A case control study of proximal calciphylaxis

Bleyer, AJ; Choi, Michael; Igwemezie, B; Torre, Ernesto de la; White, WL

doi:10.1053/ajkd.1998.v32.pm9740152

Cited by 166 publications

(139 citation statements)

References 10 publications

Supporting

Mentioning

132

Contrasting

Unclassified

Order By: Relevance

“…High P also enhances parathyroid function indirectly by decreasing calcitriol synthesis and serum ionized Ca levels, which further elevates circulating PTH (27,28). High serum PTH induces osteitis fibrosa and bone loss, thus increasing serum Ca ϫ P product (29,30) and ectopic calcification (3,31). In addition to the described effects regarding bone resorption, high PTH may also cause metastatic microcalcifications through elevations in cytosolic Ca (9,10).…”

Section: Discussionmentioning

confidence: 99%

The Effects of Sevelamer Hydrochloride and Calcium Carbonate on Kidney Calcification in Uremic Rats

Cozzolino

Dusso²,

Liapis

et al. 2002

Journal of the American Society of Nephrology

102

View full text Add to dashboard Cite

Abstract. The control of serum phosphorus (P) and calciumphosphate (Ca ϫ P) product is critical to the prevention of ectopic calcification in chronic renal failure (CRF). Whereas calcium (Ca) salts, the most commonly used phosphate binders, markedly increase serum Ca and positive Ca balance, the new calcium-and aluminum-free phosphate binder, sevelamer hydrochloride (RenaGel), reduces serum P without altering serum Ca in hemodialysis patients. Using an experimental model of CRF, these studies compare sevelamer and calcium carbonate (CaCO 3 ) in the control of serum P, secondary hyperparathyroidism (SH), and ectopic calcifications. 5/6 nephrectomized rats underwent one of the following treatments for 3 mo: uremic ϩ high-P diet (U-HP); UHP ϩ 3% CaCO 3 (U-HPϩC); UHP ϩ 3% sevelamer (U-HPϩS). Sevelamer treatment controlled serum P independent of increases in serum Ca, thus reducing serum Ca ϫ P product and further deterioration of renal function, as indicated by the highest creatinine clearances. Sevelamer was as effective as CaCO 3 in the control of high-P-induced SH, as shown by similar serum PTH levels, parathyroid (PT) gland weight, and markers of PT hyperplasia.Also, both P binders elicited similar efficacy in reducing the myocardial and hepatic calcifications induced by uremia. However, sevelamer caused a dramatic reduction of renal Ca deposition (29.8 Ϯ 8.6 g/g wet tissue) compared with both U-HP (175.5 Ϯ 45.7 g/g wet tissue, P Ͻ 0.01) and the U-HPϩC (58.9 Ϯ 13.7 g/g wet tissue, P Ͻ 0.04). Histochemical analyses using Von Kossa and Alizarin red S staining of kidney sections confirmed these findings. The high number of foci of calcification in the kidney of uremic controls (108 Ϯ 25) was reduced to 33.0 Ϯ 11.3 by CaCO 3 and decreased even further with sevelamer (16.4 Ϯ 8.9, P Ͻ 0.02 versus CaCO 3 ). Importantly, the degree of tubulointerstitial fibrosis was also markedly lower in U-HPϩS (5%) compared with either U-HPϩC (30%) or U-HP (50%). It is concluded that in experimental CRF in rats, despite a similar control of serum P and SH, sevelamer is more effective than CaCO 3 in preventing renal Ca deposition and tubulointerstitial fibrosis, including better preservation of renal function. These findings cannot be extrapolated to human disease, and further studies in patients are necessary to determine the benefits of either P binder.In end-stage renal disease, hyperphosphatemia and elevated calcium-phosphate (Ca ϫ P) product associate with ectopic calcifications and increased risk of calciphylaxis, resulting in higher prevalence of morbidity and mortality from cardiovascular events (1-6). High serum phosphorus (P) levels worsen uremia-induced secondary hyperparathyroidism by enhancing parathyroid hyperplasia and parathyroid hormone (PTH) synthesis and secretion (7-8). Elevated PTH levels cause ectopic calcification not only by enhancing serum P and Ca ϫ P product through inducing high bone turnover, but also by increasing both serum and intracellular calcium (Ca) (9 -10). The control of serum P in patients with ch...

show abstract

Section: Discussionmentioning

confidence: 99%

The Effects of Sevelamer Hydrochloride and Calcium Carbonate on Kidney Calcification in Uremic Rats

