scholarly journals 4. Urinary NAG, ^|^beta;2 Microglobulin - Renal Tubular Injury, AKI (Acute Kidney Injury) and Biomarker

2008 ◽  
Vol 97 (5) ◽  
pp. 971-978 ◽  
Author(s):  
Yukio Yuzawa ◽  
Isao Ito
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Tubular Injury ◽  
Beta 2 ◽  
Renal Tubular ◽  
Beta 2 Microglobulin

Serial Quantification of Urinary Protein Biomarkers to Predict Drug-induced Acute Kidney Injury

2019 ◽  
Vol 20 (8) ◽  
pp. 656-664 ◽  
Author(s):  
Yi Da ◽  
K. Akalya ◽  
Tanusya Murali ◽  
Anantharaman Vathsala ◽  
Chuen-Seng Tan ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cystatin C ◽  
Calcineurin Inhibitors ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Protein Biomarkers ◽  
Drug Induced ◽  
Beta 2 ◽  
Beta 2 Microglobulin

Background: : Drug-induced Acute Kidney Injury (AKI) develops in 10-15% of patients who receive nephrotoxic medications. Urinary biomarkers of renal tubular dysfunction may detect nephrotoxicity early and predict AKI. Methods:: We prospectively studied patients who received aminoglycosides, vancomycin, amphotericin, or calcineurin inhibitors, and collected their serial urine while on therapy. Patients who developed drug-induced AKI (fulfilling KDIGO criteria) were matched with non-AKI controls in a 1:2 ratio. Their urine samples were batch-analyzed at time-intervals leading up to AKI onset; the latter benchmarked against the final day of nephrotoxic therapy in non- AKI controls. Biomarkers examined include clusterin, beta-2-microglobulin, KIM1, MCP1, cystatin-C, trefoil-factor- 3, NGAL, interleukin-18, GST-Pi, calbindin, and osteopontin; biomarkers were normalized with corresponding urine creatinine. Results:: Nine of 84 (11%) patients developed drug-induced AKI. Biomarkers from 7 AKI cases with pre-AKI samples were compared with those from 14 non-AKI controls. Corresponding mean ages were 55(±17) and 52(±16) years; baseline eGFR were 99(±21) and 101(±24) mL/min/1.73m2 (all p=NS). Most biomarker levels peaked before the onset of AKI. Median levels of 5 biomarkers were significantly higher in AKI cases than controls at 1-3 days before AKI onset (all µg/mmol): clusterin [58(8-411) versus 7(3-17)], beta-2-microglobulin [1632(913-3823) versus 253(61-791)], KIM1 [0.16(0.13-0.76) versus 0.07(0.05-0.15)], MCP1 [0.40(0.16-1.90) versus 0.07(0.04-0.17)], and cystatin-C [33(27-2990) versus 11(7-19)], all p<0.05; their AUROC for AKI prediction were >0.80 (confidence intervals >0.50), with average accuracy highest for clusterin (86%), followed by beta-2-microglobulin, cystatin-C, MCP1, and KIM1 (57%) after cross-validation. Conclusion: : Serial surveillance of these biomarkers could improve the lead time for nephrotoxicity detection by days.

scholarly journals Renal tubular injury exacerbated by vasohibin-1 deficiency in a murine cisplatin-induced acute kidney injury model

2019 ◽  
Vol 317 (2) ◽  
pp. F264-F274 ◽  
Author(s):  
Satoshi Tanimura ◽  
Katsuyuki Tanabe ◽  
Hiromasa Miyake ◽  
Kana Masuda ◽  
Keigo Tsushida ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Endothelial Cells ◽  
Kidney Injury ◽  
Protective Effects ◽  
Tubular Injury ◽  
Injury Model ◽  
Peritubular Capillaries ◽  
Renal Tubular ◽  
And Function ◽  
Hospital Acquired

Acute kidney injury (AKI) is frequently encountered in clinical practice, particularly secondarily to cardiovascular surgery and administration of nephrotoxic agents, and is increasingly recognized for initiating a transition to chronic kidney disease. Clarifying the pathogenesis of AKI could facilitate the development of novel preventive strategies, because the occurrence of hospital-acquired AKI is often anticipated. Vasohibin-1 (VASH1) was initially identified as an antiangiogenic factor derived from endothelial cells. VASH1 expression in endothelial cells has subsequently been reported to enhance cellular stress tolerance. Considering the importance of maintaining peritubular capillaries in preventing the progression of AKI, the present study aimed to examine whether VASH1 deletion is involved in the pathogenesis of cisplatin-induced AKI. For this, we injected male C57BL/6J wild-type (WT) and VASH1 heterozygous knockout (VASH1+/−) mice intraperitoneally with either 20 mg/kg cisplatin or vehicle solution. Seventy-two hours after cisplatin injection, increased serum creatinine concentrations and renal tubular injury accompanied by apoptosis and oxidative stress were more prominent in VASH1+/− mice than in WT mice. Cisplatin-induced peritubular capillary loss was also accelerated by VASH1 deficiency. Moreover, the increased expression of ICAM-1 in the peritubular capillaries of cisplatin-treated VASH1+/− mice was associated with a more marked infiltration of macrophages into the kidney. Taken together, VASH1 expression could have protective effects on cisplatin-induced AKI probably by maintaining the number and function of peritubular capillaries.

