J. Tumoral calcinosis, calciphylaxis, hyperparathyroidism and tuberculosis in a dialysis patient. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2019 May 21];22:306-10. Available from: http://www.sjkdt.org/text.asp?2011/22/2/306/77612

   Introduction Top


Tuberculosis (TB) is not an uncommon di­sease in chronic hemodialysis (HD) patients and results in a significant morbidity and morta­lity. [1],[2],[3] Among the bone changes associated with renal failure, extraskeletal calcification is a com­monly observed feature, but tumoral calcinosis and calciphylaxis are uncommon. [4],[5] Increased calcium phosphate product in serum plays a sig­nificant role. The presence of a granulomatous disease (TB) may facilitate the development of the soft tissue calcifications in HD patients.

We report a case of a male HD patient with TB and both tumoral calcinosis and calciphy­laxis.


   Case Report Top


A 36-year-old man underwent HD treatment in 1998 because of end-stage renal failure from unknown initial nephropathy. He was treated by regular HD for 4 hours two times weekly using polysulfone HPS dialyzer and acetate buffer with 1.75 mmol calcium dialysate.

In June 2004, he was admitted to our center because of tumoral mass and ascites. He repor­ted bilateral shoulder and right hip pain for one year, associated with appetite loss, general fa­tigue, and systemic high fever. He was on oral CaCO3 1.5 g/day.

Physical examination revealed cachexia and fever at 38°C, and three periarticular masses be­hind sternoclavicular articulations and the left el­bow; these masses were non-tender and immo­bile. Gangrene of the third and fourth toes of the two feet was observed. Moreover, ascites with neither hepato nor splenomegaly nor collateral circulation was detected. Systemic examination was otherwise unremarkable.

The investigations showed the following: se­rum calcium: 2.42 mmol/L, serum phosphate: 3.53 mmol/L, Ca × P product: 8.53 μmol 2 /L 2 , total alkaline phosphate: 350 IU/L; parathyroid hormone (PTH) 2011 pg/L (normal: 10-60 pg/ mL). This calcium phosphate homeostasis alte­ration was associated with an inflammatory syn­drome attested by C-reactive protein at 158 mg/ L. However, liver function tests were normal. Repeated blood cultures were sterile. White cell count was 7900/mm3 , hematocrit was 25.6%, and albumin showed 28 g/L.

Peritoneal effusion was a yellow turbid liquid with protein concentration of 50 g/L and white cells/mm 3 of 120 with lymphocyte predominance (60%). Usual bacterial culture was negative. Direct examination and culture for Mycobacte­rium tuberculosis were negative.

Chest X-ray showed extensive soft tissue cal­cifications in front of the right sternoclavicular joint and the shoulders [Figure 1](a and b). Cra­nium X-ray revealed signs of hyperparathyroi­dism. X-ray of the limbs showed vascular cal­cification and soft tissue calcification in the hands, feet and knees [Figure 2], [Figure 3](a and b).
Figure 1: a and b: Chest X-ray: calcific opacity in the right superior part of thorax.

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Figure 2: Elbow X-ray: soft tissue calcification and vascular calcification.

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Figure 3: a and b: Hands and knee X-ray showing vascular calcifications.

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Cervico-thoracic computed scan showed parie­tal calcified mass in front of the right sternocla­vicular articulation and the first right chondro­costal articulation and in front of the shoulders [Figure 4](a-c). There was neither mediastinal adenopathy nor pulmonary abnormalities.
Figure 4: a, b, c: Chest CT: parietal calcification masses in front of the right sternoclavicular and the first chondrocostal articulations and the shoulders.

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Abdominal computed tomography revealed ma­ssive ascites and agglutinated intestinal loop [Figure 5].
Figure 5: Abdominopelvic CT showing ascites and agglutinated intestinal loops.

