AJP - Renal Physiology, Vol 251, Issue 3 408-F416, Copyright © 1986 by American Physiological Society
Protection by thyroxine in nephrotoxic acute renal failure
R. E. Cronin, D. M. Brown and R. Simonsen
Thyroxine (T4) protects against ischemic and nephrotoxic experimental acute
renal failure (ARF). This study examined functional, biochemical, and
morphological markers of uranyl nitrate (UN)-induced renal injury in the
rat to determine the cellular site at which T4 exerts its protective
effect. In experimental group UNT4, 1-thyroxine (10 micrograms/100 g body
wt) was given for 10 days prior to and for 4 days following a single
subcutaneous injection of UN (0.5 mg/kg body wt). Group UN received only
UN, and group CT4 received only T4 for 14 days. Five days after UN
administration, plasma creatinine rose from base line in group UNT4 (0.52
+/- 0.30 to 0.84 +/- 0.08 mg/dl, P less than 0.025) and group UN (0.52 +/-
0.03 to 1.64 +/- 0.13 mg/dl, P less than 0.001) but not in group CT4 (0.47
+/- 0.02 to 0.48 +/- 0.04 mg/dl, NS). However, plasma creatinine in group
UNT4 was significantly lower than group UN (0.84 +/- 0.08 vs. 1.64 +/- 0.13
mg/dl, P less than 0.001). T4 administration stimulated the basolateral
membrane-bound enzyme Na-K-ATPase in the renal cortex homogenate in group
UNT4 (13.9 +/- 0.5 micron X mg protein-1 X h-1, P less than 0.005) and
group CT4 (16.3 +/- 0.6 micron X mg protein-1 X h-1, P less than 0.001)
when compared with controls (11.7 +/- 0.5 micron X mg protein-1 X h-1).
Na-K-ATPase activity fell in group UN to 10.0 +/- 0.6 micron X mg protein-1
X h-1 (P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)
