Renal ostedystrophy (ROD) is a major long-term complication in uremic patients. Bone histomorphometry still remains the gold standard for the diagnosis of ROD. However, the low acceptance grade by patients makes bone biopsy a rarely performed and not easily repeatable investigation. No other instrumental assessment has been proved as yet to have sufficient sensitivity for ROD diagnosis. Many biochemical markers have been proposed for a diagnostic role, but few have a real predictive diagnostic value. Serum intact PTH (i-PTH) levels are thought to represent a good predictor of bone lesions. However, although a i-PTH level greater than 450 pg/mL and lower than 120 pg/mL may well predict high and low bone turnover disease respectively, in the wide range of values defined by the above border levels i-PTH does not have a predictive role for ROD. There is as yet no definite proof that the recently developed PTH assays might increase their diagnostic sensitivity. Bone alkaline phosphatase is a more reliable index of bone turnover than i-PTH levels. With regards to Al overload, given that an iron overburden is excluded, serum Al levels lower than 30 ug/L are seldom associated with increased Al deposition; conversely, levels above 60 mg/L are highly diagnostic for Al overload. In the latter condition, a DFO test is recommended. The main goals of ROD treatment are a) to maintain serum i-PTH levels between 120 and 150 pg/mL; b) to bring the phosphate (Pi) concentration under 5.5 mg/dL, Ca concentration between 9.2 and 10.4 mg/dL, and the Ca x Pi product under 55 mg/dL; c) to bring Al concentration under 20 ug/L; and d) to target serum bicarbonate levels between 20 and 24 mmol/L. The main therapeutic approaches include: Dietary Pi intake control (< 1200 mg/day). Intestinal phosphate binding using calcium salts and sevelamer. Calcium salts must be used at a dosage that avoids Ca overload (< 23 g/day). If Pi control is not reached, Mg and Al salts may be added at a dose lower than 2 g/day and for less than 3 months. Appropriate dialysis dose (KT/V > 1.2) and dialysis time (consider increased dialysis duration or session number for a week). Ca concentration in dialysate and infusion fluids can range between 1.25 and 2.00 mmol/L, according to the dialysis technique and to maintain an appropriate Ca balance. Vitamin D should not be used when i-PTH levels are < 120 pg/mL and/or serum Ca > 11 mg/dL and/or Pi > 6.5 mg/dL. The vitamin D dose should be proportional to PTH levels, with a larger dose given as a bolus (23 ug twice or three times per week). The intravenous route should be preferred in the case of very high i-PTH (> 700 pg/mL) or after 3 months of unsuccessful oral treatment. PTX should be prescribed on the basis of the clinical, biochemical, and instrumental data. A 7/8 PTX, when possible, is the most advisable procedure. Bone transplant disease (BTD) is caused by a combination of previous uremic ROD and bone lesions occurring after renal transplantation, mainly secondary to steroid effect. The main clinical result of BTD is the osteopenicosteoporotic syndrome, which frequently results in bone fractures. The most effective treatment of BTD is a reduction of the cumulative steroid dose. No strong evidence has been produced as yet for a preventive role of either bisphosphonates or vitamin D supplementation on BTD.

Linee Guida osteodistrofia renale = Renal osteodystrophy Guidelines / P. Messa. - In: GIORNALE ITALIANO DI NEFROLOGIA. - ISSN 0393-5590. - 20:24(2003 Sep), pp. S83-S95.

Linee Guida osteodistrofia renale = Renal osteodystrophy Guidelines

P. Messa
2003

Abstract

Renal ostedystrophy (ROD) is a major long-term complication in uremic patients. Bone histomorphometry still remains the gold standard for the diagnosis of ROD. However, the low acceptance grade by patients makes bone biopsy a rarely performed and not easily repeatable investigation. No other instrumental assessment has been proved as yet to have sufficient sensitivity for ROD diagnosis. Many biochemical markers have been proposed for a diagnostic role, but few have a real predictive diagnostic value. Serum intact PTH (i-PTH) levels are thought to represent a good predictor of bone lesions. However, although a i-PTH level greater than 450 pg/mL and lower than 120 pg/mL may well predict high and low bone turnover disease respectively, in the wide range of values defined by the above border levels i-PTH does not have a predictive role for ROD. There is as yet no definite proof that the recently developed PTH assays might increase their diagnostic sensitivity. Bone alkaline phosphatase is a more reliable index of bone turnover than i-PTH levels. With regards to Al overload, given that an iron overburden is excluded, serum Al levels lower than 30 ug/L are seldom associated with increased Al deposition; conversely, levels above 60 mg/L are highly diagnostic for Al overload. In the latter condition, a DFO test is recommended. The main goals of ROD treatment are a) to maintain serum i-PTH levels between 120 and 150 pg/mL; b) to bring the phosphate (Pi) concentration under 5.5 mg/dL, Ca concentration between 9.2 and 10.4 mg/dL, and the Ca x Pi product under 55 mg/dL; c) to bring Al concentration under 20 ug/L; and d) to target serum bicarbonate levels between 20 and 24 mmol/L. The main therapeutic approaches include: Dietary Pi intake control (< 1200 mg/day). Intestinal phosphate binding using calcium salts and sevelamer. Calcium salts must be used at a dosage that avoids Ca overload (< 23 g/day). If Pi control is not reached, Mg and Al salts may be added at a dose lower than 2 g/day and for less than 3 months. Appropriate dialysis dose (KT/V > 1.2) and dialysis time (consider increased dialysis duration or session number for a week). Ca concentration in dialysate and infusion fluids can range between 1.25 and 2.00 mmol/L, according to the dialysis technique and to maintain an appropriate Ca balance. Vitamin D should not be used when i-PTH levels are < 120 pg/mL and/or serum Ca > 11 mg/dL and/or Pi > 6.5 mg/dL. The vitamin D dose should be proportional to PTH levels, with a larger dose given as a bolus (23 ug twice or three times per week). The intravenous route should be preferred in the case of very high i-PTH (> 700 pg/mL) or after 3 months of unsuccessful oral treatment. PTX should be prescribed on the basis of the clinical, biochemical, and instrumental data. A 7/8 PTX, when possible, is the most advisable procedure. Bone transplant disease (BTD) is caused by a combination of previous uremic ROD and bone lesions occurring after renal transplantation, mainly secondary to steroid effect. The main clinical result of BTD is the osteopenicosteoporotic syndrome, which frequently results in bone fractures. The most effective treatment of BTD is a reduction of the cumulative steroid dose. No strong evidence has been produced as yet for a preventive role of either bisphosphonates or vitamin D supplementation on BTD.
human; practice guideline; renal osteodystrophy
Settore MED/14 - Nefrologia
set-2003
Article (author)
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/590560
Citazioni
  • ???jsp.display-item.citation.pmc??? 0
  • Scopus 6
  • ???jsp.display-item.citation.isi??? ND
social impact