Vitamin-D Deficiency in the Osteomalacia of Chronic Renal Failure

Eastwood, J. B.; Stamp, T. C. B.; Harris, Eric; Wardener, H. E. de

doi:10.1016/s0140-6736(76)91140-5

Cited by 102 publications

(28 citation statements)

References 13 publications

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“…In this subgroup of patients with CKD, urinary protein losses were a more important predictor than the eGFR. Nephrotic syndrome has long been recognized as an important risk factor for 25OHD deficiency osteomalacia (18,19). Consistent with the recent analyses using the NHANES III data, our study demonstrates that the graded relationship between serum 25OHD levels and proteinuria is present even at subnephrotic levels (20).…”

Section: Discussionsupporting

confidence: 91%

Hypovitaminosis D in Chronic Kidney Disease

Mehrotra¹,

Kermah²,

Budoff³

et al. 2008

Clinical Journal of the American Society of Nephrology

152

107

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Section: Discussionsupporting

confidence: 91%

Hypovitaminosis D in Chronic Kidney Disease

Mehrotra¹,

Kermah²,

Budoff³

et al. 2008

Clinical Journal of the American Society of Nephrology

152

107

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“…A drop in serum iPTH levels was absent in this study and insignificant in others (7,9). Hyperphosphoremia prevents perhaps this decrease (9).…”

Section: Discussioncontrasting

confidence: 45%

“…2 I). Moderate doses of this drug administered over a short period of time improved calcification-front (7). It has been suggested that 25 OH D3 in physiologic concentrations can have an effect on bone mineralization in chronic renal failure (6).…”

Section: Discussionmentioning

confidence: 99%

“…that represents the percent of (30 pg) of 25 O H D3 were administered, daily during the first 3 a given volume of the trabecular bone occupied by osteoid (TO). 5) 7) Calcification rate (C.R.) was evaluated in cancellous bone by measuring the mean distance between the two fluorescent labels on each site of active calcification (10).…”

Section: Radiologic E V a L U A T I O Nmentioning

confidence: 99%

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Dialysis Bone Disease in Childhood: Treatment with 25-Hydroxycholecalciferol

1979

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Summary months of the study; then, the dose was increased to 125 nmole (50 pg) daily duringthe next 5 months. During the study. calcium The effect of 8 months of administration of moderate doses of supp~ements and D2 were d~scont~nued, ~h~ 25hydroxycholecakiferol (25 OH D3) on radiolobic. biolobic. and hydroxide was followed at the same d o w No patient was receiving bone histologic changes was assessed in five children on chronic a n t~c o n v u~s~v a n l drugs, hemodialysis. Osteomalacia, defined by an increase in the thickness index of the osteoid seams and d k r e a s e of the calcification rate, was present on the initial bone biopsy of only one patient and improved with the treatment. Secondary hyperparathyroidism and its prints on bone tissue, noted in all five children, did not improve in the absence of adequate serum phosphorus control. Furthermore, cancellous bone volume diminished in two patients with the administration of 25 OH D3. This activity of the drug could be related to its inhibitory effect of osteoblastic apposition as demonstrated by the decrease in the calcification rates. while the thickness index of the osteoid seams remains normal.Despite the small number of patients studied, these results suggest the importance of limiting the prescription of 25 OH D3 to children suffering from renal osteodystrophy only after having assessed unequivocally an osteomalacic component by histodynamical criteria. Secondary hyperparathyroidism appears not to be improved with moderate doses of 25 OH D3 in the absence of adequate serum phosphorus control.

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“…Low levels of active vitamin D 3 or 25 (OH) vitamin D 3 are associated with osteomalazia, but are not useful in diagnosis of ROD [63]. Only in established cases of ABD or unexplained bone pain the determination of vitamin D 3 levels is useful for the guidance of long-term therapy.…”

Section: Vitamin Dmentioning

confidence: 99%

Diagnosis of renal osteodystrophy

Schwarz

Sulzbacher

Oberbauer

2006

Eur J Clin Investigation

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The idiom renal osteodystrophy (ROD) represents a heterogeneous pattern of bone disturbances caused by chronic renal insufficiency and concomitant diseases. For the clinical decision of therapy it is most important to differentiate between high and low or adynamic turnover ROD because the therapeutically consequences of these two ends of the ROD spectrum are fundamentally different. Bone histology remains the gold standard for the exact classification of ROD. Serological markers of bone metabolism are not suited for the accurate nomenclature of ROD but are useful for the sequential follow up of ROD after a clear diagnosis has been made. Similarly, radiological diagnosis of ROD using dual energy X-ray absorptiometry (DEXA) or quantitative computer tomography scan (q-CT) is inaccurate and thus more suited for the routine follow up of established disease.Besides mineralization, bone strength and the rate of fractures are strongly determined by the architecture of the bone matrix. This information, however, is also only available on bone biopsy sections and cannot be estimated by non-invasive diagnostic methods.In summary, bone biopsy should be used more liberally for correct classification of bone disease. The sequential follow up and guidance of therapy success can be performed by non-invasive procedures such as biochemical bone marker determination in blood. X-ray imaging and densitometry is suitable only for sequential evaluation of osteoporosis.

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Vitamin-D Deficiency in the Osteomalacia of Chronic Renal Failure

Cited by 102 publications

References 13 publications

Hypovitaminosis D in Chronic Kidney Disease

Hypovitaminosis D in Chronic Kidney Disease

Dialysis Bone Disease in Childhood: Treatment with 25-Hydroxycholecalciferol

Diagnosis of renal osteodystrophy

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