Acute Kidney Injury Induced by Various Pneumoperitoneum Pressures in a Rabbit Model of Mild and Severe Hydronephrosis

2014 ◽  
Vol 94 (2) ◽  
pp. 225-233 ◽  
Author(s):  
Wei Li ◽  
Zhixiu Cao ◽  
Zhongyuan Xia ◽  
Qingtao Meng ◽  
Wei-min Yu ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Laparoscopic Surgery ◽  
Serum Creatinine ◽  
Cell Apoptosis ◽  
Rabbit Model ◽  
Kidney Injury ◽  
Acute Injury ◽  
Intraabdominal Pressure ◽  
Pressure Tolerance ◽  
Kidney Injury Molecule 1

Objective: Increased pneumoperitoneum pressure during laparoscopic surgery can result in acute kidney injury. We aimed to clarify whether intraabdominal pressure tolerance is modified in various degrees of unilateral kidney hydronephrosis in rabbits. Methods: A total 90 rabbits were randomly allocated to three groups (group PN, PM and PS, i.e. rabbits with no, mild and severe hydronephrosis, respectively, subjected to intraabdominal pressures). Rabbits in group PM (n = 30) and group PS (n = 30) underwent a surgical procedure inducing a mild or severe left hydronephrosis. Rabbits in all groups were then allocated to 5 subgroups. Then, they were subjected to intraabdominal pressures of 0, 6, 9, 12, and 15 mm Hg, respectively. Acute kidney injury was assessed by measuring serum creatinine (Scr), blood urea nitrogen (BUN), tubular cell apoptosis, kidney injury molecule-1 (KIM-1) and cysteine-rich 61 (Cyr-61/CCN1) expression. Results: Acute kidney injury with increased tubular apoptosis and KIM-1 and Cyr-61 expression occurred when intraabdominal pressure reached 15, 15 and 9 mm Hg in PN, PM and PS groups, respectively. The Scr and BUN levels were similar in all groups. Conclusions: In rabbits, kidneys with severe hydronephrosis were more likely to suffer acute injury when they were exposed to pneumoperitoneal pressure.

scholarly journals Enhancing acute kidney injury regeneration by promoting cellular dedifferentiation in zebrafish

2018 ◽  
Author(s):  
Lauren Brilli Skvarca ◽  
Hwa In Han ◽  
Eugenel B. Espiritu ◽  
Maria A. Missinato ◽  
Elizabeth R. Rochon ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Injury ◽  
Cardiac Injury ◽  
Kidney Injury ◽  
Acute Injury ◽  
Cardiomyocyte Proliferation ◽  
Deacetylase Inhibitor ◽  
Summary Statement ◽  
Renal Tubular ◽  
Kidney Injury Molecule 1

ABSTRACTAcute kidney injury (AKI) is a serious disorder for which there is no approved pharmaceutical treatment. Following injury, native nephrons display limited regenerative capabilities, relying on the dedifferentiation and proliferation of renal tubular epithelial cells (RTECs) that survive the insult. Previously, we identified 4-(phenylthio)butanoic acid (PTBA), a histone deacetylase inhibitor (HDI) that enhances renal recovery and showed that PTBA treatment increased RTEC proliferation and reduced renal fibrosis. Here, we investigated the regenerative mechanisms of PTBA in zebrafish models of larval renal injury and adult cardiac injury. With respect to renal injury, we showed that delivery of PTBA using an esterified prodrug (UPHD25) increases the reactivation of the renal progenitor gene Pax2a, enhances dedifferentiation of RTECs, reduces Kidney injury molecule-1 expression, and lowers the number of infiltrating macrophages. Further, we find that the effects of PTBA on RTEC proliferation depend upon retinoic acid signaling and demonstrate the therapeutic properties of PTBA are not restricted to the kidney but also increase cardiomyocyte proliferation and decrease fibrosis following cardiac injury in adult zebrafish. These studies provide key mechanistic insights into how PTBA enhances tissue repair in models of acute injury and lay the groundwork for translating this novel HDI into the clinic.SUMMARY STATEMENTMortality associated with acute kidney injury (AKI) is in part due to limited treatments available to ameliorate kidney injury. We identified a compound that enhances AKI recovery by promoting cellular dedifferentiation.

