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Nephrology Dialysis Transplantation 2006 21(7):1999-2004; doi:10.1093/ndt/gfl114
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Case Report

Successful treatment of calciphylaxis with cinacalcet—an alternative to parathyroidectomy?

Nestor Velasco, Mark S. MacGregor, Andrew Innes and Ian G. MacKay

The John Stevenson Lynch Renal Unit, NHS Ayrshire & Arran, Crosshouse Hospital, Kilmarnock, Scotland

Correspondence and offprint requests to: Dr Nestor Velasco, Consultant Nephrologist, The John Stevenson Lynch Renal Unit, Crosshouse Hospital, Kilmarnock KA2 0BE, Scotland. Email: nestor.velasco{at}aaaht.scot.nhs.uk

Keywords: calciphylaxis; calcium-sensing receptors; cinacalcet; parathyroid hormone; renal replacement therapy; secondary hyperparathyroidism



   Introduction
Top
 Introduction
Case report
 Discussion
 References
 
Calciphylaxis is a rare but serious complication of end-stage renal failure, which has a high mortality due to widespread vascular calcification and refractory infections [1,2]. Parathyroidectomy has been advocated as one of the few treatments that may reverse this condition [3], although this has not been universally accepted and is not always successful [4]. The newly developed calcimimetic, cinacalcet (marketed as Mimpara® in the EU, and as Sensipar® in the USA by Amgen Inc., Thousand Oaks, CA, USA) produces rapid biochemical control of secondary hyperparathyroidism [5,6], and thus may represent an alternative treatment for patients with calciphylaxis.



   Case report
Top
 Introduction
 Case report
Discussion
 References
 
A 45-year-old man with end-stage renal failure due to autosomal dominant polycystic kidney disease started treatment with peritoneal dialysis in 2000. He had hypertension and asthma, but no other comorbidities and was a non-smoker. He transferred to haemodialysis in 2002, after bilateral nephrectomies for infection and haemorrhage. He was assessed for renal transplantation, but it was considered unsuitable for technical reasons related to extensive cystic hepatomegaly. In 2003, his secondary hyperparathyroidism became more difficult to control. Activated vitamin D was relatively contra-indicated by a persistently elevated serum calcium phosphate product (4.79–7.85 mmol2/l2) (Figure 1). Pre-dialysis corrected serum calcium was at or above the upper limit of normal at 2.50–2.72 mmol/l and serum phosphate was elevated between 1.68–2.94 mmol/l, despite therapy with 7.2 g/day of sevelamer and the use of low calcium dialysate (1.25 mmol/l). He was also on calcium carbonate as a phosphate binder, because of poor control of serum phosphate. Serum alkaline phosphatase was progressively and persistently raised to three times the upper limit of normal (reference range 50–179 IU/l). Intact parathyroid hormone levels had reached 244 pmol/l. A 99mTc-sestamibi-pertechnetate subtraction scan showed three areas of increased uptake at the lower poles of both thyroid lobes, and inferior to the left lobe, consistent with the presence of parathyroid adenomata.


Figure 1
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  		Fig. 1. Changes in corrected serum calcium (Ca), phosphate (PO4), calcium phosphate product (Product), alkaline phosphatase (Alk Phos) and parathyroid hormone (PTH) before and after treatment with cinacalcet. Calcium was corrected for the concentration of serum albumin using the formula: [serum calcium] + 0.025 x (38.0 – [serum albumin]). Laboratory reference range for corrected calcium was 2.10–2.50 mmol/l. PTH was assayed using the Nichols Advantage assays (Nichols Institute Diagnostics, San Clemente, CA, USA). Intact PTH (upper limit of normal 6 pmol/l) was measured until 5 April 2004, at which point our laboratory changed to bio-intact PTH (upper limit of normal 5 pmol/l). In our laboratory's hands, bio-intact PTH is approximately 30% lower than intact PTH. Ac, acetate.

