Pulmonary calcification in hemodialyzed patients detected by technetium-99m diphosphonate scanning

Faubert, Pierre F.; Shapiro, Warren; Porush, Jerome G.; Chou, Shyan–Yih; Gross, Joel M.; Bondi, Elliott; Gomez-Leon, Guillermo

doi:10.1038/ki.1980.114

Cited by 61 publications

(45 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tissue calcification is a well-known complication in patients with chronic renal disease [1][2][3], but rarely radiographic evidence of its presence is provided [9], and it usually occurs after a long period of HD [4], However, our case developed extensive metastatic calcifications of lung, bones, vessels, skin, uterus and other soft tissue after only 3 months of maintenance HD.…”

Section: Discussionmentioning

confidence: 81%

“…Before HD pH was 7.351, pC 02 29. 4 Before initiation of HD, she has never received aluminum salts for treatment of gastrointestinal symptoms or controlling scrum phosphate levels, although calcium carbonate and alfacalcidol were intermittently given.…”

Section: Case Reportmentioning

confidence: 99%

“…Tissue calcification has been well known in patients with chronic renal failure, especially in those undergoing maintenance hemodialysis (HD) [1][2][3], In general, such calcification occurs after a long period of HD [4] and has often been attributed to a high calcium-phosphorous product [5,6] and/or secondary hyperparathyroidism [7], We report a refractory nephrotic patient who developed acutely progressive and extensive metastatic calcification following chronic HD without those findings. …”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Acute Progressive and Extensive Metastatic Calcifications in a Nephrotic Patient following Chronic Hemodialysis

Uchida

Sakemi²,

Ikeda³

et al. 1995

Am J Nephrol

View full text Add to dashboard Cite

We report on a 46-year-old female patient with a 5-year history of refractory nephrotic syndrome who rapidly developed extensive metastatic calcifications in lung, bone, blood vessels, skin, uterus and other soft tissues following maintenance hemodialysis. She was admitted for controlling anasarca. On admission, she suffered from severe nephrotic syndrome and chronic renal failure, showing 1.3 g/dl of serum albumin and 4.6 mg/dl of serum creatinine. She received bicarbonate dialysis combined with extracorporeal ultrafiltration to control anasarca. Following hemodialysis, she was treated with alfacalcidol and an increasing dose of calcium carbonate. Although anasarca was controlled, her nephrotic state remained unchanged. After 3 months of dialysis, roentgenograms of the body disclosed multiple metastatic calcifications. At this time, though the calcium-phosphorous product in serum was almost normal, the free calcium index was confirmed to have been high for 4 weeks. We considered that administration of calcium carbonate and alfacalcidol as well as an influx of free calcium from a dialysate resulted in increased serum ionized calcium which may be unable to be bound to serum protein because of lack of total protein, leading to ectopic deposition of calcium and phosphate. Our findings suggested that intensive care is needed to prevent metastatic calcification when uremic patients with severe nephrosis are treated with bicarbonate hemodialysis.

show abstract

Section: Discussionmentioning

confidence: 81%

Section: Case Reportmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Acute Progressive and Extensive Metastatic Calcifications in a Nephrotic Patient following Chronic Hemodialysis

Uchida

Sakemi²,

Ikeda³

et al. 1995

Am J Nephrol

View full text Add to dashboard Cite

show abstract

“…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). In rats, Borle et al (16) showed that high P-induced hyperparathyroidism caused nephrocalcinosis.…”

Section: Discussionmentioning

confidence: 99%

“…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 chronic renal failure is therefore important to the prevention of increases in Ca ϫ P product, secondary hyperparathyroidism, and ectopic calcifications (9).…”

mentioning

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

Metabolic Disease

Schwarz¹,

Lynch²

1999

Diffuse Lung Disorders

View full text Add to dashboard Cite

Pulmonary calcification in hemodialyzed patients detected by technetium-99m diphosphonate scanning

Cited by 61 publications

References 17 publications

Acute Progressive and Extensive Metastatic Calcifications in a Nephrotic Patient following Chronic Hemodialysis

Acute Progressive and Extensive Metastatic Calcifications in a Nephrotic Patient following Chronic Hemodialysis

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

Metabolic Disease

Contact Info

Product

Resources

About