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The patient was switched to a daily 4-hour dialysis sessions for 6 weeks using a standard 1.75 mmol calcium dialysate since low concen­tration calcium dialysates were not available in our unit at that time, but oral CaCO 3 was dis­continued. No significant decrease in Ca × P product was noted. Due to the general fatigue, anorexia, fever of unknown origin and inflam­matory syndrome, and considering the endemic state of TB in our country and the protein rich ascites effluent with high lymphocyte count, tuberculosis peritonitis was suspected.

Laparoscopic exploration and biopsy to diag­nose the nodules of the peritoneum were not performed because of the general status of the patient. Antituberculosis treatment was then started with rifampicin 600 mg/d, isoniazide 300 mg/d, and pyrazinamide 1 g/48 h.

The patient markedly improved with antituber­culosis treatment. The elevated serum phosphate and Ca × P product dramatically decreased after antituberculosis treatment [Figure 6]. Ascites pro­gressively disappeared confirming the presumed tuberculous peritonitis. Then, subtotal parathyroi­dectomy was performed after improvement of the general state of the patient. Eventually, the Ca × P product reached normal target values [Figure 6]
Figure 6: Evolution of calcium and phosphate homeostasis after starting daily hemodialysis, antituberculosis
treatment and after parathyroidectomy.


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   Discussion Top


Our case highlights the association of vascular and soft tissue calcifications that are both com­plications of maintained high Ca × P product in a dialysis patient with peritoneal tuberculosis.

Peritoneal tuberculosis is a common extra-pul­monary localization in dialysis patients. [1] Its diag­nosis is difficult because culture for M. tuber­culosis takes several weeks and can be negative. [2] Peritoneoscopy and biopsy provide reliable diag­nostic tools, [3] but they could not be performed in our patient because of his general status. The presumed peritoneal tuberculosis was most likely correct because of the improvement of ascites after starting antituberculosis treatment.

Calciphylaxis is characterized by microvascu­lar medial calcification, intimal hypertrophy and obliteration of the arteriols' lumens with cuta­neous ischemia and ulcerations. [4] The distal areas of the lower limb are most commonly affected. Infectious complications of these lesions are associated with poor prognosis. [4]

Tumoral calcinosis is a rare inherited meta­bolic disorder characterized by massive calcium and phosphate deposits. [5] It is rare in dialyzed patients, [6] and its pathogenesis is poorly unders­tood. An elevation of the Ca × P product is the most important factor, but other factors are in­criminated (hyperparathyroidism, adynamic bone disease, aluminum intoxication, hypomagnese­mia, vitamin K excess, alkalosis and hypervita­minosis D). [7],[8],[9] Hypervitaminosis D is usually secondary to high doses of calcitriol, but ex­trarenal tissue synthesis might be observed in granulomatous diseases such as sarcoidosis and TB. [10],[11] Calcitriol production by alveolar lym­phocytes and macrophages recovered by lavage from patients with TB or active sarcoidosis has been confirmed. [12],[13]

In our case, hyperphosphatemia and elevated Ca × P product was due essentially to insuffi­cient dialysis and severe hyperparathyroidism.

Peritoneal tuberculosis may be incriminated in aggravation of phosphocalcic abnormalities by extrarenal synthesis of calcitriol by tuberculosis granuloma cells, since we observed a partial but significant decrease of Ca × P product after ini­tiating antituberculosis treatment.

Sarcoidosis and TB associated tumoral calci­nosis in dialysis patients has been reported. [11],[14]

The management of tumoral calcinosis in dia­lysis patients is difficult. The objective of treat­ment modalities is to lower the Ca × P product and the regimen should include phosphate bin­der, dialysis intensification, and parathyroidec­tomy when PTH is at high level.

Dialysis intensification was inefficient in our patient perhaps because of the elevated dialy­sate calcium concentration. We observed partial decrease of Ca × P product after antitubercu­losis treatment and normal Ca × P product after parathyroidectomy.

In conclusion, this case illustrates association of both complications, vascular and soft tissue calcification, of poor calcium and phosphate control in a patient with peritoneal tuberculosis.

