الفهرس 
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Abstract
Summary
Renal failure disrupts systemic calcium and phosphate homeostasis
and affects the bone, gut, and parathyroid glands. This occurs because of
decreased renal excretion of phosphate and diminished renal hydroxylation
of 25-hydroxyvitamin D to calcitriol (1,25-dihydroxyvitamin D). Circulating
calcitriol levels begin to fall when the glomerular filtration rate is less than
40 mL/min (occasionally even less than 80 mL/min) and are typically
markedly reduced in subjects with end-stage renal failure (Levin et al.,
2007).
The calcium-sensing receptor (CaSR), which is highly expressed in
the parathyroid glands, permits variations in the serum calcium
concentration to be sensed by the parathyroid gland, leading to the desired
changes in PTH secretion. The fall in serum calcium concentration with
renal failure, as sensed by the CaSR, is a potent stimulus to the release of
PTH. Extracellular calcium acting through the CaSR plays the predominant
role in regulating parathyroid function, resulting in this receptor being the
major therapeutic target for suppressing parathyroid gland function. This is
best shown in mouse and human genetic studies in which extracellular
calcium acting through CaSR was the major regulator of PTH transcription,
secretion, and parathyroid gland hyperplasia (Panda et al., 2004).
Since vitamin D stimulates intestinal phosphate absorption, the
decrease in active vitamin D production may be viewed as an adaptive
response to minimize hyperphosphatemia in the setting of reduced renal
phosphate excretion in patients with kidney failure (Mazess and
Elangovan., 2003).
Summary
108
The absence of vitamin D also decreases calcium and phosphorus
absorption in the gastrointestinal tract. The net effect of low vitamin D levels
is to directly increase PTH production due to removal of the normal
suppressive effect of calcitriol on the parathyroid glands, and indirectly
increase secretion through the gastrointestinal mediated hypocalcemic
stimulus.
Hyperphosphatemia is also an important factor underlying
hyperparathyroidism. Although the identity of the extracellular phosphate
sensor is unknown and may not exist, a novel phosphaturic factor, FGF23,
may be regulated by phosphate and vitamin D (Wetmore et al., 2010).
Hyperphosphatemia also lowers the levels of ionized calcium and
interferes with the production of 1,25-dihydroxyvitamin D, thereby resulting
in increased PTH levels (Saito et al.,2005).
The relationship between FGF23 and PTH is not completely
understood. As an example, although FGF23 suppresses PTH via the
activation of FGFR/Klotho complexes, elevated FGF23 concentrations do
not prevent the development of hyperparathyroidism in patients with CKD.
Rather FGF23 and PTH concentrations are directly correlated. Down
regulation of FGFR and Klotho expression may cause parathyroid gland
resistance to the suppressive effects of FGF23 (Martin et al., 2012).
In patients with ESRD, secondary hyperparathyroidism (sHPT) is a
common problem requiring surgical parathyroidectomy (PTX) if medical
treatment with active vitamin D and calcimimetics fails.
Summary
109
There are 3 approaches of surgery: Total parathyroidectomy (tPTX)
with autoimplantation, total parathyroidectomy without autoimplantation
and subtotal parathyroidectomy.
The aim of this work was to review the efficacy and the outcome of
the first 2 approaches.
This study included 40 ESRD patients on maintenance hemodialysis
thrice weekly with secondary hyperparathyroidism, underwent PTX in
Ahmad Maher teaching hospital, after failure of medical treatment
(alfacalcidol and cinacalcet) for at least 6 months. 20 patients of them
underwent total parathyroidectomy with autoimplantation (group I) and the
other 20 patients underwent total parathyroidectomy without
autoimplantation (group II).
All patients had pre-operative assessment including laboratory
investigations : Hb, s.Ca, s. phosphorus, ALP and iPTH which were done
postoperatively till discharge of the patients.
Most of our patients were suffering of hypocalcemia postoperatively
which lead to long hospital stay (ranged 5-60 days) during which they
received Ca supplementation and active vitamin D in addition to frequent
monitoring of s, Ca level.
Total parathyroidectomy with autotransplantation, and total
parathyroidectomy produced similar results when considering the regression
of osteodystrophy symptoms e.g bone aches.
As one could anticipate, group II showed increased the incidence of
hypoparathyroidism (12 patients, 60% versus 1 patient, 5%) while group I