M. Nakamura et al., ORAL CALCIUM-CARBONATE ADMINISTRATION AMELIORATES THE PROGRESSION OF RENAL-FAILURE IN RATS WITH HYPERTENSION, American journal of kidney diseases, 25(6), 1995, pp. 910-917
Oral calcium supplementation is reported to have phosphate-binding and
antihypertensive effects, Since both phosphate binders and antihypert
ensive agents are reported to attenuate renal injury, we studied the e
ffect of oral calcium carbonate (CaCO3) administration on the course o
f renal deterioration using doxorubicin-induced renal failure in rats
treated with deoxycorticosterone acetate and salt for 10 weeks. Rats w
ere divided into four groups: the CaCO3 (6.0 g/kg/d) group (n = 12), t
he aluminum hydroxide (Al(OH)(3); 6.0 g/kg/d) group (n = 11, as a phos
phate-binder control), the hydralazine (10 mg/kg/d) group (n = 11, as
an antihypertensive control), and the control group (n = 12). All agen
ts were given as a mixed chow diet, Blood pressure and urinary protein
excretion progressively increased in the control rats. CaCO3 and hydr
alazine lowered blood pressure, but Al(OH)(3) did not (185 +/- 4 mm Hg
, control; 160 +/- 5 mm Hg, CaCO3; 171 +/- 8 mm Hg, Al(OH)(3); 156 +/-
5 mm Hg, hydralazine at week 10). Proteinuria was reduced in the rats
treated with CaCO3 and Al(OH)(3) compared with those without the trea
tment (986 +/- 86 mg/d, control; 551 +/- 54 mg/d, CaCO3; 527 +/- 31 mg
/d, Al(OH)(3); and 955 +/- 68 mg/d, hydralazine at week 10). Serum pho
sphate concentration and calcium phosphate products also were signific
antly lower in both the CaCO3 and Al(OH)(3) groups than in the control
group. At week 10, increased serum urea nitrogen, impaired renal func
tion, and glomerular sclerosis present in the control group were signi
ficantly attenuated in both in the CaCO3 and Al(OH)(3) groups. No sign
ificant attenuation was observed in the hydralazine group in spite of
lower blood pressure. We conclude that oral CaCO3 administration atten
uates the progression of renal failure associated with hypertension. T
his effect appears to be primarily related to its effects on divalent
mineral metabolism and not on blood pressure. (C) 1935 by the National
Kidney Foundation, Inc.