Fracturing Dialysis Osteodystrophy and Dialysis Encephalopathy

Parkinson, Ian; Feest, Terry; Kerr, David; Ward, M. K.; Fawcett, Rodney

doi:10.1016/s0140-6736(79)90883-3

Cited by 359 publications

(97 citation statements)

References 12 publications

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“…Patients with end-stage renal disease were undergoing haemodialysis with Al-contaminated water (Platts et al 1977;Parkinson et al 1979) or receiving oral Alcontaining phosphate-binding gels, or both (Bournerais et al 1983;Andreoli et al 1984 In both types of patients Al was located in the bone-osteoid surface either by histochemical staining with aurin tricarboxylic acid (Buchanan et al 1981 ;Ott et al 1982Ott et al , 1983 or by electron-microprobe analysis (Cournot-Witmer et al 1981). The stain was quantified by measuring the amount of surface taking up the stain.…”

Section: O W -T U R N O V E R B O N E D I S E a S Ementioning

confidence: 99%

Nutritional Aspects of Aluminium Toxicity

Klein

1990

Nutr. Res. Rev.

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Table 1. Parenteral sources of aluminium contamination A1 Wl) Source Casein hydrolysate (100 g/l) Crystalline amino acids (100 g/l) Potassium phosphate (3 mmol/l) Unspecified phosphate Potassium phosphate Potassium acid phosphate (136 g/l) Sodium phosphate (3 mmol/l) Calcium gluconate (100 g/l) Calcium glucoheptonate Normal serum albumin (250 g/l) Normal serum albumin (43 g/l) Plasmanate? (50 g/l) Heparin (lo00 u/ml) Factor VIII Factor IX Trace metal solutions Multivitamin infusion

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Section: O W -T U R N O V E R B O N E D I S E a S Ementioning

confidence: 99%

Nutritional Aspects of Aluminium Toxicity

Klein

1990

Nutr. Res. Rev.

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“…A facilitating role for other nonproteinaceous substances that may accumulate in certain tissues cannot be excluded. An example of the last alternative might be furnished by aluminum salts, which are significantly increased in dialysis patients developing encephalopathy (44) or arthropathy (45). Aluminum has also been reported as a significant constituent of amyloid deposits and neurofibrillary pathology in Alzheimer's dementia (46).…”

Section: Arg-val-asn-his-val-thr-leu-ser-gln-pro-lys-ile-val-lys-trp-mentioning

confidence: 99%

Polymerization of intact beta 2-microglobulin in tissue causes amyloidosis in patients on chronic hemodialysis.

Gorevic¹,

Muñoz²,

Casey³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

159

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Systemic amyloidosis with a predilection for bone and synovium may complicate the course of patients on long-term hemodialysis. This form of amyloidosis can be typed as distinct from other amyloid diseases by using small tissue samples obtained by bone biopsy and at postmortem. Immunoblot analysis of two-dimensional gels of partially solubilized amyloid fibrils established that tissue deposits are composed of monomers, dimers, and higher polymers of beta 2-microglobulin (beta 2m) and that amyloid P component was also present. Anti-beta 2m antiserum recognized fibrils, as shown by immunoelectron microscopy. Purified monomer isolated from dissociated fibrils yielded peptides corresponding to the entire known sequence of beta 2m. Virtually all serum beta 2m, as well as that present in tissue fluid bathing amyloid fibrils, was monomeric. Hemodialysis-related amyloidosis is an example of a deposition disease occurring in hemodialysis patients. We have shown conclusively that, in this amyloid disease, polymerization of an intact normal serum protein to a fibrillar configuration may occur without proteolysis. We propose the designation A beta 2m for this form of amyloid fibril subunit protein.

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“…(14) Defective mineralization (M) may result in bone pain and/or fracture. (15)(16)(17)(18) Abnormalities in bone balance will lead to changes in bone volume (V), which result in either osteoporosis or osteosclerosis. (19,20) No up-to-date information is available on with active vitamin D or phosphate binders have not been studied in patients with CKD.…”

Section: Introductionmentioning

confidence: 99%

Renal osteodystrophy in the first decade of the new millennium: Analysis of 630 bone biopsies in black and white patients

Malluche

Mawad

Monier‐Faugere

2010

Journal of Bone and Mineral Research

282

235

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Renal osteodystrophy occurs early during loss of kidney function. There are 26 million American patients with chronic kidney disease (CKD), and almost all patients with CKD stage 5 have abnormal bone histology. Six hundred and thirty bone biopsies from adult CKD-5 patients on dialysis were evaluated by histomorphometry and analyzed using the turnover (T), mineralization (M), and volume (V) classification. There were racial differences; whites exhibited predominantly low turnover (62%), whereas blacks showed mostly normal or high turnover (68%). A mineralization defect was observed in only 3% of patients. In whites, cancellous bone volume was low, normal, or high in approximately the same number of patients, whereas in blacks, cancellous bone volume was high in two-thirds of the patients. More than 80% of blacks and whites with low cancellous bone volume had thin trabeculae owing to low bone formation. Cortical thickness was low in half the whites, whereas it was normal in three-quarters of blacks. Cortical porosity was high in 50% of whites, whereas three-quarters of blacks had high porosity. In summary, the TMV system gives relevant information. It should be expanded to include the architecture of cancellous and cortical bone. There are racial differences. Low bone volume and low bone turnover are more frequent than heretofore appreciated, whereas mineralization defects nowadays are observed rarely in adults. These findings call for an adjustment of the current therapeutic paradigm that takes into consideration race and risk of low bone volume and turnover. The latter have been shown to be associated with increased vascular calcifications. ß

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Fracturing Dialysis Osteodystrophy and Dialysis Encephalopathy

Cited by 359 publications

References 12 publications

Nutritional Aspects of Aluminium Toxicity

Nutritional Aspects of Aluminium Toxicity

Polymerization of intact beta 2-microglobulin in tissue causes amyloidosis in patients on chronic hemodialysis.

Renal osteodystrophy in the first decade of the new millennium: Analysis of 630 bone biopsies in black and white patients

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