URINE CALCIUM EXCRETION, NEPHROGENOUS CYCLIC-ADENOSINE MONOPHOSPHATE AND SERUM PARATHYROID-HORMONE LEVELS IN PATIENTS WITH ESSENTIAL-HYPERTENSION

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3044618 5 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
URINE CALCIUM EXCRETION, NEPHROGENOUS CYCLIC-ADENOSINE MONOPHOSPHATE AND
SERUM PARATHYROID-HORMONE LEVELS IN PATIENTS WITH ESSENTIAL-HYPERTENSION
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
To evaluate the role of calcium and the parathyroid gland in the
pathophysiology of essential hypertension, creatinine clearance, urinary
excretion of sodium, calcium and nephrogenous cyclic adenosine
monophosphate (NcAMP) and serum parathyroid hormone (PTH) levels were
measured in 25 newly diagnosed essentially hypertensive patients before
institution of any treatment and in 25 age- and sex-matched normal
volunteers. While no significant differences in creatinine clearance,
serum total calcium levels of 24-hour sodium excretion existed between
the two groups, hypertensives had a higher mean (+/- SD) 24-hour calcium
excretion rate (199.0 +/- 44.7 vs. 152.8 +/- 33.6 mg, p < 0.001), a
higher mean NcAMP excretion rate (2.54 +/- 0.8 vs. 1.87 +/- 0.5 nmol/100
ml glomerular filtrate, p < 0.001) and a higher mean serum PTH
concentration (1.87 +/- 0.6 vs. 1.53 +/- 0.4 ng/ml, p < 0.001) than the
normotensives. A significant positive correlation existed between
calcium and sodium excretion in both hypertensives (r = 0.66, p <
0.001)) and normotensives (r = 0.67, p < 0.001), but given the same
levels of creatinine clearance and sodium excretion, hypertensives
excreted more calcium than normotensives (p < 0.001)). In both
hypertensives and normotensives, serum PTH levels were positively
correlated with NcAMP excretion (r = 0.42, p < 0.05, and r = 0.41, p <
0.05, respectively) and the ratio of urinary sodium to urinary calcium
excretion (r = 0.59, p < 0.001, and r = 0.75, p < 0.001), respectively).
The above results suggest that in essential hypertension, increased
activity of parathyroid glands may occur as a consequence of increased
urinary calcium losses which are presumably due to an intrinsic defect
in renal calcium handling.
Έτος δημοσίευσης:
1991
Συγγραφείς:
PAPAGALANIS, ND
SKOPELITIS, P
KOURTI, A
KOSTOGIANNI, G and
KARABATSOS, A
GENNADIOU, M
THOMAS, S
SAMARTZIS, M and
MOUNTOKALAKIS, T
Περιοδικό:
Nephron Extra
Εκδότης:
Karger
Τόμος:
59
Αριθμός / τεύχος:
2
Σελίδες:
226-231
Λέξεις-κλειδιά:
HYPERTENSION; PARATHYROID GLANDS; CALCIUM; PARATHYROID HORMONE
Επίσημο URL (Εκδότης):
DOI:
10.1159/000186555
Το ψηφιακό υλικό του τεκμηρίου δεν είναι διαθέσιμο.