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|Year : 2011 | Volume : 22 | Issue : 2 | Page : 306-310 |
|Tumoral calcinosis, calciphylaxis, hyperparathyroidism and tuberculosis in a dialysis patient |
Khawla Kammoun1, Faiçal Jarraya1, Mohamed Ben Hmida1, Abedelmajid Khebir2, Mahmoud Kharrat1, Tahia Boudawara2, Jamel Mnif3, Jamil Hachicha1
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 Publication ||18-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 2014 Mar 4];22:306-10. Available from: http://www.sjkdt.org/text.asp?2011/22/2/306/77612
| Introduction || || |
Tuberculosis (TB) is not an uncommon disease in chronic hemodialysis (HD) patients and results in a significant morbidity and mortality. ,, Among the bone changes associated with renal failure, extraskeletal calcification is a commonly observed feature, but tumoral calcinosis and calciphylaxis are uncommon. , 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 || || |
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 || || |
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.  Its diagnosis is difficult because culture for M. tuberculosis takes several weeks and can be negative.  Peritoneoscopy and biopsy provide reliable diagnostic tools,  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.  The distal areas of the lower limb are most commonly affected. Infectious complications of these lesions are associated with poor prognosis. 
Tumoral calcinosis is a rare inherited metabolic disorder characterized by massive calcium and phosphate deposits.  It is rare in dialyzed patients,  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). ,, 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. , Calcitriol production by alveolar lymphocytes and macrophages recovered by lavage from patients with TB or active sarcoidosis has been confirmed. ,
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. ,
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.
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Department of Nephrology, Hedi Chaker Hospital, 3029 Sfax
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
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