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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2006  |  Volume : 17  |  Issue : 4  |  Page : 589-595
Tumorlysis by Dialysis

Nephrology Division, Security Forces Hospital Program, Riyadh, Saudi Arabia

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Keywords: Hyperparathyroid, Hyperphosphatemia, Haemodialysis, Phosphate binders, Vitamin D, Calcimimetics.

How to cite this article:
Al-Abadi AM, Al-Harbi AS, Al-Mohaya SA, Kechrid M, Azhari O, Shetia S. Tumorlysis by Dialysis. Saudi J Kidney Dis Transpl 2006;17:589-95

How to cite this URL:
Al-Abadi AM, Al-Harbi AS, Al-Mohaya SA, Kechrid M, Azhari O, Shetia S. Tumorlysis by Dialysis. Saudi J Kidney Dis Transpl [serial online] 2006 [cited 2022 Oct 5];17:589-95. Available from: https://www.sjkdt.org/text.asp?2006/17/4/589/32504

   Introduction Top

Soft tissue calcification in renal failure has been recognized since 1901. [1] The exact incidence of soft tissue calcification in patients with renal failure is unknown since the detection of visceral calcification is difficult during the patient's life. The combination of marked hyperphosphatemia and a normal or low-normal serum calcium concentration results in an elevated calcium-phosphate product, which is associated with increased mortality. [2],[3],[4],[5] When the calcium-phosphate product is high (due in part to the increased intake of calcium [via calcium-based phosphate binders]), there is a tendency for calcium phosphate to precipitate in arteries, joints, soft tissues, and the viscera; this process is called metastatic calcification or, when very severe and leading to tissue ischemia by affecting dermal arterioles, calciphylaxis. [2],[6] Tumoral collections of calcium phosphate crystals may also be a consequence of hyper­phosphatemia and an elevated calcium­phosphate product. [7] Soft tissue calcification involves most frequently kidneys, lungs, stomach and heart. [8],[9],[10] It starts before end stage renal disease [8] and increases during the progression of chronic kidney disease. Although, there are a myriad of factors that contribute to metastatic calcification, including high PTH, calcitriol treatment, local tissue pH, high calcium-phosphate product, and magnesium deficiency, [6],[11] calcium and phosphate overload are perhaps the major factors leading to soft tissue calcification in renal failure.

   Case Top

A 31 year single male, end stage renal disease secondary to chronic glomeruloneph­ritis started hemodialysis in November 1999 in Security Forces Hospital (SFH) then con­tinued his dialysis in a local hospital, presented to our institution in S.F.H 5 years later in June 2004 in a wheelchair complaining of painful masses at his right thigh, left & right shoulders which started before one year with progressive enlargment and tenderness.

O/E: patient was feeling unwell, malnourished and he had uremic frost. vital signs were stable, he had multiple, hard and tender swellings over the lateral aspect of the right thigh measuring 20x20 cm, at the anterior-superior aspect of the right shoulder measuring about 10x10cm and. The left acromio-clavicular joint was also involved with two small masses sized 2x3 cm with restricted mobility of affected areas, no joint effusion, no neuro­logical deficits, cardiovascular, pulmonary and abdominal exam were normal. [Figure - 1]

His x-rays showed extensive, diffuse soft tissue calcifications at right hip, right & left shoulder obliterating the joint spaces as seen in [Figure - 2].

Laboratory investigations showed:

Urea 14.5 mmol/l, alk.p 377 u/l, Creatinine 484 mmol/l, iPTH 1.616 pg/ml, Albumin 37 g/, HBSAg +ve, Ca,2.53mmol/l HCV +ve, po4 3.42 mmol/l Ca x P product 82.0 mg2/d, Parathyroid scan Diffuse parathyroid hyper­plasia.

   Echocardiogram Top

Left ventricular hypertrophy - normal global left ventricular function with ejection fraction of 62%- calcified posterior mitral valve leaflet and mitral annulus- mild tricuspid regurgitation - calcification in anterior aortic cusp- no pericardial effusion.