scholarly journals Short-term Changes in Urine Beta 2 Microglobulin Following Recovery of Acute Kidney Injury Resulting From Snake Envenomation

2019 ◽  
Vol 4 (5) ◽  
pp. 667-673 ◽  
Author(s):  
Challa Jaswanth ◽  
P.S. Priyamvada ◽  
Bobby Zachariah ◽  
Sathish Haridasan ◽  
Sreejith Parameswaran ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Short Term ◽  
Snake Envenomation ◽  
Beta 2 ◽  
Beta 2 Microglobulin

scholarly journals Role of Urinary Beta 2 Microglobulin and Kidney Injury Molecule-1 in Predicting Kidney Function at One Year Following Acute Kidney Injury

2021 ◽  
Vol Volume 14 ◽  
pp. 225-234
Author(s):  
Dhanin Puthiyottil ◽  
PS Priyamvada ◽  
Mattewada Naveen Kumar ◽  
Anand Chellappan ◽  
Bobby Zachariah ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Function ◽  
Kidney Injury ◽  
Beta 2 ◽  
One Year ◽  
Beta 2 Microglobulin ◽  
Kidney Injury Molecule 1

scholarly journals Inhibition of Mitochondrial Complex I Aggravates Folic Acid-Induced Acute Kidney Injury

2019 ◽  
Vol 44 (5) ◽  
pp. 1002-1013 ◽  
Author(s):  
Wen Zhang ◽  
Yunwen Yang ◽  
Huiping Gao ◽  
Yue Zhang ◽  
Zhanjun Jia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Folic Acid ◽  
Mitochondrial Dysfunction ◽  
Complex I ◽  
Kidney Injury ◽  
Mitochondrial Complex I ◽  
Tubular Injury ◽  
Mitochondrial Complex ◽  
Renal Tubular

Background: Some researches revealed that mitochondrial dysfunction is associated with various kidney injury. However, the role of mitochondrial dysfunction in the pathogenesis of acute kidney injury (AKI) still needs evidence. Methods: We evaluated the effect of mitochondrial complex I inhibitor rotenone on folic acid (FA)-induced AKI in mice. Results: Strikingly, the mice pretreated with rotenone at a dose of 200 ppm in food showed exacerbated kidney injury as shown by higher levels of blood urea nitrogen and creatinine compared with FA alone group. Meanwhile, both renal tubular injury score and the expression of renal tubular injury marker neutrophil gelatinase-associated lipocalin were further elevated in rotenone-pretreated mice, suggesting the deteriorated renal tubular injury. Moreover, the decrements of mitochondrial DNA copy number and the expressions of mitochondrial Cytochrome c oxidase subunit 1, mitochondrial NADH dehydrogenase subunit 1, and mitochondria-specific superoxide dismutase (SOD2) in the kidneys of FA-treated mice were further reduced in rotenone-pretreated mice, indicating the aggravated mitochondrial damage. In parallel with the SOD2 reduction, the oxidative stress markers of malondialdehyde and HO-1 displayed greater increment in AKI mice with rotenone pretreatment in line with the deteriorated apoptotic response and inflammation. Conclusion: Our results suggested that the inhibition of mitochondrial complex I activity aggravated renal tubular injury, mitochondrial damage, oxidative stress, cell apoptosis, and inflammation in FA-induced AKI.

scholarly journals Lack of significant renal tubular injury despite acute kidney injury in acute decompensated heart failure

2012 ◽  
Vol 14 (6) ◽  
pp. 597-604 ◽  
Author(s):  
Matthias Dupont ◽  
Kevin Shrestha ◽  
Dhssraj Singh ◽  
Adiveh Awad ◽  
Cynthia Kovach ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Kidney Injury ◽  
Acute Decompensated Heart Failure ◽  
Kidney Injury ◽  
Decompensated Heart Failure ◽  
Tubular Injury ◽  
Renal Tubular

scholarly journals Effects of Exercise on Acute Kidney Injury Biomarkers and the Potential Influence of Fluid Intake

2021 ◽  
pp. 1-7
Author(s):  
Loris Allan Juett ◽  
Lewis J. James ◽  
Stephen Andrew Mears
Keyword(s):  
Acute Kidney Injury ◽  
Muscle Damage ◽  
Fluid Intake ◽  
Kidney Injury ◽  
Strenuous Exercise ◽  
Physical Work ◽  
Tubular Injury ◽  
Potential Influence ◽  
Water Ingestion ◽  
Renal Tubular

