Bone loss in diabetic patients with chronic kidney disease

Objective  We investigated whether loss of bone is detectable during follow‐up of diabetic patients with chronic kidney disease (CKD). Research design and methods  In 40 initially non‐dialysed diabetic patients with CKD (isotopic glomerular filtration rate < 60 ml/min/1.73 m2 or albumin excretion...

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Published in:Diabetic medicine Vol. 24; no. 1; pp. 91 - 93
Main Authors: Rigalleau, V., Lasseur, C., Raffaitin, C., Perlemoine, C., Barthe, N., Chauveau, P., Aparicio, M., Combe, C., Gin, H.
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Publishing Ltd 01.01.2007
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ISSN:0742-3071, 1464-5491
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Abstract Objective  We investigated whether loss of bone is detectable during follow‐up of diabetic patients with chronic kidney disease (CKD). Research design and methods  In 40 initially non‐dialysed diabetic patients with CKD (isotopic glomerular filtration rate < 60 ml/min/1.73 m2 or albumin excretion rate > 30 mg/24 h), body composition (DEXA scan) and glomerular filtration rate (GFR determined from 51Cr‐EDTA clearance) were measured at a 2‐year interval, and compared by paired t‐tests. Results  The 40 patients, mainly with Type 2 diabetes (n = 28), were men (n = 28), aged 65 ± 11 years, with diabetes duration 18 ± 11 years. GFR was initially 38.0 (range 8–89) ml/min/1.73 m2. CKD progressed during follow‐up: eight started haemodialysis and GFR declined in the 32 others (P < 0.05 vs. initial). T‐scores for total body (initial −0.61 ± 1.11, final −1.11 ± 1.40; P < 0.001) and femoral neck (initial −1.88 ± 0.15, final −2.07 ± 0.15; P < 0.05) declined. Ten patients were osteopaenic at baseline (no osteoporosis), whereas most were osteopaenic (n = 21, P < 0.05) and five were osteoporotic at final assessment. The 16 patients who became osteopaenic or osteoporotic during follow‐up did not differ from the others for the type of diabetes, age, GFR, albumin excretion rate, HbA1c, GFR reduction and the requirement for dialysis during follow‐up. They were all men (P < 0.01 by chi‐squared test), with reduced initial total body T‐score (−1.20 ± 0.82, others −0.32 ± 1.13; P < 0.05) and a lower body mass index (24.6 ± 4.3; others 27.7 ± 4.3; P < 0.05). Conclusion  Bone loss, especially in the femoral neck, is progressive in diabetic patients with CKD.
AbstractList AbstractObjectiveWe investigated whether loss of bone is detectable during follow-up of diabetic patients with chronic kidney disease (CKD).Research design and methodsIn 40 initially non-dialysed diabetic patients with CKD (isotopic glomerular filtration rate < 60 ml/min/1.73 m2 or albumin excretion rate > 30 mg/24 h), body composition (DEXA scan) and glomerular filtration rate (GFR determined from 51Cr-EDTA clearance) were measured at a 2-year interval, and compared by paired t-tests.ResultsThe 40 patients, mainly with Type 2 diabetes (n = 28), were men (n = 28), aged 65 plus or minus 11 years, with diabetes duration 18 plus or minus 11 years. GFR was initially 38.0 (range 8-89) ml/min/1.73 m2. CKD progressed during follow-up: eight started haemodialysis and GFR declined in the 32 others (P < 0.05 vs. initial). T-scores for total body (initial -0.61 plus or minus 1.11, final -1.11 plus or minus 1.40; P < 0.001) and femoral neck (initial -1.88 plus or minus 0.15, final -2.07 plus or minus 0.15; P < 0.05) declined. Ten patients were osteopaenic at baseline (no osteoporosis), whereas most were osteopaenic (n = 21, P < 0.05) and five were osteoporotic at final assessment. The 16 patients who became osteopaenic or osteoporotic during follow-up did not differ from the others for the type of diabetes, age, GFR, albumin excretion rate, HbA1c, GFR reduction and the requirement for dialysis during follow-up. They were all men (P < 0.01 by chi-squared test), with reduced initial total body T-score (-1.20 plus or minus 0.82, others -0.32 plus or minus 1.13; P < 0.05) and a lower body mass index (24.6 plus or minus 4.3; others 27.7 plus or minus 4.3; P < 0.05).ConclusionBone loss, especially in the femoral neck, is progressive in diabetic patients with CKD.Diabet. Med. 24, 91-93 (2007)