 
He developed pain in his legs, and in November 2003 was reviewed by a vascular surgeon who noted a superficial area of discolouration in the left great toe. Good pulses were present at femoral, popliteal and postero-tibial levels, and it was concluded that there was no major occlusive large-vessel disease (subsequently confirmed by arteriography in April 2005). Control of hyperparathyroidism continued to deteriorate. His liver cysts were becoming calcified. In 2002, his chest radiogram was essentially normal, but by September 2004 there was evidence of miliary calcification in the lung fields. In 1999, there was no vascular calcification evident on radiograms of foot and pelvis. By 2002, mild patchy, arterial calcification could be seen, becoming far more extensive and dense on subsequent films in February 2004. Bone density appeared normal in radiograms in 1999. Coincident with the development of extra-osseous calcification, bone density appeared to deteriorate rapidly on films in 2004. He began to develop a proximal myopathy and had progressive difficulty with mobility. Over the course of 5 months, he developed painful superficial ulcers in both shins and subsequently a deeper ulcer in the left calf that were consistent with a clinical diagnosis of calciphylaxis (Figure 2A).


Figure 2
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  		Fig. 2. (A) Typical lesions of calciphylaxis affecting both lower legs. (B) Complete healing of the same lesions after 35 weeks of cinacalcet therapy.

 
In November 2004, he was admitted for parathyroidectomy, but unfortunately, just before going to the theatre he slipped in the shower and suffered a fractured right neck of femur and left patella causing cancellation of the parathyroidectomy. A bipolar arthroplasty of the right hip was carried out. Cinacalcet (30 mg daily) was commenced, and within a few days an improvement in the control of his hyperphosphataemia and hypercalcaemia was noted. Within 2 weeks, the dose of cinacalcet was increased to 60 mg/day. Sevelamer was discontinued due to normalization of serum phosphate. After 4 weeks, activated vitamin D was introduced, as the corrected serum calcium had fallen below the lower limit of normal.

By January 2005, corrected serum calcium was 2.07 mmol/l and serum phosphate was 1.10 mmol/l, giving a product of 2.28 mmol2/l2 (Figure 1). Alkaline phosphatase had fallen to the lowest level in 2 years and parathyroid hormone levels had also decreased dramatically to 49.9 pmol/l. His general condition also improved with increased appetite, muscular strength improved from being incapable of standing in the immediate few weeks after his arthroplasty to the extent of being able to walk again, first with crutches, and then with a single walking stick. He also described a non-specific feeling of well-being. By December 2005, he was receiving 120 mg/day of cinacalcet and 2 µg/day of calcitriol. Corrected calcium was 2.10 mmol/l. Phosphate control was variable with the most recent value being 2.24 mmol/l, giving a product of 4.70 mmol2/l2. Alkaline phosphatase had fallen further to 157 U/l, and parathyroid hormone had fallen to 12.7 pmol/l. Pulmonary and vascular calcification have not progressed further in extent or severity since starting cinacalcet, but as yet there is no evidence of regression. Bone density appears to be continuing to deteriorate on a foot radiogram in September 2005. Throughout this period, the leg ulcers improved dramatically with near complete healing (Figure 2B).



   Discussion
Top
 Introduction
 Case report
 Discussion
References
 
Calciphylaxis, also known as calcific uraemic arteriolopathy, typically occurs in dialysis patients and manifests as skin ulceration, as a result of medial calcification of arterial walls leading to downstream ischaemia and necrosis. It was first described by Selye in the 1960s [7], who also noted an association with hyperparathyroidism. With the subsequent advent of chronic haemodialysis, the association with secondary hyperparathyroidism and poor phosphate control, as well as the beneficial role of parathyroidectomy, was established [7,8]. Since then, several historical reviews have confirmed both the high mortality and the improved prognosis following parathyroidectomy [3,9–13]. Calciphylaxis may also present in the context of primary hyperparathyroidism [14] and is well-described following kidney transplantation, which can exacerbate hypercalcaemia, before resolution of hyperparathyroidism occurs [15,16]. Very rarely, calciphylaxis may be associated with coagulopathies or malignancy in the absence of renal failure [17–19]. Visceral and pulmonary calcification, although rare, have also been described [4,20,21].