Acute kidney injury (AKI) incidence (diagnosed by changes in serum creatinine [Cr]) following prolonged endurance events has been reported to be anywhere from 4 to 85%, and hypohydration may contribute to this. Whilst an increase in serum Cr indicates impaired kidney function, this might be influenced by muscle damage. Therefore, the use of other AKI biomarkers which can detect renal tubular injury may be more appropriate. The long-term consequences of AKI are not well understood, but there are some potential concerns of an increased subsequent risk of chronic kidney disease (CKD). Therefore, this brief review explores the effects of exercise training/competition on novel AKI biomarkers and the potential influence of fluid intake. The increase in novel AKI biomarkers following prolonged endurance events suggests renal tubular injury. This is likely due to the long duration and relatively high exercise intensity, producing increased sympathetic tone, body temperature, hypohydration, and muscle damage. Whilst muscle damage appears to be an important factor in the pathophysiology of exercise-associated AKI, it may require coexisting hypohydration. Fluid intake seems to play a role in exercise-associated AKI, as maintaining euhydration with water ingestion during simulated physical work in the heat appears to attenuate rises in AKI biomarkers. The composition of fluid intake may also be important, as high-fructose drinks have been shown to exacerbate AKI biomarkers. However, it is yet to be seen if these findings are applicable to athletes performing strenuous exercise in a temperate environment. Additionally, further work should examine the effects of repeated bouts of strenuous exercise on novel AKI biomarkers.

scholarly journals Isoliquiritigenin attenuates LPS-induced acute kidney injury through suppression of HMGB1 pathway in renal tubular against ferritinophagy

2020 ◽  
Author(s):  
Yun Tang ◽  
Yanmei Wang ◽  
Chan Wang ◽  
Meidie Yu ◽  
Li Li ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Dysfunction ◽  
Kidney Injury ◽  
Tubular Injury ◽  
Renal Tubular Cells ◽  
Septic Acute Kidney Injury ◽  
Life Threatening ◽  
Renal Tubular

Abstract Septic acute kidney injury (AKI) mainly results in life-threatening renal dysfunction involving renal tubular injury to bring heavy burden to patients in intensive care unit (ICU). However, there is still a lack of therapy to prevent septic AKI effectively and inexpensive. To observe the role and novel mechanism of isoliquiritigenin (ISL) which isolated from the roots of licorice in septic AKI, we used LPS to induce renal tubular injury upon septic AKI both in vitro and in vivo. 50mg/kg ISL and 5 mg/kg Ferrostatin-1 were once given to the male C57BL/6 mice one hour before 1 mg/kg LPS i.p injection. 50 μM and 100 μM ISL respectively pre-treat the human renal tubular cells 5 hrs before 2 μg/ml LPS stimulation. We found ISL pretreatment apparently reversed LPS-induced renal dysfunction and ameliorated murine renal tubular injury by suppression HMGB1 pathway. Furthermore, we observed that LPS induced autophagy and ferroptosis in renal tubular, whereas ISL pretreatment significantly suppress autophagy and ferroptosis of renal tubular both in vitro and in vivo. Mechanically, autophagy activated ferroptosis via NCOA4-mediated ferritinophagy. Moreover, HMGB1 is required for ferritinophagy in renal tubular. ISL treatment inhibited the expression of HMGB1. Taken together, these results suggest that ISL protects LPS-induced acute kidney injury through suppression of HMGB1 pathway in renal tubular against ferritinophagy.

scholarly journals Impact of Ciprofloxacin With Autophagy on Acute Kidney Injury

2021 ◽  
Author(s):  
Woo Yeong Park ◽  
Sun-Ha Lim ◽  
Yaerim Kim ◽  
Jin Hyuk Paek ◽  
Kyubok Jin ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Caspase 3 ◽  
Kidney Injury ◽  
Underlying Mechanism ◽  
Beclin 1 ◽  
Control Group ◽  
Renal Tubules ◽  
Tubular Injury ◽  
Renal Tubular Cells ◽  
Renal Tubular

Abstract Renal tubular injury caused by oxidative stress and inflammation results in acute kidney injury. Recent research reported that antibiotics may restore deteriorated renal tubules, but the underlying mechanism remains unclear. Therefore, we investigated the efficacy and mechanism of action of antibiotics against renal tubular injury. We screened ciprofloxacin, ceftizoxime, minocycline, and netilmicin and selected ciprofloxacin to examine further because of its low toxicity towards renal tubular cells. We evaluated the effect of ciprofloxacin on cell survival by analyzing apoptosis and autophagy. TUNEL assay results showed that the ciprofloxacin group had less apoptotic cells than the control group. The ratio of cleaved caspase 3 to caspase 3, the final effector in the apoptosis process, was decreased, but the ratio of Bax to Bcl-2 located upstream of caspase 3 was not decreased in the ciprofloxacin group. Therefore, apoptosis inhibition does not occur via Bax/Bcl-2. Conversely, the levels of phosphorylated Bcl-2, and Beclin-1, an autophagy marker, were increased, and that of caspase-3 was decreased in the ciprofloxacin group. This indicates that ciprofloxacin enhanced autophagy, increasing the amount of free Beclin-1 via phosphorylated Bcl-2, and inhibited caspase activity. Therefore, ciprofloxacin might increase renal cell viability through the autophagy activation in acute kidney injury.

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