Abstract
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They observed that KIM-1 and NAG levels significantly increased post-SWL and returned to baseline within 2 weeks after SWL. They proposed that poor renal function was significantly associated with increased biomarker activity both in baseline and post-SWL measurements and suggested that those two urinary biomarkers could be used in identifying patients with higher risk of renal injury. It was not the case, however, for patients who were treated with URS. No significant change in urinary KIM-1 and NAG concentrations were noticed before and after URS operation.
Accordingly, we were interested in the changes in renal Doppler ultrasonographic parameters in patients treated with rigid URS. 1 Our hypothesis while planning this prospective study was dependent on the idea that, because of the irrigation fluid used, the irrigation pressures generated within the collecting system could be elevated, and could cause pyelovenous and pyelolymphatic backflow. This backflow might create a pressure on intrarenal vasculature and might also contribute to the increase in renal vascular resistance. The amount of irrigation pressures transmitted to the renal pelvis, collecting ducts, and subsequently to the parenchyma determined the degree of the vasoconstrictive response that would eventually lead to an increase in resistivity index (RI) values.
Therefore, we suggested that RI and delta RI values of the operated kidneys would be significantly higher than the values for nonoperated kidneys. As we hypothesized, we observed significant P values when RI was considered in operated kidneys. Delta RI was regarded as the mean difference between the postoperative and preoperative RI values in the same kidney. In addition, we noticed that delta RI was found to be correlated with the parameters “operative time” and “irrigation fluid volume.” In our study, renal Doppler measurements were obtained 24 hours before URS and 24 hours after URS, so acute changes were investigated.
Similarly, we also investigated the effects of SWL on renal blood flow in patients who were treated for renal/ureteral stones. 2 Color Doppler ultrasonography and pulsed wave spectral analysis were performed before, 1 hour, and 7 days after SWL to both ipsilateral and contralateral kidneys to measure RI. In this trial, we observed that RI showed significant increase from pre-SWL values in both ipsilateral and contralateral kidneys. Seven days after SWL, RI in the contralateral kidney returned to pre-SWL values, but RI in the ipsilateral kidney did not return to pre-SWL values, although a decrease was noticed.
In the study by Fahmy and colleagues, KIM-1 and NAG levels returned to baseline within 2 weeks after SWL, suggesting that SWL might cause temporary renal hemodynamic changes that would eventually lead to an acute increase in tissue injury biomarkers such as KIM-1 and NAG. During SWL, the vasoconstrictive response detected via the measurement of RI may cause transient secretion of various urinary and serum biomarkers such as neutrophil gelatinase-associated lipocalin, KIM-1, cystatin C, interleukin-6, interleukin-8, interleukin-18, NAG, glutathione transferases, and liver fatty acid binding protein. 3 Of course, the secretion of those markers does not depend solely on renal hemodynamic changes, but this vasoconstrictive response should at least be a part of the tubular secretion process of those certain biomarkers.
As Dr. Fahmy and associates already suggested in the article, these urinary markers may be used in identifying patients at higher risk of tissue injury, but in this perspective, RI should also be regarded as a sensitive parameter for monitoring vascular and tubulointerstitial diseases of the kidneys. Noninvasive Doppler measurements may give the clinician an idea about the degree of acute renal injury, especially after urologic interventions such as SWL. Prospective, randomized trials with large series mainly focusing on the correlation between Doppler parameters and serum/urinary biomarker levels in acute renal injury may give more conclusive data.