Hyperparathyroidism commonly develops in chronic kidney disease, and causes bone disease with high turnover, fibrosis and an increased risk of fractures. Partly as a result of the currently available therapeutic agents, there are frequent increases in serum calcium, serum phosphate and the calcium phosphate product, which are associated with vascular and valvular calcification, increased vascular stiffness and calcification of soft tissues and joints [22]. Elevated serum calcium, serum phosphate and calcium phosphate product are all independently associated with increased mortality [23]. Symptomatically, patients experience bone pain with weak and painful muscles. These symptoms are usually improved by control of the hyperparathyroidism.

The pathogenesis of calciphylaxis remains unclear. Calciphylaxis usually occurs in the setting of hyperparathyroidism and elevated serum calcium phosphate product, but unlike these conditions, it remains relatively rare. The use of activated vitamin D and calcium-containing phosphate binders is also associated and may partly explain the apparent rising incidence [13,24]. It has also been associated with relatively minor trauma [1], female gender [11,13], obesity [11], diabetes mellitus and the use of warfarin [25] or steroids.

Cinacalcet is the first of a new class of drugs, the calcimimetics. It acts by increasing the sensitivity of the calcium-sensing receptor to calcium, thus leading to a reduction of the parathyroid hormone, and yet at the same time a reduction in serum calcium, serum phosphate and calcium phosphate product. In three randomized, double-blind, placebo-controlled trials in 1136 dialysis patients with poorly controlled secondary hyperparathyroidism, cinacalcet was shown to reduce parathyroid hormone by a median of 48.2–54.1%, with a concomitant reduction in calcium phosphate product of 14.9–19.7%. The major side effects were nausea and vomiting [5,6]. It has also been found to be effective in patients with advanced renal impairment but not yet requiring dialysis [26] and in patients with renal transplants [27,28] or on peritoneal dialysis [6].

In our patient, cinacalcet produced rapid control of hyperphosphataemia and hypercalcaemia with simultaneous lowering of parathyroid hormone levels. This was accompanied by a rapid improvement and healing of leg ulcers. Some authors believe that histology is essential to make the diagnosis of calciphylaxis [29]. But others feel that the clinical picture can in itself be diagnostic, and point out that biopsies can be less than definitive. Furthermore, skin biopsies can lead to clinical deterioration with non-healing biopsy sites and subsequent sepsis [2,13,30]. We did not obtain histology because we believed the clinical picture to be convincingly that of calciphylaxis, and because we were concerned about the potential negative impact of skin biopsies on patient outcome. The patient (as has often been observed following parathyroidectomy) also noted a non-specific sense of well-being. Muscle strength and mobility have also improved along with the control of hyperparathyroidism. Pulmonary and vascular calcification appear to have stabilized in our patient, but we are unable to demonstrate any regression of extra-osseous calcification as yet. It should of course be appreciated that the levels of parathyroid hormone and alkaline phosphatase have only been normalized for a matter of months. It is perhaps disappointing that bone density appears to be deteriorating further, at least in the feet, but plain radiography is not a reliable method to assess bone density. One previous study showed that cinacalcet increased femoral, though not lumbar, bone density after only 6 months therapy [31], and another study demonstrated a reduction in fractures with cinacalcet [32]. Initially, control was obtained in our patient by using relatively low doses of cinacalcet (30–60 mg/day) but later, while receiving higher doses, we observed no adverse effects in him. The lowering of serum calcium allowed the re-introduction of calcitriol, which, in the context of a healing femoral fracture, was therapeutically desirable. A marked fall in alkaline phosphatase was also seen.

We used calcium carbonate as a phosphate binder in combination with sevelamer for 6 months immediately prior to the planned parathyroidectomy in an attempt to improve serum phosphate levels. It is conceivable that this additional calcium load in combination with a high calcium phosphate product and high parathyroid hormone levels may have contributed to the onset of calciphylaxis, although it did lower the product to a certain degree. Should we have used aluminium-based phosphate binders? In accordance with the Kidney Disease Outcomes Quality Initiative guidelines [33], we generally limit the use of aluminium-based binders to a 4 week course, which we do not repeat in any individual patient, mainly because of concerns about the impact of aluminium on renal osteodystrophy, though also because of the potential risks of encephalopathy and anaemia. We think it unlikely that a 4 week course of aluminium salts would have had a major impact on outcome in this patient.