scholarly journals Serum Cystatin C, Kidney Injury Molecule-1, Neutrophil Gelatinase-Associated Lipocalin, Klotho and Fibroblast Growth Factor-23 in The Early Prediction of Acute Kidney Injury Associated With Sepsis in a Chinese Emergency Cohort Study

2021 ◽  
Author(s):  
Yuanyuan Pei ◽  
Guangping Zhou ◽  
Pengfei Wang ◽  
Fang'e Shi ◽  
Xiaolu Ma ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Cystatin C ◽  
Fibroblast Growth Factor 23 ◽  
Kidney Injury ◽  
Serum Levels ◽  
Serum Cystatin C ◽  
Serum Cystatin ◽  
Kidney Injury Molecule 1 ◽  
Fgf 23

Abstract Background: Acute kidney injury (AKI) was a common and critical complication of sepsis, and is associated with unacceptable morbidity and mortality. Current diagnostic criteria for AKI was insensitive for early detection. Novel biomarkers included cystatin C, KIM-1, NGAL, klotho and FGF-23 which can predict AKI earlier may allow immediate interventions. We aimed to determine the diagnostic performance of these biomarkers for detecting AKI in sepsis patients.Methods: This prospective observational study was conducted from May 2018 and November 2020, enrolling sequential 162 sepsis patients. AKI’s definition was according to 2012 KDIGO criteria and we divided patients into non-AKI (n=102) and AKI (n=60) groups. Serum levels of several AKI biomarkers were detected by ELISA. The relationship between biomarker levels on admission of AKI were analyzed and discrimination performances comparison were performed.Results: AKI incidence was up to 37.0% (60/162) during hospitalization. Compared with non-AKI group, both serum cystatin C, KIM-1, NGAL and FGF-23 were significantly elevated at admission in septic AKI patients. The areas under the receiver operating curves demonstrated that serum cystatin C had modest discriminative powers for predicting AKI after sepsis, and cystatin C combined with serum creatinine in the prediction of septic AKI increased the diagnostic sensitivity prominently.Conclusion: Serum cystatin C, KIM-1, NGAL and FGF-23 levels are both increased in septic AKI patients. Our study provides reliable evidence that cystatin C solely and combined with serum creatinine may accurately and sensitively predict septic AKI when patients on admission.

scholarly journals The Marker of Tubular Injury, Kidney Injury Molecule-1 (KIM-1), in Acute Kidney Injury Complicating Acute Pancreatitis: A Preliminary Study

2020 ◽  
Vol 9 (5) ◽  
pp. 1463 ◽  
Author(s):  
Justyna Wajda ◽  
Paulina Dumnicka ◽  
Witold Kolber ◽  
Mateusz Sporek ◽  
Barbara Maziarz ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Acute Pancreatitis ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Care Hospital ◽  
Tubular Injury ◽  
Fatty Acid Binding ◽  
Number Of Patients ◽  
Initial Symptoms ◽  
Kidney Injury Molecule 1

Acute pancreatitis (AP) may be associated with severe inflammation and hypovolemia leading to organ complications including acute kidney injury (AKI). According to current guidelines, AKI diagnosis is based on dynamic increase in serum creatinine, however, creatinine increase may be influenced by nonrenal factor and appears late following kidney injury. Kidney injury molecule-1 (KIM-1) is a promising marker of renal tubular injury and it has not been studied in AP. Our aim was to assess if urinary KIM-1 may be used to diagnose AKI complicating the early stage of AP. We recruited 69 patients with mild to severe AP admitted to a secondary care hospital during the first 24 h from initial symptoms of AP. KIM-1 was measured in urine samples collected on the day of admission and two subsequent days of hospital stay. AKI was diagnosed based on creatinine increase according to Kidney Disease: Improving Global Outcomes 2012 guidelines. Urinary KIM-1 on study days 1 to 3 was not significantly higher in 10 patients who developed AKI as compared to those without AKI and did not correlate with serum creatinine or urea. On days 2 and 3, urinary KIM-1 correlated positively with urinary liver-type fatty acid-binding protein, another marker of tubular injury. On days 2 and 3, urinary KIM-1 was higher among patients with systemic inflammatory response syndrome, and several correlations between KIM-1 and inflammatory markers (procalcitonin, urokinase-type plasminogen activator receptor, C-reactive protein) were observed on days 1 to 3. With a limited number of patients, our study cannot exclude the diagnostic utility of KIM-1 in AP, however, our results do not support it. We hypothesize that the increase of KIM-1 in AKI complicating AP lasts a short time, and it may only be observed with more frequent monitoring of the marker. Moreover, urinary KIM-1 concentrations in AP are associated with inflammation severity.

