Osteopathien und Calcium-Phosphat-Stoffwechsel bei chronischer H�modialyse

Kuhlencordt, F.; Bauditz, W; Lozano-Tonkin, C; Kruse, H.‐P.; Augustin, Herbert; Rehpenning, W.; Bartelheimer, H

doi:10.1007/bf01496807

Cited by 19 publications

(2 citation statements)

References 32 publications

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“…In contrast, cancellous bone mass is increased in endstage renal failure [11]; it may stay increased, as in our experiments, under haemodialysis; or it may become decreased, as in the studies of other authors [12].…”

Section: Changes O F Skeletal Mass In Dialysis Bone Diseasecontrasting

confidence: 47%

Skeletal Complications of Renal Insufficiency and Maintenance Haemodialysis

Ritz¹,

Krempien²,

Mehls³

et al. 1973

Nephron

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Some more controversial points in the interpretation of metabolic bone disease in end-stage renal failure are dealt with in this communication. The pattern of clinical signs changes with duration of dialysis and is strikingly different in dialysed children as compared with adults. Haemodialysed women bear children with apparently no skeletal disease. Animal experiments failed to show defective mineralisation in the fetal skeleton of the offsprings of uraemic pregnant rats, possibly pointing to a compensatory role of the fetal kidney in the metabolism of vitamin D. Some fallacies in the interpretation of X-ray signs in azotaemic patients are stressed: replacement of lamellar bone by woven bone and especially replacement of primary spongiosa underneath the growth plate by fibrous tissue (roentgenologically misinterpreted as rickets) are mentioned. The discrepant behaviour of cancellous vs. cortical bone is analysed.

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Section: Changes O F Skeletal Mass In Dialysis Bone Diseasecontrasting

confidence: 47%

Skeletal Complications of Renal Insufficiency and Maintenance Haemodialysis

Ritz¹,

Krempien²,

Mehls³

et al. 1973

Nephron

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“…A variety of pathogenic mechanisms closely related to each other have been proposed to be the reason for the secondary hyperparathyroidism which is frequently of critical im portance for bone disease. These include retention of in organic phosphate [1][2][3], impaired synthesis of the impor tant vitamin D metabolite l,25(OH)2Ds with the conse quence of diminished intestinal calcium absorption [4][5][6], sceletal resistance to parathyroid hormone (PTH) [7,8] and delayed metabolism of PTH [9][10][11][12], These abnormalities result in increased PTH values in most patients with chronic renal disease [10,[13][14][15] and in hyperparathyroid ism as a predominant feature of histological changes in the bone of such patients [16][17][18][19][20], The significance of the mechanisms proposed to induce the disturbance of cal cium metabolism in early renal failure which might well represent one underlying abnormality is uncertain. How-1 2 ever, secondary hyperparathyroidism must be present when one or the other of the mentioned mechanisms lead to a decreased serum calcium concentration.…”

Section: Introductionmentioning

confidence: 99%

Immunoreactive Parathyroid Hormone in Early and Advanced Renal Failure

Lilienfeld-Toal¹,

Gerlach²,

Klehr³

et al. 1982

Nephron

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Immunoreactive parathyroid hormone (iPTH) was measured in the serum of 20 patients with early renal failure (ERF) using three assays with different specificity. Half of these patients had elevated iPTH in one or more assays, up to twice the upper limit of normal. In contrast, 36 patients with a creatinine clearance below < 20 ml/min had an 80% elevated iPTH, up to 5 times the upper limit of normal. The patients with ERF and elevated iPTH had a lower serum calcium but no higher serum phosphate than those with normal iPTH. The differences in iPTH in early and end-stage renal failure can be explained by known differences in metabolism of different PTH forms in uremia.

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