The correct treatment for calciphylaxis is uncertain, but most authorities recommend vigorous attempts to control serum calcium and phosphate, and parathyroidectomy [9]. Unfortunately, parathyroidectomy had to be postponed in this patient. Other therapies which have been suggested include hyperbaric oxygen [34–38], intravenous sodium thiosulphate [30,39], steroids [13] and bisphosphonates [40], but their efficacy is based on scant evidence. We used cinacalcet as an interim measure to control serum calcium, phosphate and parathyroid hormone levels, pending fitness for operation. Due to the rapid control of the hyperparathyroidism following the introduction of cinacalcet, which resulted in hypocalcaemia, improvement of serum phosphate and the reintroduction of activated vitamin D combined with healing of the cutaneous lesions, parathyroidectomy was avoided, perhaps indefinitely. This may indicate that cinacalcet is an appropriate alternative to parathyroidectomy in patients with calciphylaxis. This observation is especially important in the context of an increasingly frail and elderly dialysis population, many of whom would be at a significant risk from parathyroidectomy. Parathyroidectomy in dialysis patients is associated with an increased mortality for 6 months after the operation [41].

In conclusion, administration of cinacalcet to a haemodialysis patient with calciphylaxis led to rapid biochemical control of secondary hyperparathyroidism and resolution of skin ulcers. Although our results require confirmation in further patients, cinacalcet should be considered as a treatment for patients with calciphylaxis, particularly when doubts exist about fitness for parathyroidectomy.



   Acknowledgments
 
We are grateful to Amgen Ltd, Cambridge, UK for the provision of cinacalcet for compassionate use, prior to its licensing in the European Union, and for providing it free of charge pending review by the Scottish Medicines Consortium. Amgen had no input to this manuscript.

Conflict of interest statement. MMacG reports receiving consultancy and lecture fees, and also financial assistance from Amgen to attend academic meetings. The other authors have no conflicts of interest to report.