Evaluation of urinary neutrophil gelatinase-associated lipocalin and urinary kidney injury molecule-1 as biomarkers of renal function in cancer patients treated with cisplatin

2020 ◽  
Vol 26 (7) ◽  
pp. 1643-1649
Author(s):  
Elliyeh Ghadrdan ◽  
Sholeh Ebrahimpour ◽  
Sanambar Sadighi ◽  
Samira Chaibakhsh ◽  
Zahra Jahangard-Rafsanjani
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Characteristic Curve ◽  
Kidney Injury ◽  
Acute Kidney Injury Network ◽  
The Novel ◽  
Urinary Ngal ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Kidney Injury Molecule 1 ◽  
Neutrophil Gelatinase

Introduction Cisplatin-associated acute kidney injury (AKI) is the major limitation to the use of cisplatin-based chemotherapy regimens. Serum creatinine as a traditional marker did not increase in a timely enough fashion in AKI patients. Therefore, recently, the novel markers such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were considered for early detection of AKI. The aim of this study was to compare the sensitivity and specificity of urinary NGAL and KIM-1 with serum creatinine in cisplatin related AKI. Methods Patients ≥18 years with solid tumors who received cisplatin-based chemotherapy were included. Urine samples were collected 0, 6 and 24 h after cisplatin infusion and the urinary NGAL, KIM-1, and creatinine concentrations were evaluated. NGAL and KIM-1 concentrations were adjusted based on urine creatinine to eliminate hydration effects. Serum creatinine levels were assessed at the base and 72 h after cisplatin administration. Results Seven out of the 35 recruited patients (20%) suffered from AKI defined by Acute Kidney Injury Network criteria. In AKI patients, the ratio of urinary KIM-1–creatinine at 24 h compared to baseline (24 h/baseline) and NGAL–creatinine 24 h/baseline were significantly higher than those of non-AKI group ( p = 0.037 and 0.047 respectively). The area under the receiver-operating characteristic curve for KIM-1–creatinine 24 h/baseline and NGAL–creatinine 24 h/baseline were 0.78 (0.59–0.96, p = 0.032) and 0.77 (0.57–0.97, p = 0.036) respectively. Conclusions Our findings showed that the changes in urinary NGAL–creatinine and KIM-1–creatinine ratios, 24 h after cisplatin administration can be utilized to predict AKI in cisplatin recipients.

scholarly journals Serial Serum Creatinine and Urinary Acute Kidney Injury Biomarker Measurements in Dogs Envenomated by the European Adder (Vipera Berus).

2020 ◽  
Author(s):  
Hannah Harjen ◽  
Tove Nicolaysen ◽  
Tale Negard ◽  
Hege Lund ◽  
Bente Sævik ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
High Morbidity ◽  
Reference Limit ◽  
Vipera Berus ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Serial Serum ◽  
Kidney Injury Molecule 1 ◽  
Glutamyl Transferase