The patient started treatment as follows: low phosphate diet about one gram per day and intensive hemodialysis in the form of 6 sessions /weekly for 6months (each session of 5 hours, blood flow of 400ml/min, high flux dialyser, surface area of 1.7m2 with Kt/V of 1.2-1.36) followed by another 6 months with 5 sessions/wk, dialysis with low calcium dialysate (of 0.75 mmol). Calcium free phosphate binders (sevelamer 800 mg 3 times/day).

Our patient showed good clinical response in the form of increasing weight improve movement of the joints and marked regression of the swelling with the following results done 16 months after his presentation: Ca2.17 mmol/L, Phosphorous 1.12 mmol/L Ca x P, 46.1, Mg2/dl2 iPTH 466 pg/ml X­ray [Figure - 3].

   Parathyroid Scan Top

Repeated parathyroid scan showed no more significant abnormalities and reported as negative study.

   Discussion Top

The objectives of secondary hyperparathy­roidism (SHPT) treatment are to achieve and maintain optimal PTH levels ,while main­taining controlled serum phosphorus and calcium levels and normal bone turnover rates in order to prevent osseous and particularly, extra osseous complications. Target ranges for intact PTH (iPTH), calcium and phosphorus in renal patients were published recently by the US National Kidney Foundation (NKF) as part of the Kidney Disease Outcomes Quality Initiative (K/DOQI) see [Figure - 4].

Due to the progressive nature of renal SHPT, prophylactic measures to suppress parathyroid function should be instituted early, ideally before iPTH exceeds the proposed target range. iPTH >600 pg/ml as an independent risk factor for mortality. [4]

Restricting phosphate intake can be attem­pted, with about 800 mg per day being the lowest level that at least some patients will find acceptable. Limiting phosphate intake can be accomplished only by limiting protein intake. However, different considerations are present in maintenance dialysis. A large fraction of dialyzed patients have either overt or borderline malnutrition. Thus, protein supplementation rather than protein restriction is the goal. In this setting, the patient should be encouraged to avoid unnecessary dietary phosphate (as in dairy products, certain vege­tables, many processed foods, and colas) while increasing the intake of high biologic value sources of protein (such as meat and eggs). [12]

The current thrice weekly renal replace­ment therapies fail to remove the daily absorbed phosphate, and we have to use the calcium carbonate as a primary phosphate binding agent to reduce intestinal phosphate absorption. Recent studies have indicated that phosphate restriction alone independent of plasma calcitriol or calcium can lower plasma PTH in renal failure and prevent hyperplasia in parathyroid gland. [13],[14],[15],[16]

Comparing conventional thrice weekly hemo­dialysis with nocturnal (extended) dialysis in a randomized study from Toronto published in 1998 concluded that conversion of dialysis from routine thrice weekly to daily extended dialysis (nocturnal) has an important impact in controlling the phosphorus and markedly decreasing serum PTH levels. [17]

Although calcitriol and alfacalcidol have been mainstay of SHPT therapy since the 1980 and, their efficacy and safety have been demonstrated in several studies. However for the benefit of active vitamin D metabolites, there are also some possible risks: (i) rises in serum calcium and/or phosphorus through increases in intestinal absorption;(ii) over suppression of plasma PTH resulting in reduced bone turnover (adynamic bone) with the concomitant risk of extra osseous calci­fications; (iii) development of resistance toward active vitamin D metabolites [18],[19] in as many as 30% of patients;(iv) pharmacological amounts of vitamin D may have detrimental effects on elastogenesis and inflammation of the arterial wall. Considering theses reasons, there have been attempts to develop chemically modified vitamin D analogues with fewer hypercalcaemic and hyperphosphatemia side effects. [20] Paricalcitol, a vitamin D2-derived analogue was found in preclinical studies to induce less hypercalcaemia and hyperphos­phatemia than calcitriol. Paricalcitol is approved for therapy of SHPT in the US and has recently received European approval. In recent rando­mized multicentre study in dialysis patients, paricalcitol reduced plasma iPTH somewhat faster than calcitriol, and with fewer sustained episodes of hypercalcaemia. [21] However, in both groups, more than 60% of patients still experienced at least one episode of hypercal­caemia (>11mg/dl) and/or Ca x P >75mg2/dl2, in contrast to the available experimental data.