We investigated whether loss of bone is detectable during follow-up of diabetic patients with chronic kidney disease (CKD).OBJECTIVEWe investigated whether loss of bone is detectable during follow-up of diabetic patients with chronic kidney disease (CKD).In 40 initially non-dialysed diabetic patients with CKD (isotopic glomerular filtration rate < 60 ml/min/1.73 m(2) or albumin excretion rate > 30 mg/24 h), body composition (DEXA scan) and glomerular filtration rate (GFR determined from (51)Cr-EDTA clearance) were measured at a 2-year interval, and compared by paired t-tests.RESEARCH DESIGN AND METHODSIn 40 initially non-dialysed diabetic patients with CKD (isotopic glomerular filtration rate < 60 ml/min/1.73 m(2) or albumin excretion rate > 30 mg/24 h), body composition (DEXA scan) and glomerular filtration rate (GFR determined from (51)Cr-EDTA clearance) were measured at a 2-year interval, and compared by paired t-tests.The 40 patients, mainly with Type 2 diabetes (n = 28), were men (n = 28), aged 65 +/- 11 years, with diabetes duration 18 +/- 11 years. GFR was initially 38.0 (range 8-89) ml/min/1.73 m(2). CKD progressed during follow-up: eight started haemodialysis and GFR declined in the 32 others (P < 0.05 vs. initial). T-scores for total body (initial -0.61 +/- 1.11, final -1.11 +/- 1.40; P < 0.001) and femoral neck (initial -1.88 +/- 0.15, final -2.07 +/- 0.15; P < 0.05) declined. Ten patients were osteopaenic at baseline (no osteoporosis), whereas most were osteopaenic (n = 21, P < 0.05) and five were osteoporotic at final assessment. The 16 patients who became osteopaenic or osteoporotic during follow-up did not differ from the others for the type of diabetes, age, GFR, albumin excretion rate, HbA(1c), GFR reduction and the requirement for dialysis during follow-up. They were all men (P < 0.01 by chi-squared test), with reduced initial total body T-score (-1.20 +/- 0.82, others -0.32 +/- 1.13; P < 0.05) and a lower body mass index (24.6 +/- 4.3; others 27.7 +/- 4.3; P < 0.05).RESULTSThe 40 patients, mainly with Type 2 diabetes (n = 28), were men (n = 28), aged 65 +/- 11 years, with diabetes duration 18 +/- 11 years. GFR was initially 38.0 (range 8-89) ml/min/1.73 m(2). CKD progressed during follow-up: eight started haemodialysis and GFR declined in the 32 others (P < 0.05 vs. initial). T-scores for total body (initial -0.61 +/- 1.11, final -1.11 +/- 1.40; P < 0.001) and femoral neck (initial -1.88 +/- 0.15, final -2.07 +/- 0.15; P < 0.05) declined. Ten patients were osteopaenic at baseline (no osteoporosis), whereas most were osteopaenic (n = 21, P < 0.05) and five were osteoporotic at final assessment. The 16 patients who became osteopaenic or osteoporotic during follow-up did not differ from the others for the type of diabetes, age, GFR, albumin excretion rate, HbA(1c), GFR reduction and the requirement for dialysis during follow-up. They were all men (P < 0.01 by chi-squared test), with reduced initial total body T-score (-1.20 +/- 0.82, others -0.32 +/- 1.13; P < 0.05) and a lower body mass index (24.6 +/- 4.3; others 27.7 +/- 4.3; P < 0.05).Bone loss, especially in the femoral neck, is progressive in diabetic patients with CKD.CONCLUSIONBone loss, especially in the femoral neck, is progressive in diabetic patients with CKD.