Abstract Background Acute kidney injury (AKI) is associated with high morbidity and mortality in dogs, but diagnosis may be impaired due the insensitivity of routine renal function biomarkers to detect earlier or milder forms of injury. Snake envenomation is one of several causes of AKI in dogs and humans. Dogs are commonly envenomated by the European adder (Vipera berus) between April and October each year, but few studies exist examining serial serum creatinine (sCr) measurements and AKI biomarkers in these dogs. Novel urinary biomarkers could improve clinical outcome by allowing earlier diagnosis of and intervention in AKI. The aim of this study was to assess the presence of AKI in dogs envenomated by V. berus at 12, 24 and 36 hours after bite, as well as 14 days later, using sCr and a panel of urinary AKI biomarkers normalised to urine creatinine (uCr), compared to a group of healthy control dogs.Results Thirty-five envenomated dogs and 37 control dogs were included. Serum creatinine did not exceed the upper reference limit at any time point in any dog after envenomation. Compared to controls, urinary albumin /uCr, neutrophil gelatinase-associated lipocalin/uCr and monocyte chemotactic protein-1 /uCr were significantly elevated 12 hours (p < 0.001, p< 0.001, p = 0.01), 24 hours (p < 0.001, p < 0.001, p = 0.003) and 36 hours ( p < 0.001, p< 0.001, p = 0.001) after bite. Osteopontin /uCr was higher 24 and 36 hours after bite (p < 0.001), kidney injury molecule-1 /uCr, interleukin-8 /uCr and γ- glutamyl transferase /uCr were significantly higher 36 hours after bite (p = 0.0007, p = 0.0005, p= 0.001). Urinary cystatin C /uCr was not significantly different to controls at any timepoint. Biomarker/uCr ratios were not significantly different 14 days after envenomation compared to controls. Conclusion Urinary biomarker/Cr ratios are indicative of transient non-azotaemia AKI in dogs envenomated by V. berus.

scholarly journals Kidney Injury Molecule 1 (KIM-1) as an Early Predictor for Acute Kidney Injury in Post-Cardiopulmonary Bypass (CPB) in Open Heart Surgery Patients

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Nora A. Khreba ◽  
Mostafa Abdelsalam ◽  
A. M. Wahab ◽  
Mohammed Sanad ◽  
Rania Elhelaly ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Kidney Injury ◽  
Open Heart ◽  
Post Surgery ◽  
Significant Difference ◽  
Kidney Injury Molecule 1 ◽  
Early Predictor

Introduction. Postoperative acute kidney injury is associated with a higher mortality, a more complicated hospital course with longer hospital stay. Urinary kidney injury molecule 1 may play an important role as an early predictor of acute kidney injury post-cardiopulmonary in open heart surgery. Methods. We evaluated 45 patients who underwent open heart surgery from January 2016 to June 2016. Both urinary kidney injury molecule 1 and serum creatinine were evaluated before operation and 3hs and 24hs after operation. Acute kidney injury was diagnosed according to Kidney Disease: Improving Global Outcomes, 2012 guidelines. Results. In this study, 27 patients developed acute kidney injury. The three hour-post-surgery urinary kidney injury molecule 1 was significantly higher in the acute kidney injury group (P<0.015) and, at the same time, we did not find any significant difference in the serum creatinine levels between the two groups. Conclusion. Although serum creatinine is still the gold standard for diagnosis of acute kidney injury searching for other new markers is mandatory. Urinary kidney injury molecule 1 can be used as simple noninvasive and specific biomarker for early diagnosis of acute kidney injury.

Acute Kidney Injury

2016 ◽  
Author(s):  
Lee Grodin ◽  
Joshua McHugh ◽  
Richard Sinert
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Signs And Symptoms ◽  
Absolute Increase ◽  
Mortality And Morbidity ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Kidney Injury Molecule 1 ◽  
Parenchymal Disease ◽  
Neutrophil Gelatinase