 
   References Top

1.Chou KJ, Fang HC, Bai KJ, Hwang SJ, Yang WC, Chung HM. Tuberculosis in maintenance dialysis patients. Nephron 2001;88:138-43.  Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.Khan R, Abid S, Jafri W, Abbas Z, Hameed K, Ahmad Z. Diagnostic dilemma of abdominal tuberculosis in non-HIV patients: an ongoing challenge for physicians. World J Gastroenterol 2006;12(39):6371-5.  Back to cited text no. 2
    
3.Hung YM, Chan HH, Chung HM. Tuberculous peritonitis in different dialysis patients in Southern Taiwan. Am J Trop Med Hyg 2004;70 (5):532-5.  Back to cited text no. 3
    
4.Coates T, Kirkland GS, Dymock RB, et al Cuta­neous necrosis from calcific uremic arteriolo­pathy. Am J Kidney Dis 1998;32(3):384-91.  Back to cited text no. 4
    
5.Mohamed S, Jong-Hun J, Weon-Yoo K. Tumo­ral calcinosis of the foot with unusual presen­tation in an 11-year-old boy: a case report and review of literature. J Postgrad Med 2007;53(4): 247-9.  Back to cited text no. 5
    
6.Scuteri RM, Otero AB, Chitchoty E, et al. More about tumoral calcinosis in maintenance hemo­dialysis patients. Nephron 1993;65(2):334-5.  Back to cited text no. 6
    
7.Eisenberg B, Tzamaloukas AH, Hartshorne MF, Listrom MB, Arrington ER, Sherrard DJ. Peri­articular tumoral calcinosis and hypercalcemia in a hemodialysis patient without hyperpara­thyroidism: A case report. J Nucl Med 1990; 31(6):1099-103.  Back to cited text no. 7
    
8.Drueke TB. A clinical approach to the uraemic patient with extra-skeletal calcifications. Nephrol Dial Transplant 1996;11[Suppl 3]:37-42.  Back to cited text no. 8
    
9.Zins B, Zingraff J, Basile C, et al. Tumoral calcifications in hemodialysis patients: possible role of aluminum intoxication. Nephron 1992; 60(3):260-7.  Back to cited text no. 9
    
10.Peces R, Pobes A, Díaz-Corte C, Gago E. Hyp­ercalcemia, inappropriate calcitriol levels, and tuberculosis on hemodialysis. Scand J Urol Nephrol 2000;34(4):287-8.  Back to cited text no. 10
    
11.Naito T, Nitta K, Kimata N, et al. Progressive tumoral calcinosis as the presenting feature of sarcoidosis in a patient on haemodialysis treat­ment. Nephrol Dial Transplant 1999;14(11): 2716-9.  Back to cited text no. 11
    
12.Cadranel J, Garabedian M, Milleron B. 1,25 (OH)2 D3 production by T lymphocytes and alveolar macrophages recovered by lavage from normocalcemic patients with tuberculosis. J Clin Investig 1990;85:93.9.  Back to cited text no. 12
    
13.Adams JS, Gacad MA. Characterization of 1 alpha-hydroxylation of vitamin D3 sterols by cultured alveolar macrophages from patients with sarcoidosis. J Exp Med 19 8 5;161:755-65.  Back to cited text no. 13
    
14.Santos-Ocampo AS, Tupasi TE, Villanueva F, Roxas FK, Ramos CP. Mycobacterium tuber­culosis infection of a tophaceous pseudogout nodule. J Rheumatol 2002;29(5):1093-6.1093-6.  Back to cited text no. 14
    

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Correspondence Address:
Khawla Kammoun
Department of Nephrology, Hedi Chaker Hospital, 3029 Sfax
Tunisia
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PMID: 21422631

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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]



 

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    Abstract
    Introduction
    Case Report
    Discussion
    References
    Article Figures
 

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