In the past aluminum hydroxide was used to bind ingested phosphate, but its use is now discouraged due to toxic effects caused by aluminum accumulation in tissues leading to encephalopathy, aluminium-associted osteo­malacia, and osteodystrophy. [22]

The calcium salts, calcium acetate and calcium carbonate, are most widely used to control hyperphosphatemia. Calcium salts may result in increased serum calcium levels, since 20­30% of ingested calcium is absorbed into the bloodstream. [23]

Sevelamer is calcium-and aluminum free phosphate binder that has been shown to significantly reduce serum phosphorus and to improve lipid profiles in haemodialysis patients. [16] In comparative study with calcium­containing phosphate binders, sevelamer limited the progression of coronary artery calcification. [24] A cost-benefit analysis indi­cated that, in the absence of hypercalcaemia, calcium salts should remain the treatment of choice for hyperphosphatemia in haemodialysis patients. [25] The question of whether sevelamer can improve survival of chronic dialysis patients is currently addressed in the DCOR study. A press release at the end of July 2005 indicates that in post-hoc analysis the study shows a significant decrease in mortality over calcium-containing phosphate binders, in patients who completed two or more years of sevelamer treatment, and those whom were 65 years of age or older.

Lanthanum carbonate is another aluminum­free, calcium-free phosphate binder that was recently approved in both Europe and the US. It has been shown to reduce serum phos­phorus levels in short-term and long-term studies in ESRD patients. [26],[27] An abstract reporting lanthanum carbonate treatment data for up to 3 years has shown good tolerability and no increase in the frequency of adverse events. [1]

Calcimimetics are a new class of pharmaco­logical compounds with a novel mode of action for the control of PTH. These agents offer the benefit of suppressing PTH release from parathyroid glands without increasing calcium and phosphorus concentrations. Calci­mimetics act directly on the parathyroid cells by modulating the activity of the Ca receptor (CaR) and by increasing its sensitivity to serum calcium, resulting in enhanced signal transduction and suppression of PTH release. [28]

   Conclusion Top

Intensive hemodialysis is another modality to treat soft tissue calcifications in end stage renal disease. In our patient we used calcium­free phosphate binders but we think that the major role was related to intensive hemo­dialysis.

   Questions and Answers Top

Dr. Ramesh Kumar (Riyadh Medical Complex) Chairman of the club: Now the presentation is open for disucussion.

Dr. Jamal Al Wakeel (King Khaled University Hospital): Were there any other signs of calcification related to hyperparathyroidism like bone resorption in hands or vascular lesions.

Dr. Al-Abbadi: The atient had calcified valvular heart disease, hut no other calcifications or bone lesions; we noticed only the soft tissue calcification which was resolved by intensive dialysis regime.

Dr. Al Wakeel: what was your regimen during hemodialysis therapy? Was the patient on vitamin D?

Dr. Ali Al-Harbi (Security Forces Hospital): In the first weeks we stoped the Vitamin D. because of severe hypercalcimia. Then we restarted the Vitamin D in the later phase after the reduction of PX Ca product. In addition to that, the patient was on low calcium dialysate and sevelamer as calcium and aluminium free phosphate binder Dr. Jamal Al Wakeel: In this case may be the patient was suffering from Vitamin D toxicity more than hyperparathyroidism because of the absence of other future of hyperpara­thyroidism.