Acute kidney injury (AKI) is defined as a syndrome in which there is an abrupt (hours to days) absolute increase in serum creatinine (SCr) of 0.5 mg/dL or a 25% increase from baseline. Even a modest rise in SCr of 0.3 mg/dL during hospitalization is associated with increased mortality and morbidity. Because of difficulties using SCr as a determinant of AKI, a variety of serum (neutrophil gelatinase–associated lipocalin, interleukin-18) and urine (kidney injury molecule–1) biomarkers of AKI are currently undergoing intense investigation. AKI may be defined pathophysiologically, as a decrease in renal blood flow (prerenal), or an intrinsic renal parenchymal disease (renal), or obstruction of urine flow (postrenal). Indications for emergent dialysis include hyperkalemia, fluid overload, acidosis, and signs and symptoms of uremia. If AKI is diagnosed in the emergency department, the patient should be admitted for further workup. In the majority of patients who survive AKI, renal function essentially returns to normal.  Key words: acute kidney injury, dialysis, hyperkalemia, serum creatinine This review contains 3 highly rendered figures, 11 tables, and 49 references.

Abstract 13920: Impact of Diabetes on Acute Kidney Injury After Myocardial Infarction: Possible Involvement of Toll-like Receptor in the Kidney

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Kohei Ohno ◽  
Atsushi Kuno ◽  
Shingo Muratsubaki ◽  
Hiromichi Murase ◽  
Hidemichi Kouzu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Early Stage ◽  
Mrna Level ◽  
Kidney Injury ◽  
Mrna Levels ◽  
Toll Like Receptor ◽  
Increased Risk ◽  
Kidney Injury Molecule 1

Background: Comorbid acute kidney injury (AKI) predicts poor prognosis in patients with acute myocardial infarction (MI). Although type 2 diabetes (T2D) is a well-known risk factor of AKI after MI, the mechanism of the increased risk remains unclear. Here we hypothesized that T2D increases AKI after MI via toll-like receptor (TLR)-mediated inflammation. Methods and Results: OLETF, a rat model of obese T2D, and LETO, non-diabetic controls, at 25-30 weeks of age were randomized into sham and permanent coronary ligation (MI) groups. At baseline, body weight (617±23 vs. 537±13 g), fasting plasma glucose (267±32 vs. 153±15 mg/dl) and urinary protein level (6.4 vs. 0.6 g/gCr), but not serum creatinine, were significantly higher in OLETF than in LETO. Histologically, glomerular size was increased by 17% without mesangial proliferation in OLETF compared to that in LETO, indicating that OLETF developed early-stage nephropathy by this age. At 12 h after MI, mRNA levels of TLR2, TLR4, IL-6 and TNF-α in the kidney were increased by 1.6-, 1.2-, 2.6-, 1.5-fold, respectively, in OLETF but not in LETO. Furthermore, immunoblot analyses showed that phosphorylation levels of p38 MAPK and JNK, downstream mediators of the TLR signal, were significantly elevated by MI in OLETF. Histological abnormalities in the kidney or increase in serum creatinine were not detected in either LETO or OLETF 12 h after MI. However, in immunohistochemical analyses, areas positive for neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were significantly increased by 4.0- and 5.3-fold, respectively, and NGAL mRNA level was increased by 1.8-fold after MI in OLETF but not in LETO. In sham-operated LETO and OLETF, areas positive for NGAL and KIM-1 were barely detected. Infarct sizes were similar and cardiac BNP mRNA levels in the non-infarcted left ventricle were equally elevated at 12 h after MI in LETO and OLETF, suggesting that MI-induced cardiac loads were comparable in the two groups. However, mortality at 48 h after MI was significantly higher in OLETF than in LETO (68% vs. 18%, P<0.05). Conclusion: The results suggest that AKI after MI is enhanced in T2D via TLR-mediated inflammation. The cardio-renal interaction may underlie increased post-MI mortality in T2D.

scholarly journals Acute kidney injury in children

2014 ◽  
Vol 142 (5-6) ◽  
pp. 371-377 ◽  
Author(s):  
Amira Peco-Antic ◽  
Dusan Paripovic
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Developed Countries ◽  
Multiple Organ ◽  
Critically Ill Children ◽  
Creatinine Concentration ◽  
Fatty Acid Binding ◽  
Kidney Injury Molecule 1 ◽  
Sudden Decrease

