Abstract
Shockwave lithotripsy (SWL) induces acute kidney injury (AKI) that extends from the papilla to the outer cortex by causing ischemia and the production of nephrotoxic agents. Direct ischemic damage and the generation of free radicals cause injury to the proximal tubular cells. Kidney injury molecule-1 (KIM-1) is a transmembrane glycoprotein that is upregulated in proximal tubular cells after ischemic or nephrotoxic injury and is not expressed in healthy kidneys. We evaluated the extent of free radical production in response to SWL by measuring urinary total antioxidant capacity (TAC) and total oxidant status (TOS). Furthermore, we investigated the severity of SWL-induced kidney injury by measuring KIM-1 expression levels. The study population comprised 30 patients who were carefully selected and 30 age and sex matched control subjects. All patients received the same SWL procedure. Midstream urine samples were collected from patients before SWL and at 120 minutes after SWL. Urine KIM-1 levels were measured by enzyme-linked immunosorbent assay, and TAC and TOS were measured via spectrophotometry. Mean levels of TAC (2.88±0.56 mmolTxEq/L),TOS (8.27±1.57 μmolH2O2Eq/L), and KIM-1 (0.55±0.08 ng/mL) before SWL were not significantly different from mean TAC, TOS, and KIM-1 levels measured from the control group at 2.81±0.42 mmolTxEq/L, 10.73±1.4 μmolH2O2Eq/L, and 0.51±0.07 ng/mL, respectively. Two hours after SWL, mean urine TAC levels (2.81±0.85 mmolTxEq/L, P=0.02) were decreased and mean KIM-1 expression (0.85±0.11 ng/mL, P=0.01) was significantly increased, but there was no significant difference in mean TOS levels (11.24±1.9 μmolH2O2Eq/L, P=0.627) compared with the control group. The increased burden of free radical oxidants in the setting of decreasing antioxidant capacity may be one of the initial indicators of AKI after SWL. Moreover, KIM-1 demonstrates great potential as an early and noninvasive biomarker of SWL-induced kidney injury.
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