Objective  We investigated whether loss of bone is detectable during follow‐up of diabetic patients with chronic kidney disease (CKD). Research design and methods  In 40 initially non‐dialysed diabetic patients with CKD (isotopic glomerular filtration rate < 60 ml/min/1.73 m2 or albumin excretion rate > 30 mg/24 h), body composition (DEXA scan) and glomerular filtration rate (GFR determined from 51Cr‐EDTA clearance) were measured at a 2‐year interval, and compared by paired t‐tests. Results  The 40 patients, mainly with Type 2 diabetes (n = 28), were men (n = 28), aged 65 ± 11 years, with diabetes duration 18 ± 11 years. GFR was initially 38.0 (range 8–89) ml/min/1.73 m2. CKD progressed during follow‐up: eight started haemodialysis and GFR declined in the 32 others (P < 0.05 vs. initial). T‐scores for total body (initial −0.61 ± 1.11, final −1.11 ± 1.40; P < 0.001) and femoral neck (initial −1.88 ± 0.15, final −2.07 ± 0.15; P < 0.05) declined. Ten patients were osteopaenic at baseline (no osteoporosis), whereas most were osteopaenic (n = 21, P < 0.05) and five were osteoporotic at final assessment. The 16 patients who became osteopaenic or osteoporotic during follow‐up did not differ from the others for the type of diabetes, age, GFR, albumin excretion rate, HbA1c, GFR reduction and the requirement for dialysis during follow‐up. They were all men (P < 0.01 by chi‐squared test), with reduced initial total body T‐score (−1.20 ± 0.82, others −0.32 ± 1.13; P < 0.05) and a lower body mass index (24.6 ± 4.3; others 27.7 ± 4.3; P < 0.05). Conclusion  Bone loss, especially in the femoral neck, is progressive in diabetic patients with CKD.
We investigated whether loss of bone is detectable during follow-up of diabetic patients with chronic kidney disease (CKD). In 40 initially non-dialysed diabetic patients with CKD (isotopic glomerular filtration rate < 60 ml/min/1.73 m(2) or albumin excretion rate > 30 mg/24 h), body composition (DEXA scan) and glomerular filtration rate (GFR determined from (51)Cr-EDTA clearance) were measured at a 2-year interval, and compared by paired t-tests. The 40 patients, mainly with Type 2 diabetes (n = 28), were men (n = 28), aged 65 +/- 11 years, with diabetes duration 18 +/- 11 years. GFR was initially 38.0 (range 8-89) ml/min/1.73 m(2). CKD progressed during follow-up: eight started haemodialysis and GFR declined in the 32 others (P < 0.05 vs. initial). T-scores for total body (initial -0.61 +/- 1.11, final -1.11 +/- 1.40; P < 0.001) and femoral neck (initial -1.88 +/- 0.15, final -2.07 +/- 0.15; P < 0.05) declined. Ten patients were osteopaenic at baseline (no osteoporosis), whereas most were osteopaenic (n = 21, P < 0.05) and five were osteoporotic at final assessment. The 16 patients who became osteopaenic or osteoporotic during follow-up did not differ from the others for the type of diabetes, age, GFR, albumin excretion rate, HbA(1c), GFR reduction and the requirement for dialysis during follow-up. They were all men (P < 0.01 by chi-squared test), with reduced initial total body T-score (-1.20 +/- 0.82, others -0.32 +/- 1.13; P < 0.05) and a lower body mass index (24.6 +/- 4.3; others 27.7 +/- 4.3; P < 0.05). Bone loss, especially in the femoral neck, is progressive in diabetic patients with CKD.
