In this study, we intend to establish a connection between star fruit and a
cute oxalate nephropathy and also investigate predisposing factors for its
development. Male Sprague-Dawley rats of 180 to 200 g were assigned to four
groups; namely, control, experimental, fasting, and water-deprivation grou
ps. The former two groups were subjected to both fasting and water deprivat
ion, whereas the latter two groups were subjected to either fasting or wate
r deprivation, respectively. Except for tap water for controls, the remaini
ng groups were administered 4 mL/100 g of body weight of sour star fruit ju
ice with an oxalate concentration of 2.46 g/dL. After these procedures, ser
ial measurement of serum creatinine levels and kidney pathological examinat
ion were performed. Peak serum creatinine levels in the control, experiment
al, fasting, and water-deprivation groups were 0.50 +/- 0.04, 1.46 +/- 0.26
, 0.68 +/- 0.20, and 0.52 +/- 0.08 mg/dL, respectively. The experimental gr
oup had a greater peak serum creatinine level (P < 0.05). Mean serum creati
nine levels of the experimental group days 0, 1, 2, 3, 4, and 5 were 0.43 /- 0.03, 1.11 +/- 0.18, 1.31 +/- 0.27,1.16 +/- 0.28, 0.8 +/- 0.26, and 0.82
+/- 0.28 mg/dL, respectively. Mean serum creatinine levels days 1 to 3 wer
e greater than that day 0 (P < 0.05). Pearson's correlation analysis of pea
k serum creatinine level and kidney weight for the experimental group showe
d a significant correlation (R = 0.75; P < 0.05; n = 9). In addition to typ
ical changes of oxalate nephropathy, kidney pathological examination showed
many refractile oxalate crystals with all rainbow colors under polarized l
ight microscopy in the experimental group. In conclusion, sour star fruit w
ith abundant oxalate contents could cause acute oxalate nephropathy in rats
under the conditions of fasting and water deprivation. (C) 2001 by the Nat
ional Kidney Foundation, Inc.