Die renale Osteodystrophie

Based on a literature survey the present thesis analyses symptoms
of renal osteodystrophy, a consequence of chronic renal failure.
Within the disease complex of chronic renal failure renal
osteodystrophy represents one of the main reasons for the morbidity
of the affected patients (Ferreira, 2006). One target of this
dissertation is to describe the origin of different types of renal
osteodystrophy, its pathogenesis, clinical phenomenons and
diagnostic routines. Evaluating the current state of therapy is
another main focus. At this point, mode of action, dosage, side
effects and risks of different therapeutics have been proved by
current research results. There are two different kinds of renal
osteodystrophy: high turnover bone disease and low turnover bone
disease. Current literature studies indicate that incidences have
changed over the last three decades: In the 1970s and 1980s the
high turnover bone disease caused by secondary hyperparathyroidism
and lack of vitamin D were predominant. Due to intensified
application of vitamin D-metabolites in order to treat high
turnover bone disease, increasing occurrence of diabetes mellitus
and the higher age of patients, a strong parathyroid suppression
and low turnover bone disease has appeared more often in the
meantime. With regard to diagnostic routines, bone biopsy for
histomorphometric evaluation is still the only secure way to
diagnose renal osteodystrophy. Up to now, the search for new
chemical parameters to substitute histomorphometric examination has
remained without any result. However, there are certain laboratory
parameters successfully applied for controlling the current therapy
approaches to renal osteodystrophy. These therapies form another
main focus of the dissertation. Administration of different vitamin
D-metabolites in order to balance a lack of vitamin D is one of the
principal components of treating the high turnover bone disease.
Hypercalcaemia remains the most serious side effect of these
compounds which can lead possibly to metastatic calcifications and
also to the low turnover bone disease. Vitamin D must only be
prescribed very carefully and well dosed, particularly if the low
turnover bone disease was caused by therapy of the secondary
hyperparathyroidism with vitamin D-metabolites. In this point, the
thesis also presents innovative therapy approaches, such as the
application of solanum glaucophyllum as natural source for active
vitamin D. In order to reduce a high phosphate level, which is
another problem of renal osteodystrophy, phosphatebinders are to be
applied. In summery, considerable deficits in therapy even exist
today. Bone defects caused by renal osteodystrophy can only be
remedied very slowly and most of the time therapy approaches lead
to complications. Therefore, early diagnosis and treatment of renal
osteodystrophy are of vital importance.