Objective  We investigated whether loss of bone is detectable during follow‐up of diabetic patients with chronic kidney disease (CKD). Research design and methods  In 40 initially non‐dialysed diabetic patients with CKD (isotopic glomerular filtration rate < 60 ml/min/1.73 m 2 or albumin excretion rate > 30 mg/24 h), body composition (DEXA scan) and glomerular filtration rate (GFR determined from 51 Cr‐EDTA clearance) were measured at a 2‐year interval, and compared by paired t ‐tests. Results  The 40 patients, mainly with Type 2 diabetes ( n  = 28), were men ( n  = 28), aged 65 ± 11 years, with diabetes duration 18 ± 11 years. GFR was initially 38.0 (range 8–89) ml/min/1.73 m 2 . CKD progressed during follow‐up: eight started haemodialysis and GFR declined in the 32 others ( P <  0.05 vs. initial). T‐scores for total body (initial −0.61 ± 1.11, final −1.11 ± 1.40; P  < 0.001) and femoral neck (initial −1.88 ± 0.15, final −2.07 ± 0.15; P  < 0.05) declined. Ten patients were osteopaenic at baseline (no osteoporosis), whereas most were osteopaenic ( n  = 21, P  < 0.05) and five were osteoporotic at final assessment. The 16 patients who became osteopaenic or osteoporotic during follow‐up did not differ from the others for the type of diabetes, age, GFR, albumin excretion rate, HbA 1c , GFR reduction and the requirement for dialysis during follow‐up. They were all men ( P <  0.01 by chi‐squared test), with reduced initial total body T‐score (−1.20 ± 0.82, others −0.32 ± 1.13; P  < 0.05) and a lower body mass index (24.6 ± 4.3; others 27.7 ± 4.3; P  < 0.05). Conclusion  Bone loss, especially in the femoral neck, is progressive in diabetic patients with CKD.
Author Chauveau, P.
Combe, C.
Barthe, N.
Raffaitin, C.
Lasseur, C.
Perlemoine, C.
Aparicio, M.
Rigalleau, V.
Gin, H.
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Keywords Endocrinopathy
Kidney disease
Human
Urinary system disease
osteopaenia
Diabetes mellitus
Renal failure
Diseases of the osteoarticular system
Bone mineral density
Chronic kidney disease
diabetes
Osteopenia
Language English
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PublicationTitle Diabetic medicine
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Rix M, Andreassen H, Eskildsen P, Langdahl B, Olgaard K. Bone mineral density and biochemical markers of bone turnover in patients with predialysis chronic renal failure. Kidney Int 1999; 56: 1084-1093.
Hruska KA. Renal osteodystrophy. Baillieres Clin Endocrinol Metab 1997; 11: 165-194.
Goliat E, Marusza W, Ostrowski K, Lipinska A. Microalbuminuria as a risk factor for diabetic osteopathy in patients with IDDM and renal sufficiency. Pol Arch Med Wewn 1998; 100: 111-118.
Hovind P, Rossing P, Tarnow L, Smidt UM, Parving HH. Progression of diabetic nephropathy. Kidney Int 2001; 59: 702-709.
Pei Y, Hercz G, Greenwood C, Segre G, Manuel A, Saiphoo C et al. Renal osteodystrophy in diabetic patients. Kidney Int 1993; 44: 159-164.
Spasovski GB, Bervoets AR, Behets GJ, Ivanovski N, Sikole A, Dams G et al. Spectrum of renal bone disease in end-stage renal failure patients not yet on dialysis. Nephrol Dial Transplant 2003; 18: 1159-1166.
Tuominen JT, Impivaara O, Puukka P, Ronnemaa T. Bone mineral density in patients with type 1 and type 2 diabetes. Diabetes Care 1999; 22: 1196-1200.