Dr. Ali Al-Harbi: all these future indicate the inappropriate dialysis regimen and may be the non-compliance by the patient. The soft tissue calcification was completely resolved after intensive dialysis. Audience: did you check the valvular heart disease after the correction of the PX Ca disturbance?

Dr. Al- Abaddi: we did not, but the patient will be evaluated for renal transplant work-up and an echocadigram will be done. So it will be interesting to compare the new finding with the previous one.

Dr. Sulaiman Al-Muhaya (Security Forces Hospital): I would like to mention that the calcium and aluminium free phosphate binders are not available in most dialysis units and they are expensive drugs.

So the buttom-line of this presentation is the importance of applying the basic strategies of proper diet and efficient dialysis. Dr. Faissal Shaheen (KFH, SCOT): On the other hand, we have to consider the use this expensive new phosphate binder drugs for specific situations and remember that the application of intensive dialysis is more


   References Top

1.Goodman WG. Calcimimetic agents and secondary hyperparathyroidism: treatment and prevention. Nephrol Dial Transplant 2002;17:204-7.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Block GA, Hulbert S, Levin NW, Port FK. Association of serum phosphorus and calcium x phosphate product with mortality risk in chronic hemodialysis patients: a national study. Am J Kidney Dis 1998;31: 607-17.  Back to cited text no. 2    
3.Ganesh SK, Stack AG, Levin NW, Hulbert­Shearon T, Port FK. Association of elevated serum PO(4), Ca x PO(4) product, and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients. J Am Soc Nephrol 2001;12:2131-8.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Block GA, Klassen PS, Lazarus JM, Ofsthun N, Lowrie EG, Chertow GM. Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. J Am Soc Nephrol 2004;15:2208-18.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Young EW, Albert JM, Satayathum S, et al. Predictors and consequences of altered mineral metabolism: the dialysis outcomes and practice patterns study. Kidney Int 2005;67:1179-87.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Lau K. Phosphate excess and progressive renal failure: the precipitation- calcification hypothesis [clinical conference]. Kidney Int 1989;36:918-37.  Back to cited text no. 6  [PUBMED]  
7.Cofan F, Garcia S, Combalia A, et al. Uremic tumoral calcinosis in patients receiving long-term hemodialysis therapy. J Rheumatol 1999;26:379  Back to cited text no. 7  [PUBMED]  
8.Kuzela DC, Huffer WE, Conger JD, Winter SD, Hammond WS. Soft tissue calcification in chronic dialysis patients. Am J Pathol 1977;86:403-24.  Back to cited text no. 8  [PUBMED]  
9.Quarles LD, Sherrard DJ, Adler S, et al. The calcimimetic AMG 073 as a potential treatment for secondary hyperparathyroidism of end-stage renal disease. J Am Soc Nephrol 2003;14:575-83.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Lindberg JS, Moe SM, Goodman WG, et al. The calcimimetic AMG 073 reduces para­thyroid hormone and calcium x phosphorus in secondary hyperparathyroidism. Kidney Int 2003;63:248-54.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Gallieni M, Brancaccio D, Padovese P, et al. Low-dose intravenous calcitriol treat­ment of secondary hyperparathyroidism in hemodialysis patients. Italian Group for the Study of Intravenous Calcitriol. Kidney Int 1992;42:1191-8.  Back to cited text no. 11    
12.Quarles LD, Yohay DA, Carroll BA, et al. Prospective trial of pulse oral versus intravenous calcitriol treatment of hyper­parathyroidism in ESRD. Kidney Int 1994; 45:1710-21.  Back to cited text no. 12  [PUBMED]  
