Intravenous Calcitriol Improves Anaemia and Reduces the Need for Erythropoietin in Haemodialysis Patients

Goicoechea, Marián; Vázquez, Miguél; Ruiz, M A; Gómez-Campderá, Francisco; Pérez‐García, Rafael; Valderrábano, Fernando

doi:10.1159/000044877

Cited by 87 publications

(68 citation statements)

References 9 publications

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“…As for the effect of PTX on hemoglobin levels, beneficial effects have been seen following correction of secondary hyperparathyroidism in chronic renal failure [19, 20, 21]. Ureña et al [19]have reported an increase in circulating erythropoietin levels following PTX in chronic renal failure.…”

Section: Introductionmentioning

confidence: 99%

Parathyroidectomy in Chronic Renal Failure: Short- and Long-Term Results on Parathyroid Function, Blood Pressure and Anemia

Coen¹,

Calabria²,

Bellinghieri³

et al. 2001

Nephron

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To evaluate the long-term results of parathyroidectomy (PTX) on parathyroid function, blood pressure and anemia, data of 45 patients with secondary Hyperparathyroidism in dialysis who had undergone PTX were collected retrospectively from 8 different dialysis units. The patients, 25 M and 20 F, mean age 56 ± 11 years, who were followed up for an average period of 3.3 ± 2.3 years, were divided into four groups according to the surgical procedure: 19 patients had had a subtotal PTX; 10 patients had undergone total PTX with autotransplantation (AT); 10 patients had had total PTX without AT, and 6 patients had undergone partial PTX. Taking a reduction in intact PTH >50% as sign of successful PTX, only 5 patients did not attain this result. Considering values of PTH between 20 and 200 pg/ml at the mid-term observation (1–2 years) as the optimal result, values under 20 pg/ml as an expression of permanent hypoparathyroidism, and those above 200 pg/ml as indicating persistent/recurrent hyperparathyroidism, 65.5% of patients operated with subtotal PTX and total PTX + AT had a therapeutic success, versus 31.2% of patients in the other two groups, due to excess permanent hypoparathyroidism and persistent/recurrent hyperparathyroidism; 20 of 45 patients with preoperative hypertension experienced a statistically and clinically significant decrease in blood pressure levels. An increase in serum hemoglobin was also observed, despite a reduction of administered erythropoietin. In conclusion, the results of PTX obtained from this multicenter study are comparable to those reported by single leading centers. Recommended surgical procedures are subtotal PTX and total PTX with AT. The fall in blood pressure in hypertensive patients is clinically significant, and improvement in anemia is also observed with a reduction in erythropoietin dosage.

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Section: Introductionmentioning

confidence: 99%

Parathyroidectomy in Chronic Renal Failure: Short- and Long-Term Results on Parathyroid Function, Blood Pressure and Anemia

Coen¹,

Calabria²,

Bellinghieri³

et al. 2001

Nephron

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“…For example, intervention with calcitriol improves glucose tolerance 75,76 and lipid parameters, 77 and reduces erythropoietin requirements. 78 In addition to our efforts on cardiac structure and function, ongoing trials are currently testing the role of 1,25(OH) 2 D 3 or a related analog in inflammation (NCT00294866), vascular calcification (NCT00752102), endothelial cell health (NCT00528788), and proteinuria and renal disease (NCT00421733), to name a few.The biology for nutritional replacement of vitamin D also should not be ignored given the magnitude of 25OHD 3 deficiency in chronic renal failure. Recent data on 25OHD 3 and antimicrobial peptides are quite compelling, 79 and this has not gone unnoticed by the nephrology community (e.g., study NCT00749736) given infection is the second most common cause of mortality in chronic renal failure.…”

mentioning

confidence: 99%

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confidence: 99%

Is Calcitriol Life-Protective for Patients with Chronic Kidney Disease?

Thadhani¹

2009

Journal of the American Society of Nephrology

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In nephrology we are frequently confronted with association studies reporting novel biomarkers or mediators. Which among the myriad of potential candidates are amenable to intervention and, thereafter, which do we carry forward into clinical trials? Our group and others have considered the potential of vitamin D. Before commenting on vitamin D in chronic kidney disease, lessons learned from Alfred Sommer's initial observational studies and subsequent clinical trials with vitamin A-a journey of humility and perseverance-are worthy of reminder.Alfred Sommer, Dean Emeritus of the Johns Hopkins Bloomberg School of Public Health, received the Lasker Award in 1997 for his seminal work showing vitamin A deficiency is linked to increased risk of mortality and for demonstrating that correcting this deficiency reduces mortality. His series of studies started as simple observations, which led to community-based randomized trials. When Sommer initiated his work, vitamin A deficiency was highly prevalent, yet the connection between vitamin A deficiency and mortality had not been established. With the intent of examining night-blindness and dry eyes, Sommer and his colleagues stumbled across the observation that death rates in children with these ophthalmic conditions were several-fold higher than children without these conditions. 1 When Sommer first published his prospective observational study linking vitamin A deficiency with a 16% increased risk in mortality, 2 the field hardly took notice. As he articulated in a commentary written at the time of winning the Lasker, "The initial report associating vitamin A deficiency with increased mortality was received with deafening silence." 1 This response, as we know all too well, is common.Treatment with activated vitamin D, or calcitriol [1,25(OH) 2 D 3 ], has been used for over three decades to manage the secondary hyperparathyroidism and hypocalcemia accompanying chronic renal disease. [3][4][5][6] This intervention markedly changed the management of renal osteodystrophy, historically a severe debilitating condition. 7,8 By the late 1990s our attention in nephrology turned to altered mineral metabolism and its relationship to adverse outcomes. 9 The classic role for 1,25(OH) 2 D 3 is to maintain calcium homeostasis. 10 As an expected "side effect," it also raises serum levels of phosphate. 11 We were keenly interested in understanding the contribution of 1,25(OH) 2 D 3 to alterations in serum minerals and whether these alterations associated with increased mortality. In this effort, we accidentally came across a rather strong and consistent association between activated vitamin D therapy and reduced mortality, a finding independent of alterations in serum minerals. 12,13 Linking vitamin D therapy with altered minerals, and the two with increased mortality, would have "fit the prevailing paradigm" 1 and would have been more easily accepted. Speculating that 1,25(OH) 2 D 3 compounds-such as retinoic acid that activates nuclear receptors and leads to changes in gene transcription...

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“…Appropriate iron stores seem to be protective [76] because aluminum and iron share common pathways for intestinal absorption, serum transport and cellular uptake. Vice versa, aluminum overload may be one reason for iron-resistant anemia and resistance to erythropoietin [77] which might be overcome by intravenous calcitriol [78]. …”

Section: The Many Faces Of Renal Osteodystrophymentioning

confidence: 99%

Renal Osteodystrophy: New Insights in Pathophysiology and Treatment Modalities with Special Emphasis on the Insulin-Like Growth Factor System

Jehle

Mohan

et al. 1998

Nephron

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Intravenous Calcitriol Improves Anaemia and Reduces the Need for Erythropoietin in Haemodialysis Patients

Cited by 87 publications

References 9 publications

Parathyroidectomy in Chronic Renal Failure: Short- and Long-Term Results on Parathyroid Function, Blood Pressure and Anemia

Parathyroidectomy in Chronic Renal Failure: Short- and Long-Term Results on Parathyroid Function, Blood Pressure and Anemia

Is Calcitriol Life-Protective for Patients with Chronic Kidney Disease?

Renal Osteodystrophy: New Insights in Pathophysiology and Treatment Modalities with Special Emphasis on the Insulin-Like Growth Factor System

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