Clausen P, Feldt-Rasmussen B, Jacobsen P, Rossing K, Parving HH, Nielsen PK et al. Microalbuminuria as an early indicator of osteopenia in male insulin-dependent diabetic patients. Diabet Med 1997; 14: 1038-1043.
Johnell O, Kanis JA, Oden A, Johansson H, De Laet C, Delmas P et al. Predictive value of BMD for hip and other fractures. J Bone Miner Res 2005; 20: 1185-1194.
Ahmed LA, Joakimsen RM, Berntsen GK, Fonnebo V, Schirmer H. Diabetes mellitus and the risk of non-vertebral fractures: the Tromso study. Osteoporos Int 2006; 17: 495-500.
Vestergaard P, Rejnmark L, Mosekilde L. Relative fracture risk in patients with diabetes mellitus, and the impact of insulin and oral anti-diabetic medication on relative fracture risk. Diabetologia 2005; 48: 1292-1299.
Kaji H, Suzuki M, Yano S, Sugimoto T, Chihara K, Hattori S et al. Risk factors for hip fracture in hemodialysis patients. Am J Nephrol 2002; 22: 325-331.
Strotmeyer ES, Cauley JA, Schwartz AV, Nevitt MC, Resnick HE, Bauer DC et al. Non-traumatic fracture risk with diabetes mellitus and impaired fasting glucose in older white and black adults: the health, aging, and body composition study. Arch Intern Med 2005; 165: 1612-1617.
Nicodemus KK, Folsom AR; Iowa Women's Health Study. Type 1 and type 2 diabetes and incident hip fractures in post-menopausal women. Diabetes Care 2001; 24: 1192-1197.
Miao J, Brismar K, Nyren O, Ugarph-Morawski A, Ye W. Elevated hip fracture risk in type 1 diabetic patients: a population-based cohort study in Sweden. Diabetes Care 2005; 28: 2850-2855.
Rossing K, Christensen PK, Hovind P, Tarnow L, Rossing P, Parving HH. Progression of nephropathy in type 2 diabetic patients. Kidney Int 2004; 66: 1596-1605.
De Liefde II, Van Der Klift M, De Laet CE, Van Daele PL, Hofman A, Pols HA. Bone mineral density and fracture risk in type-2 diabetes mellitus: the Rotterdam Study. Osteoporos Int 2005; 16: 1713-1720.
Nishitani H, Miki T, Morii H, Nishizawa Y, Ishimura E, Hagiwara S et al. Decreased bone mineral density in diabetic patients on hemodialysis. Contrib Nephrol 1991; 90: 223-227.
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References_xml – reference: Nicodemus KK, Folsom AR; Iowa Women's Health Study. Type 1 and type 2 diabetes and incident hip fractures in post-menopausal women. Diabetes Care 2001; 24: 1192-1197.
– reference: Vestergaard P, Rejnmark L, Mosekilde L. Relative fracture risk in patients with diabetes mellitus, and the impact of insulin and oral anti-diabetic medication on relative fracture risk. Diabetologia 2005; 48: 1292-1299.
– reference: Tuominen JT, Impivaara O, Puukka P, Ronnemaa T. Bone mineral density in patients with type 1 and type 2 diabetes. Diabetes Care 1999; 22: 1196-1200.
– reference: Hovind P, Rossing P, Tarnow L, Smidt UM, Parving HH. Progression of diabetic nephropathy. Kidney Int 2001; 59: 702-709.
– reference: Hruska KA. Renal osteodystrophy. Baillieres Clin Endocrinol Metab 1997; 11: 165-194.
– reference: Rakic V, Davis WA, Chubb SAP, Islam FMA, Prince RL, Davis TME. Bone mineral density and its determinants in diabetes: the Fremantle Diabetes Study. Diabetologia 2006; 49: 863-871.
– reference: Goliat E, Marusza W, Ostrowski K, Lipinska A. Microalbuminuria as a risk factor for diabetic osteopathy in patients with IDDM and renal sufficiency. Pol Arch Med Wewn 1998; 100: 111-118.