   References
Top
 Introduction
 Case report
 Discussion
 References
 

  1. Janigan DT, Hirsch DJ, Klassen GA, MacDonald AS. Calcified subcutaneous arterioles with infarcts of the subcutis and skin (‘calciphylaxis’) in chronic renal failure. Am J Kidney Dis 2000; 35: 588–597[Medline]
  2. Wilmer WA, Magro CM. Calciphylaxis: emerging concepts in prevention, diagnosis, and treatment. Sem Dial 2002; 15: 172–186
  3. Arch-Ferrer JE, Beenken SW, Rue LW, Bland KI, Diethelm AG. Therapy for calciphylaxis: an outcome analysis. Surgery 2003; 134: 941–944[CrossRef][ISI][Medline]
  4. Oikawa S, Osajima A, Tamura M et al. Development of proximal calciphylaxis with penile involvement after parathyroidectomy in a patient on hemodialysis. Intern Med 2004; 43: 63–68[Medline]
  5. Block GA, Martin KJ, de Francisco AL et al. Cinacalcet for secondary hyperparathyroidism in patients receiving hemodialysis. N Engl J Med 2004; 350: 1516–1525[Abstract/Free Full Text]
  6. Lindberg JS, Culleton B, Wong G et al. Cinacalcet HCl, an oral calcimimetic agent for the treatment of secondary hyperparathyroidism in hemodialysis and peritoneal dialysis: a randomized, double-blind, multicenter study. J Am Soc Nephrol 2005; 16: 800–807[Abstract/Free Full Text]
  7. Selye H, Gabbiani G, Tuchweber B. Effect of parathyroidectomy and ferric dextrin upon calciphylactic sensitization by uremia. J Urol 1963; 90: 120–124[Medline]
  8. Gipstein RM, Coburn JW, Adams DA et al. Calciphylaxis in man. A syndrome of tissue necrosis and vascular calcification in 11 patients with chronic renal failure. Arch Intern Med 1976; 136: 1273–1280[Abstract]
  9. Hafner J, Keusch G, Wahl C et al. Uremic small-artery disease with medial calcification and intimal hyperplasia (so-called calciphylaxis): a complication of chronic renal failure and benefit from parathyroidectomy. J Am Acad Dermatol 1995; 33: 954–962[CrossRef][ISI][Medline]
  10. Kang AS, McCarthy JT, Rowland C, Farley DR, van Heerden JA. Is calciphylaxis best treated surgically or medically? Surgery 2000; 128: 967–971[CrossRef][ISI][Medline]
  11. Mazhar AR, Johnson RJ, Gillen D et al. Risk factors and mortality associated with calciphylaxis in end-stage renal disease. Kidney Int 2001 60: 324–332[CrossRef][ISI][Medline]
  12. Girotto JA, Harmon JW, Ratner LE, Nicol TL, Wong L, Chen H. Parathyroidectomy promotes wound healing and prolongs survival in patients with calciphylaxis from secondary hyperparathyroidism. Surgery 2001; 130: 645–650[CrossRef][ISI][Medline]
  13. Fine A, Zacharias J. Calciphylaxis is usually non-ulcerating: risk factors, outcome and therapy. Kidney Int 2002; 61: 2210–2217[CrossRef][ISI][Medline]
  14. Mirza I, Chaubay D, Gunderia H, Shih W, El-Fanel H. An unusual presentation of calciphylaxis due to primary hyperparathyroidism. Arch Pathol Lab Med 2001; 125: 1351–1353[Medline]
  15. Wenzel-Seifert K, Harwig S, Keller F. Fulminant calcinosis in two patients after kidney transplantation. Am J Nephrol 1991; 11: 497–500[ISI][Medline]
  16. Barbur MA, Kurjak M, Becker K. Systemische Kalziphylaxie bei chronischer Niereninsuffizienz: fulminanter Verlauf nach Nierentransplantation. Pathologe 1997; 18: 453–458[Medline]
  17. Korkmaz C, Dundar E, Zubaroglu I. Calciphylaxis in a patient with rheumatoid arthritis without renal failure and hyperparathyroidism: the possible role of long-term steroid use and protein S deficiency. Clin Rheumatol 2002; 21: 66–69[CrossRef][ISI][Medline]
  18. Riegert-Johnson DL, Kaur JS, Pfeifer EA. Calciphylaxis associated with cholangiocarcinoma treated with low-molecular-weight heparin and vitamin K. Mayo Clin Proc 2001; 76: 749–752[ISI][Medline]
  19. Goyal S, Huhn KM, Provost TT. Calciphylaxis in a patient without renal failure or elevated parathyroid hormone: possible aetiological role of chemotherapy. Br J Dermatol 2000; 143: 1087–1090[Medline]
  20. Giacobetti R, Feldman SA, Ivanovich P, Huang CM, Levin ML. Sudden fatal pulmonary calcification following renal transplantation. Nephron 1977; 19: 295–300[Medline]