13.Brown AJ, Finch J, Takahashi F, Slatopolsky E. Calcemic activity of 19-Nor-1,25 (OH) (2)D(2) decreases with duration of treatment. J Am Soc Nephrol 2000;11:2088-94.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Sprague SM, Llach F, Amdahl M, Taccetta C, Batlle D. Paricalcitol versus calcitriol in the treatment of secondary hyperparathy­roidism. Kidney Int 2003;63:1483-90.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Teng M, Wolf M, Lowrie E, Ofsthun N, Lazarus JM, Thadhani R. Survival of patients undergoing hemodialysis with paricalcitol or calcitriol therapy. N Engl J Med 2003; 349:446-56.  Back to cited text no. 15  [PUBMED]  [FULLTEXT]
16.Ott SM. Aluminium-related osteomalacia. Int J Artif Organs 1983;6:173-5.  Back to cited text no. 16  [PUBMED]  
17.Mucsi I, Hercz G, Uldall R, Ouwendyk M, Francoeur R, Pierratos A. Control of serum phosphate binders in patients treated with nocturnal hemodialysis. Kidney Int 1998; 53(5):1399-404.  Back to cited text no. 17    
18.Emmett M, Sirmon MD, Kirkpatrick WG, Nolan CR, Schmitt GW, Cleveland MB. Calcium acetate control of serum phosphorus in hemodialysis patients. Am J Kidney Dis 1991;17:544-50  Back to cited text no. 18  [PUBMED]  
19.Goodman WG, Goldin J, Kuizon BD, et al. Coronary-artery calcification in young adults with end-stage renal disease who are under­going dialysis. N Engl J Med 2000;342: 1478-83.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Guerin AP, London GM, Marchais SJ, Metivier F. Arterial stiffening and vascular calcifications in end-stage renal disease. Nephrol Dial Transplant 2000;15:1014-21.  Back to cited text no. 20  [PUBMED]  [FULLTEXT]
21.Locatelli F, Cannata A, Drueke TB, et al. Management of disturbances of calcium and phosphate metabolism in chronic renal insufficiency, with emphasis on the control of hyperphosphataemia. Nephrol Dial Transplant 2002;17:723-31.  Back to cited text no. 21    
22.Chertow GM, Burke SK, Dillon MA, Slatopolsky E. Long-term effects of sevelamer hydrochloride on the calcium x phosphate product and lipid profile of haemodialysis patients. Nephrol Dial Transplant 1999;14: 2907-14.  Back to cited text no. 22  [PUBMED]  [FULLTEXT]
23.Chertow GM, Burke SK, Raggi P. Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients. Kidney Int 2002;62:245-52.  Back to cited text no. 23    
24.Coladonato JA, Ritz E. SHPT and its therapy as a cardiovascular risk factor among end­stage renal disease patients. Adv Ren Replace Ther 2002;9:193-9.  Back to cited text no. 24  [PUBMED]  
25.Qunibi WY, Hootkins RE, McDowell LL, et al. Treatment of hyperphosphatemia in hemodialysis patients: The Calcium Acetate Renagel Evaluation (CARE study). Kidney Int 2004;65:1914-26.  Back to cited text no. 25  [PUBMED]  [FULLTEXT]
26.Hutchison AJ, Speake M, Al Baaj F. Redu­cing high phosphate levels in patients with chronic renal failure undergoing dialysis: a 4-week, dose-finding, open-label study with lanthanum carbonate. Nephrol Dial Transplant 2004;19:1902-6.  Back to cited text no. 26    
27.Hutchison AJ, Maes B, Vanwalleghem J, et al. Efficacy, tolerability, and safety of lanthanum carbonate in hyperphosphatemia: a 6-month, randomised, comparative trial versus calcium carbonate. Nephron Clin Pract 2005;100: c8-c19.  Back to cited text no. 27  [PUBMED]  [FULLTEXT]
28.Block GA, Martin KJ, de Francisco AL, et al. Cinacalcet for secondary hyperparathy­roidism in patients receiving hemodialysis. N Engl J Med 2004;350:1516-25.  Back to cited text no. 28  [PUBMED]  [FULLTEXT]

Correspondence Address:
Abdulnaser Mohammed Al-Abadi
Department of Internal Medicine, Security Forces Hospital Program, P.O. Box 3643, Riyadh 11481
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

PMID: 17186701

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