– reference: Ahmed LA, Joakimsen RM, Berntsen GK, Fonnebo V, Schirmer H. Diabetes mellitus and the risk of non-vertebral fractures: the Tromso study. Osteoporos Int 2006; 17: 495-500.
– reference: Rossing K, Christensen PK, Hovind P, Tarnow L, Rossing P, Parving HH. Progression of nephropathy in type 2 diabetic patients. Kidney Int 2004; 66: 1596-1605.
– reference: De Liefde II, Van Der Klift M, De Laet CE, Van Daele PL, Hofman A, Pols HA. Bone mineral density and fracture risk in type-2 diabetes mellitus: the Rotterdam Study. Osteoporos Int 2005; 16: 1713-1720.
– reference: Spasovski GB, Bervoets AR, Behets GJ, Ivanovski N, Sikole A, Dams G et al. Spectrum of renal bone disease in end-stage renal failure patients not yet on dialysis. Nephrol Dial Transplant 2003; 18: 1159-1166.
– reference: Miao J, Brismar K, Nyren O, Ugarph-Morawski A, Ye W. Elevated hip fracture risk in type 1 diabetic patients: a population-based cohort study in Sweden. Diabetes Care 2005; 28: 2850-2855.
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– reference: Kaji H, Suzuki M, Yano S, Sugimoto T, Chihara K, Hattori S et al. Risk factors for hip fracture in hemodialysis patients. Am J Nephrol 2002; 22: 325-331.
– reference: Johnell O, Kanis JA, Oden A, Johansson H, De Laet C, Delmas P et al. Predictive value of BMD for hip and other fractures. J Bone Miner Res 2005; 20: 1185-1194.
– reference: Nishitani H, Miki T, Morii H, Nishizawa Y, Ishimura E, Hagiwara S et al. Decreased bone mineral density in diabetic patients on hemodialysis. Contrib Nephrol 1991; 90: 223-227.
– reference: Pei Y, Hercz G, Greenwood C, Segre G, Manuel A, Saiphoo C et al. Renal osteodystrophy in diabetic patients. Kidney Int 1993; 44: 159-164.
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Snippet Objective  We investigated whether loss of bone is detectable during follow‐up of diabetic patients with chronic kidney disease (CKD). Research design and...
Objective  We investigated whether loss of bone is detectable during follow‐up of diabetic patients with chronic kidney disease (CKD). Research design and...
We investigated whether loss of bone is detectable during follow-up of diabetic patients with chronic kidney disease (CKD). In 40 initially non-dialysed...
AbstractObjectiveWe investigated whether loss of bone is detectable during follow-up of diabetic patients with chronic kidney disease (CKD).Research design and...
We investigated whether loss of bone is detectable during follow-up of diabetic patients with chronic kidney disease (CKD).OBJECTIVEWe investigated whether...
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StartPage 91
SubjectTerms Adult
Aged
Aged, 80 and over
Biological and medical sciences
Body Mass Index
Bone Density - physiology
Bone Diseases, Metabolic - etiology
Bone Diseases, Metabolic - physiopathology
bone mineral density
chronic kidney disease
diabetes
Diabetes Mellitus, Type 1 - complications
Diabetes Mellitus, Type 2 - complications
Diabetes. Impaired glucose tolerance
Diseases of the osteoarticular system
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Female
Femoral Neck Fractures - etiology
Follow-Up Studies
Humans
Kidney Failure, Chronic - complications
Male
Medical sciences
Middle Aged
osteopaenia
Osteoporosis. Osteomalacia. Paget disease
Risk Factors
Title Bone loss in diabetic patients with chronic kidney disease
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https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1464-5491.2007.02026.x
https://www.ncbi.nlm.nih.gov/pubmed/17227330
https://www.proquest.com/docview/20437006
https://www.proquest.com/docview/68924342
Volume 24
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