  21. Khafif RA, Delima C, Silverberg A, Frankel R, Groopman J. Acute hyperparathyroidism with systemic calcinosis. Report of a case. Arch Intern Med 1989; 149: 681–684[Abstract]
  22. Llach F, Velasquez Forero F. Secondary hyperparathyroidism in chronic renal failure: pathogenic and clinical aspects. Am J Kidney Dis 2001; 38 [Suppl 5]: S20–S33[Medline]
  23. 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: 2208–2218[Abstract/Free Full Text]
  24. Zacharias JM, Fontaine B, Fine A. Calcium use increases risk of calciphylaxis: a case-control study. Peritoneal Dial Int 1999; 19: 248–252[Abstract/Free Full Text]
  25. Coates T, Kirkland GS, Dymock RB et al. Cutaneous necrosis from calcific uremic arteriolopathy. Am J Kidney Dis 1998; 32: 384–391[ISI][Medline]
  26. Charytan C, Coburn JW, Chonchol M et al. Cinacalcet hydrochloride is an effective treatment for secondary hyperparathyroidism in patients with CKD not receiving dialysis. Am J Kidney Dis 2005; 46: 58–67[CrossRef][ISI][Medline]
  27. Kruse AE, Eisenberger U, Frey FJ, Mohaupt MG. The calcimimetic cinacalcet normalizes serum calcium in renal transplant patients with persistent hyperparathyroidism. Nephrol Dial Transplant 2005; 20: 1311–1314[Abstract/Free Full Text]
  28. Serra AL, Schwarz AA, Wick FH, Marti HP, Wuthrich RP. Successful treatment of hypercalcemia with cinacalcet in renal transplant recipients with persistent hyperparathyroidism. Nephrol Dial Transplant 2005; 20: 1315–1319[Abstract/Free Full Text]
  29. Goldsmith DJ. Calcifying panniculitis or ‘simple’ inflammation? Biopsy is better than a bone scan. Nephrol Dial Transplant 1997; 12: 2463–2464[Free Full Text]
  30. Cicone JS, Petronis JB, Embert CD, Spector DA. Successful treatment of calciphylaxis with intravenous sodium thiosulfate. Am J Kidney Dis 2004; 43: 1104–1108[CrossRef][ISI][Medline]
  31. Lien YH, Silva AL, Whittman D. Effects of cinacalcet on bone mineral density in patients with secondary hyperparathyroidism. Nephrol Dial Transplant 2005;20: 1232–1237[Abstract/Free Full Text]
  32. Cunningham J, Danese M, Olson K, Klassen P, Chertow GM. Effects of the calcimimetic cinacalcet HCl on cardiovascular disease, fracture, and health-related quality of life in secondary hyperparathyroidism. Kidney Int 2005; 68: 1793–1800[CrossRef][ISI][Medline]
  33. National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis 2003; 42 [Suppl 3]: S1–S201
  34. Vassa N, Twardowski ZJ, Campbell J. Hyperbaric oxygen therapy in calciphylaxis-induced skin necrosis in a peritoneal dialysis patient. Am J Kidney Dis 1994; 23: 878–881[ISI][Medline]
  35. Dean SM, Werman H. Calciphylaxis: a favorable outcome with hyperbaric oxygen. Vascular Med 1998; 3: 115–120[CrossRef]
  36. Podymow T, Wherrett C, Burns KD. Hyperbaric oxygen in the treatment of calciphylaxis: a case series. Nephrol Dial Transplant 2001; 16: 2176–2180[Abstract/Free Full Text]
  37. Dwyer KM, Francis DM, Hill PA, Murphy BF. Calcific uraemic arteriolopathy: local treatment and hyperbaric oxygen therapy. Nephrol Dial Transplant 2002; 17: 1148–1149[Free Full Text]
  38. Basile C, Montanaro A, Masi M, Pati G, De Maio P, Gismondi A. Hyperbaric oxygen therapy for calcific uremic arteriolopathy: a case series. J Nephrol 2002; 15: 676–680[Medline]
  39. Guerra G, Shah RC, Ross EA. Rapid resolution of calciphylaxis with intravenous sodium thiosulfate and continuous venovenous haemofiltration using low calcium replacement fluid: case report. Nephrol Dial Transplant 2005; 20: 1260–1262[Free Full Text]
  40. Monney P, Nguyen QV, Perroud H, Descombes E. Rapid improvement of calciphylaxis after intravenous pamidronate therapy in a patient with chronic renal failure. Nephrol Dial Transplant 2004; 19: 2130–2132[Free Full Text]
  41. Foley RN, Li S, Liu J, Gilbertson DT, Chen SC, Collins AJ. The fall and rise of parathyroidectomy in U.S. hemodialysis patients, 1992 to 2002. J Am Soc Nephrol 2005; 16: 210–218[Abstract/Free Full Text]
Received for publication: 14.12.05
Accepted in revised form: 21. 2.06


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