BACKGROUND: Serum levels of low molecular weight (LMW) proteins, such as cystatin C and beta-2-microglobulin (MG), are used as GFR markers. Ureteral obstruction is a cause of acute kidney injury (AKI). However, it is unclear whether serum concentrations of LMW proteins are increased in postrenal AKI like in intrinsic AKI. To evaluate this question, the responses of serum levels of cystatin C and beta-2-MG were investigated in rats with bilateral ureteral obstruction (BUO) and bilateral nephrectomy (BNX). METHODS: Sixteen SD rats were divided into sham (sham operated), BUO and BNX groups. Serum levels of creatinine, BUN, cystatin C, beta 2-MG and creatine phosphokinase (CPK) were measured after 24 h of the treatments. Cystatin C and beta 2-MG were measured using rat ELISA kits. RESULTS: In the sham group, the mean +/- SD of creatinine, BUN, cystatin C and beta-2-MG were 0.19 +/- 0.01 mg/dl, 22.6 +/- 1.9 mg/dl, 1.27 +/- 0.18 mg/l and 3.57 +/- 0.42 mg/l, respectively. Following BNX, the values significantly rose to 4.79 +/- 0.17 mg/dl, 116.9 +/- 2.6 mg/dl, 2.59 +/- 0.18 mg/l and 9.03 +/- 0.52 mg/l compared with sham, respectively. Following BUO, they were 3.99 +/- 0.25 mg/dl, 130.3 +/- 12.9 mg/dl, 1.94 +/- 0.35 mg/l and 4.78 +/- 0.24 mg/l, respectively. Increasing amounts of creatinine and BUN in BUO were similar to those in BNX. On the other hand, cystatin C and beta-2 MG in BUO were much lower compared with BNX (P < 0.01 and <0.001, respectively). Fold increases of cystatin C and beta-2-MG in BUO were only 51% and 22% of those in BNX, respectively. There was no significant difference in CPK levels between the BUO and BNX groups. CONCLUSION: We showed a discrepancy between serum levels of LMW proteins in AKI model rats with BUO and BNX. The reasons for the discrepancy are discussed.
BACKGROUND: Serum levels of low molecular weight (LMW) proteins, such as cystatin C and beta-2-microglobulin (MG), are used as GFR markers. Ureteral obstruction is a cause of acute kidney injury (AKI). However, it is unclear whether serum concentrations of LMW proteins are increased in postrenal AKI like in intrinsic AKI. To evaluate this question, the responses of serum levels of cystatin C and beta-2-MG were investigated in rats with bilateral ureteral obstruction (BUO) and bilateral nephrectomy (BNX). METHODS: Sixteen SD rats were divided into sham (sham operated), BUO and BNX groups. Serum levels of creatinine, BUN, cystatin C, beta 2-MG and creatine phosphokinase (CPK) were measured after 24 h of the treatments. Cystatin C and beta 2-MG were measured using rat ELISA kits. RESULTS: In the sham group, the mean +/- SD of creatinine, BUN, cystatin C and beta-2-MG were 0.19 +/- 0.01 mg/dl, 22.6 +/- 1.9 mg/dl, 1.27 +/- 0.18 mg/l and 3.57 +/- 0.42 mg/l, respectively. Following BNX, the values significantly rose to 4.79 +/- 0.17 mg/dl, 116.9 +/- 2.6 mg/dl, 2.59 +/- 0.18 mg/l and 9.03 +/- 0.52 mg/l compared with sham, respectively. Following BUO, they were 3.99 +/- 0.25 mg/dl, 130.3 +/- 12.9 mg/dl, 1.94 +/- 0.35 mg/l and 4.78 +/- 0.24 mg/l, respectively. Increasing amounts of creatinine and BUN in BUO were similar to those in BNX. On the other hand, cystatin C and beta-2 MG in BUO were much lower compared with BNX (P < 0.01 and <0.001, respectively). Fold increases of cystatin C and beta-2-MG in BUO were only 51% and 22% of those in BNX, respectively. There was no significant difference in CPK levels between the BUO and BNX groups. CONCLUSION: We showed a discrepancy between serum levels of LMW proteins in AKI model rats with BUO and BNX. The reasons for the discrepancy are discussed.