Cozzolino

Dusso²,

Liapis

et al. 2002

Journal of the American Society of Nephrology

102

View full text Add to dashboard Cite

show abstract

“…An additional risk factor such as concurrent warfarin use should be taken note of and any observations of elevations in the calcium × phosphorus product and/or PTH levels over past months may support the diagnosis. However, it is very important to mention that although we have many ESRD patients on dialysis, the prevalence of calcific uremic arteriolopathy (CUA) is rare with a multifactorial etiology not completely understood currently and requires more than one risk factor (Table 2 [4][5][6][7][8][9][10][11][12]). …”

Section: Discussionmentioning

confidence: 99%

Calciphylaxis: Early Detection and Off-Label Treatment With Sodium Thiosulfate

London

Eter

2017

World J Nephrol Urol

View full text Add to dashboard Cite

Calciphylaxis or calcific uremic arteriolopathy (CUA) is a rare disorder of calcium and phosphate metabolism most often manifesting in end-stage renal disease (ESRD) patients. The typical clinical picture is that of a necrotic cutaneous ulceration with focal or diffuse distribution, most often manifesting on the lower extremities. We report a 49-year-old Caucasian male with ESRD on hemodialysis who presented to the emergency department with complaints of lower extremity pain and multiple cutaneous necrotic lesions on his lower extremities. Patient reports seeking assistance from several medical providers over a 3-month period. Upon admission and further evaluation, a diagnosis of calciphylaxis was made clinically and confirmed by a skin biopsy. Sodium thiosulfate was initiated and the clinical picture improved significantly. Sodium thiosulfate is traditionally used as an antidote for cyanide poisoning, and it has demonstrated beneficial outcomes in most patients afflicted with CUA. The rationale behind sodium thiosulfate therapy in CUA is its role in chelating calcium into calcium thiosulfate, which increases its solubility leading to improved renal clearance. It is essential to raise awareness amongst physicians and medical practitioners alike, as early recognition and initiation of appropriate treatment can improve the patients' quality of life and more importantly, decrease mortality.

show abstract

“…5,10 Areas rich in adipose tissue may be more prone to small vessel damage, thus promoting calcification before the cutaneous lesions become clinically apparent. In obese patients, CUA develops in the abdomen, buttocks, and thighs as deeply seated, painful nodules.…”

Section: Discussionmentioning

confidence: 99%

“…The use of calcium containing phosphate binders should be avoided because ingestion of a large amount of calcium can trigger CUA. 10 One study showed that the use of nil calcium dialysate along with aggressive dialysis 5-6 days per week for 7-11 weeks was a highly effective treatment for CUA. 7 A second important therapeutic step is aggressive wound care.…”

Section: Discussionmentioning

confidence: 99%

Calcific uremic arteriopathy in a patient with long-standing uremia and severe hyperparathyroidism

et al. 2006

View full text Add to dashboard Cite

Calcific uremic arteriopathy (CUA) is a rare complication of uremia. Its pathogenesis is not known, and there is no well-defined treatment for it. In this report we describe CUA in a patient with end-stage renal failure who had undergone hemodialysis (HD) for 12 years. The patient developed end-stage renal failure 12 years prior to this report because of chronic glomerulonephritis, and was managed by HD. He had a renal transplant soon after initiation of HD, but this graft failed within a month because of acute rejection, and HD was resumed. He became hepatitis C positive 2 years later, and tests showed the development of impaired liver function. A year prior to this report, the patient developed tubercular ascites and responded well to antituberculous drugs. Six months prior to this report he noticed the development of multiple ulcerations in his toes and digits with ischemic pain. These lesions slowly increased in number and size. The patient was managed by strictly controlling phosphorus and by anticoagulation, followed by parathyroidectomy. This led to complete healing of most ischemic lesions and improvement of others. We attribute the CUA in this patient to prolonged hyperphosphatemia and hyperparathyroidism. Control of hyperphosphatemia, parathyroidectomy, local care, and anticoagulation are important therapeutic measures for this rare but life-threatening complication of chronic uremia.

show abstract

A case control study of proximal calciphylaxis

Cited by 166 publications

References 10 publications

The Effects of Sevelamer Hydrochloride and Calcium Carbonate on Kidney Calcification in Uremic Rats

The Effects of Sevelamer Hydrochloride and Calcium Carbonate on Kidney Calcification in Uremic Rats

Calciphylaxis: Early Detection and Off-Label Treatment With Sodium Thiosulfate

Calcific uremic arteriopathy in a patient with long-standing uremia and severe hyperparathyroidism

Contact Info

Product

Resources

About