Although controversial, chronic uric acid nephropathy is a tubulointerstiti
al disease capable of developing renal function loss. On the other hand, po
tassium citrate (KCi) administration has demonstrated to be effective in ca
lcium as well as uric acid nephrolithiasis therapy. Therefore, the aim of t
he present study was to evaluate the possible benefit of KCi treatment in t
he prevention or amelioration of renal interstitial damage in uric acid nep
hropathy. Two-month-old male Sprague-Dawley rats were divided into 3 groups
: GI hyperuricemic (HU), G2 hyperuricemic + KCi (HU+KCi), and G3 KCi. G1 an
d G2 were fed on oxonic acid (inhibitor of rat liver uricase), and a uric a
cid supplement, during 4 weeks. G2 and G3 were given 2% KCi in drinking wat
er, and G I regular tap water and standard rat chow. At the end of the stud
y, renal tissue was processed for light and electron microscopy and immunos
taining by ct-smooth muscle actin (SMA). Tubulointerstitial lesions and the
amount of a-SMA immunostaining in renal tissue were evaluated by histomorp
hometric quantitation. Rats belonging to the hyperuricemic groups treated w
ith KCi (G2) showed fewer tubulointerstitial lesions as follows: % tubular
atrophy: 1.7 +/- 0.3 versus 7.2 +/- 1.2, p < 0.05. inflammatory cells infil
trate (number of cells/area): 0.6 +/- 0.1 versus 2.4 +/- 0.2, p < 0.01; % i
nterstitial fibrosis (cortex): 3.3 +/- 0.3 versus 9.3 +/- 0.5, p < 0.05, %
interstitial fibrosis (medulla): 5.2 +/- 0.3 versus 21.9 +/- 1.2, p < 0.01,
lower albuminuria (32.8 +/- 11.2 mg/day versus 128.5 +/- 10.4 p < 0.01), h
igher creatinine clearance (1.36 +/- 0.02 ml/min versus 0.74 +/- 0.0 1, p <
0.0 1) and less percentage of (x-SMA in renal tissue (1.8 +/- 0.1 versus 1
0.5 +/- 1.4 p < 0.05). when compared with the hyperuricemic group not treat
ed with KCi (G I). These data suggest that KCi administration could provide
a substantial benefit in the chronic hyperuricemic states treatment with r
egard to tubulointerstitial lesion and progressive renal damage.