Acutely accumulated systemic mediators following renal failure in the absence of kidneys vary from those due to combined renal failure with ischemic-reperfused kidneys and consequently they induce ALI with distinct characteristics.

Biochemical and histological assays are currently used for the diagnosis and characterization of kidney injury. The purpose of this study was to compare technetium-99m-labeled dimercaptosuccinic acid (Tc-DMSA) renal scintigraphy, as a non-invasive method, with common biochemical and histopathological methods in two animal models of acute kidney injury. Nephrotoxicity was induced either by gentamicin (100 mg/kg/day for one week) or unilateral ureteral ligation (UUO). Renal scintigraphy was performed 1 h after intravenous injection of 99mTc-DMSA (3 mCi). Furthermore, plasma levels of blood urea nitrogen (BUN), creatinine, sodium, and potassium were determined using an autoanalyzer. At the end of experiments, kidneys were excised for the measurement of activity uptake (mCi/gr) using a dose calibrator as well as histopathological examinations with hematoxylin and eosin (H&E) staining. There was a significant decrease in 99mTc-DMSA uptake in both gentamicin (P value = 0.049) and UUO (P value = 0.034) groups, and it was more significant in the former. The levels of BUN and creatinine increased in both gentamicin and UUO groups, while the levels of sodium and potassium remained unchanged. Furthermore, a strong correlation was found between DMSA uptake and histopathological findings. Scintigraphy with 99mTc-DMSA is capable of detection of kidney injury in both gentamicin and UUO groups. Moreover, a significant correlation was found between scintigraphy parameters and histopathological findings. This suggests 99mTc-DMSA as a non-invasive method for the evaluation of kidney injury induced by drugs or anatomical disorders.

Keyword:Acute kidney injury, inducible nitric oxide synthase, reactive oxygen species, unilateral nephrectomy, unilateral renal ischemia https://mc06.manuscriptcentral.com/cjpp-pubs AbstractAcute kidney injury is usually associated with distant organ dysfunction. The roles of inducible nitric oxide synthase (iNOS) and reactive oxygen species (ROS) in this phenomenon were investigated following 2-h unilateral renal ischemia and 24-h reperfusion. There were three groups of rats subjected to either unilateral ischemia/reperfusion (UIR group), unilateral nephrectomy (UNX group), or shamoperation. Two further groups were given α-tocopherol and aminoguanidine with UIR (treated-UIR group) and UNX (treated-UNX group). Plasma nitrite/nitrate and malondialdehyde were elevated only in the UIR group. Creatinine clearance and blood flow increased in non-ischemic kidney of the UIR, but not to the same extent as remnant kidney of the UNX group, while they had equal compensatory rises in absolute Na + -and K + -excretion and urine flow. Non-ischemic kidney of the treated-UIR group, but not remnant kidney of the treated-UNX group, showed more elevation in blood flow, whereas both kidneys had reductions in absolute Na + -excretion and urine flow.Respiratory functional variable were not different between all groups. Therefore, 2-h unilateral renal ischemia and 24-h reperfusion did not affect lung but had distant effects on contralateral kidney partly mediated by ROS and NO-derived from iNOS to dampen compensatory increases in renal hemodynamics and to decrease tubular reabsorption.Keywords: Acute kidney injury, acute lung injury, alpha-tocopherol, aminoguanidine, inducible nitric oxide synthase, ischemia/reperfusion, reactive oxygen species, unilateral nephrectomy, unilateral renal ischemia.

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Background. Polycystic ovary syndrome (PCOS) is the most common reproductive disorder in premenopausal women. This syndrome is also associated with many metabolic and cardiovascular complications. These complications are major risk factors for renal injury and kidney disease. Therefore, this study aimed to investigate the types of functional and structural kidney injuries in a hyperandrogenic female rat model. Methods. Female Sprague-Dawley rats were randomly divided into three groups (n=10 each): control, sham, and dehydroepiandrosterone (DHEA). Plasma total testosterone and kidney functional indices were measured using enzyme-linked immunosorbent assay (ELISA) and colorimetric techniques. Ovarian and renal histological changes were also evaluated qualitatively and quantitatively by Hematoxylin-Eosin (H&E) staining. Results. Plasma total testosterone in the DHEA group increased about 9-fold compared to the control and sham groups. There was also a significant increase in Cr, BUN, and absolute excretion of sodium ion. Insignificant increases in glomerular filtration rate (GFR), urine flow rate (V0), and absolute excretion of potassium ion were observed in DHEA group compared to other groups. However, significant damages were observed in the glomerular and tubular parts of the kidneys and the follicular parts of the ovaries in DHEA-receiving rats. Conclusion. Hyperandrogenemia is likely to cause systemic abnormalities through a variety of mechanisms, followed by obvious destruction of kidney and ovarian tissues. Accordingly, DHEA administration provides a useful animal model for studying the mechanism of PCOS-mediated renal injury. Practical Implications. The present study Findings can be helpful in identifying the mechanism of PCOS-induced renal injury, especially in younger women.