
parathyroid function in chronic renal failure.  a statistical survey
of the plasma biochemistry in azotaemic renal osteodystrophy.
   a collection has been made of 134 personal and
published cases of azotemic osteodystrophy in which
adequate information was available concerning the
pathological state of the bones.  measurements were
available of the plasma calcium, plasma phosphate, and
blood-urea-nitrogen in all cases, and of plasma bicarbonate
and plasma proteins in a representative sample.
the plasma levels of calcium and phosphate in the whole
series of 134 cases were not related reciprocally but
were correlated directly.  these data were further analyzed
by allocating each case to either of 2 sub-groups,
according to the type of pathological lesions present in
the bones.  in one group there was evidence of defective
mineralization of skeletal tissues, in the form of either
rickets or osteomalacia, and the plasma-calcium was
found to be statistically sub-normal.  in the other group
there was no primary defect of mineralization but the
lesions of generalized osteitis fibrosa were present and
the plasma calcium was statistically normal.  there was
no significant correlation between the plasma levels of
calcium and phosphate in either sub-group; and the plasma
phosphate was significantly higher in the group with
the higher plasma calcium levels.  the data indicate that
in patients with renal osteodystrophy, contrary to general
belief, the plasma calcium varies independently of the
plasma phosphate.  since these results imply differences
in parathyroid function among patients with azotemic
osteodystrophy, a survey has also been made of
the recorded parathyroid weights in chronic renal failure.
generalized osteitis fibrosa and the accompanying normal
levels of plasma calcium are associated with greater
parathyroid hypertrophy than is found in most cases
of chronic renal failure or cases with defective mineralization.
the various data are interpreted in relation
to the known metabolic disturbances and natural history
of azotemic osteodystrophy.  by analogy with states of
simple vitamin d deficiency, it is suggested that hypocalcemia
and relative unresponsiveness to the calcemic
action of parathyroid hormone are related to an acquired
resistance to vitamin d.  the group of cases with statistically
normal plasma-calcium prove that the parathyroid
glands can function effectively in some patients
with chronic renal failure, irrespective of the level of
the plasma phosphate.  the size of the glands and the
effects of sub-total parathyroidectomy in patients of this
group suggest that the normal plasma calcium results
from an increased production of parathyroid hormone.
the more advanced renal failure in the normocalcemic,
as compared with the hypocalcemic, cases could mean
that the development of an effective degree of secondary
hyperparathyroidism is a function of the duration of the
renal disease.  it seems likely that when the parathyroid
response is sufficient to overcome the effects of the vitamin
d resistance it also entails the development of generalized
osteitis fibrosa, healing of the defect of mineralization
and increased liability to metastatic calcification.