Acute kidney injury (AKI) is a clinical condition considered to be the consequence of a sudden decrease (>25%) or discontinuation of renal function. The term AKI is used instead of the previous term acute renal failure, because it has been demonstrated that even minor renal lesions may cause far-reaching consequences on human health. Contemporary classifications of AKI (RIFLE and AKIN) are based on the change of serum creatinine and urinary output. In the developed countries, AKI is most often caused by renal ischemia, nephrotoxins and sepsis, rather than a (primary) diffuse renal disease, such as glomerulonephritis, interstitial nephritis, renovascular disorder and thrombotic microangiopathy. The main risk factors for hospital AKI are mechanical ventilation, use of vasoactive drugs, stem cell transplantation and diuretic-resistant hypervolemia. Prerenal and parenchymal AKI (previously known as acute tubular necrosis) jointly account for 2/3 of all AKI causes. Diuresis and serum creatinine concentration are not early diagnostic markers of AKI. Potential early biomarkers of AKI are neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule-1 (KIM-1), interleukins 6, 8 and 18, and liver-type fatty acid-binding protein (L-FABP). Early detection of kidney impairment, before the increase of serum creatinine, is important for timely initiated therapy and recovery. The goal of AKI treatment is to normalize the fluid and electrolyte status, as well as the correction of acidosis and blood pressure. Since a severe fluid overload resistant to diuretics and inotropic agents is associated with a poor outcome, the initiation of dialysis should not be delayed. The mortality rate of AKI is highest in critically ill children with multiple organ failure and hemodynamically unstable patients.

scholarly journals Serial serum creatinine, SDMA and urinary acute kidney injury biomarker measurements in dogs envenomated by the European adder (Vipera berus)

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Hannah J. Harjen ◽  
Tove V. Nicolaysen ◽  
Tale Negard ◽  
Hege Lund ◽  
Bente K. Sævik ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
High Morbidity ◽  
Reference Limit ◽  
Vipera Berus ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Serial Serum ◽  
Kidney Injury Molecule 1 ◽  
Glutamyl Transferase

Abstract Background Acute kidney injury (AKI) is associated with high morbidity and mortality in dogs, but diagnosis may be impaired due the insensitivity of routine renal function biomarkers to detect earlier or milder forms of injury. Snake envenomation is one of several causes of AKI in dogs and humans. Dogs are commonly envenomated by the European adder (Vipera berus) between April and October each year, but few studies exist examining serial serum creatinine (sCr) and symmetric dimethylarginine (SDMA) measurements and AKI biomarkers in these dogs. Novel urinary biomarkers could improve clinical outcome by allowing earlier diagnosis of and intervention in AKI. The aim of this study was to assess the presence of AKI in dogs envenomated by V. berus at 12, 24 and 36 h after bite, as well as 14 days later, using sCr, SDMA and a panel of urinary AKI biomarkers normalised to urine creatinine (uCr), compared to a group of healthy control dogs. Results Thirty-five envenomated dogs and 35 control dogs were included. Serum creatinine did not exceed the upper reference limit at any time point in any dog after envenomation. Serum SDMA did not exceed 0.89 μmol/L in any dog. Compared to controls, urinary albumin/uCr, neutrophil gelatinase-associated lipocalin/uCr and monocyte chemotactic protein-1/uCr were significantly elevated 12 h (P <  0.0001, P <  0.0001, P = 0.01), 24 h (P <  0.001, P <  0.001, P = 0.002) and 36 h (P <  0.001, P <  0.001, P = 0.0008) after bite. Osteopontin/uCr was higher 24 and 36 h after bite (P < 0.0001), kidney injury molecule-1/uCr, interleukin-8/uCr and γ- glutamyl transferase/uCr were significantly higher 36 h after bite (P = 0.003, P = 0.0005, P = 0.001). Urinary cystatin C/uCr was not significantly different to controls at any timepoint. Biomarker/uCr ratios were not significantly different 14 days after envenomation compared to controls. Conclusion Urinary biomarker/Cr ratios are indicative of mild transient, non-azotaemic AKI in dogs envenomated by V. berus.

Sign in / Sign up

Export Citation Format

Share Document