scholarly journals Acute Kidney Injury Biomarker Responses to Short-Term Heat Acclimation

Author(s):  
Riana R. Pryor ◽  
J. Luke Pryor ◽  
Lesley W. Vandermark ◽  
Elizabeth L. Adams ◽  
Rachel M. Brodeur ◽  
...  

The combination of hyperthermia, dehydration, and strenuous exercise can result in severe reductions in kidney function, potentially leading to acute kidney injury (AKI). We sought to determine whether six days of heat acclimation (HA) mitigates the rise in clinical biomarkers of AKI during strenuous exercise in the heat. Twenty men completed two consecutive 2 h bouts of high-intensity exercise in either hot (n = 12, 40 °C, 40% relative humidity) or mild (n = 8, 24 °C, 21% relative humidity) environments before (PreHA) and after (PostHA) 4 days of 90–120 min of exercise per day in a hot or mild environment. Increased clinical biomarkers of AKI (CLINICAL) was defined as a serum creatinine increase ≥0.3 mg·dL−1 or estimated glomerular filtration rate (eGFR) reduction >25%. Creatinine similarly increased in the hot environment PreHA (0.35 ± 0.23 mg·dL−1) and PostHA (0.39 ± 0.20 mg·dL−1), with greater increases than the mild environment at both time points (0.11 ± 0.07 mg·dL−1, 0.08 ± 0.06 mg·dL−1, p ≤ 0.001), respectively. CLINICAL occurred in the hot environment PreHA (n = 9, 75%), with fewer participants with CLINICAL PostHA (n = 7, 58%, p = 0.007), and no participants in the mild environment with CLINICAL at either time point. Percent change in plasma volume was predictive of changes in serum creatinine PostHA and percent changes in eGFR both PreHA and PostHA. HA did not mitigate reductions in eGFR nor increases in serum creatinine during high-intensity exercise in the heat, although the number of participants with CLINICAL was reduced PostHA.

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Gianluca Villa ◽  
Silvia De Rosa ◽  
Caterina Scirè Calabrisotto ◽  
Alessandro Nerini ◽  
Thomas Saitta ◽  
...  

Abstract Background Postoperative acute kidney injury (PO-AKI) is a leading cause of short- and long-term morbidity and mortality, as well as progression to chronic kidney disease (CKD). The aim of this study was to explore the physicians’ attitude toward the use of perioperative serum creatinine (sCr) for the identification of patients at risk for PO-AKI and long-term CKD. We also evaluated the incidence and risk factors associated with PO-AKI and renal function deterioration in patients undergoing major surgery for malignant disease. Methods Adult oncological patients who underwent major abdominal surgery from November 2016 to February 2017 were considered for this single-centre, observational retrospective study. Routinely available sCr values were used to define AKI in the first three postoperative days. Long-term kidney dysfunction (LT-KDys) was defined as a reduction in the estimated glomerular filtration rate by more than 10 ml/min/m2 at 12 months postoperatively. A questionnaire was administered to 125 physicians caring for the enrolled patients to collect information on local attitudes regarding the use of sCr perioperatively and its relationship with PO-AKI. Results A total of 423 patients were observed. sCr was not available in 59 patients (13.9%); the remaining 364 (86.1%) had at least one sCr value measured to allow for detection of postoperative kidney impairment. Among these, PO-AKI was diagnosed in 8.2% of cases. Of the 334 patients who had a sCr result available at 12-month follow-up, 56 (16.8%) developed LT-KDys. Data on long-term kidney function were not available for 21% of patients. Interestingly, 33 of 423 patients (7.8%) did not have a sCr result available in the immediate postoperative period or long term. All the physicians who participated in the survey (83 out of 125) recognised that postoperative assessment of sCr is required after major oncological abdominal surgery, particularly in those patients at high risk for PO-AKI and LT-KDys. Conclusion PO-AKI after major surgery for malignant disease is common, but clinical practice of measuring sCr is variable. As a result, the exact incidence of PO-AKI and long-term renal prognosis are unclear, including in high-risk patients. Trial registration ClinicalTrials.gov, NCT04341974.


Author(s):  
Ahmad El Samra ◽  
Ayesa Mian ◽  
Marc Lande ◽  
Hongyue Wang ◽  
Ronnie Guillet

Objective The aim of this study was to determine the effects of a 2-day prenatal course of indomethacin on the premature kidney as reflected by serum creatinine and urinary biomarkers. Study Design Urine of infants ≤ 32 weeks was collected for the first 14 days and analyzed for cystatin C, neutrophil gelatinase-associated lipocalin, osteopontin, β2 microglobulin, epidermal growth factor, uromodulin, and microalbumin. Bivariate analysis compared serum creatinine and biomarkers of exposed (INDO) and unexposed (CONT) subjects. Results Fifty-seven infants (35 CONT and 22 INDO) were studied. The cohorts were similar in gestational age, birthweight, race, gender, nephrotoxic medication exposure, and Apgar scores. CONT had more dopamine exposure and included more pre-eclamptic mothers (p = 0.005). No difference in creatinine-based acute kidney injury or the log transformed mean, maximum, and minimum values of urinary biomarkers was detected. Conclusion Our findings suggest that a short course of tocolytic indomethacin does not result in neonatal acute kidney injury. Key Points


2015 ◽  
Vol 62 ◽  
pp. S380 ◽  
Author(s):  
F. Wong ◽  
J.G. O’Leary ◽  
K.R. Reddy ◽  
G. Garcia-Tsao ◽  
M.B. Fallon ◽  
...  

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Natalia Stepanova ◽  
Ganna Tolstanova ◽  
Valentyn Nepomnyashchii ◽  
Iryna Akulenko ◽  
Svitlana Savchenko ◽  
...  

Abstract Background and Aims Gut microbiota is considered an important factor affecting oxalate handling in the intestine. It has been demonstrated that intestinal oxalate secretion provides a complementary route of excretion, and it becomes more evident when kidney function declines. A diversity of gut oxalate-degrading bacteria (ODB) has been hypothesized to play a role in this process. However, there is a general lack of research on the long-term effects of acute kidney injury (AKI) on ODB and their total oxalate-degrading activity (ODA) in fecal microbiota. In this study, we evaluated whether renal dysfunction could affect intestinal ODB and their total ODA in a rat model of glycerol-induced AKI. Method The Male Wistar rats (200-300 g, n=20) on oxalate-free diet were randomly divided into 2 groups. After 24-h of water deprivation, Group 1 (n=10) received an intramuscular injection of 50% glycerol (10 ml/kg of body weight), and Group 2 (n=10) served as control. The numbers of ODB (incubated in a highly selective Oxalate Medium and determined using culture method) and total fecal ODA were measured after injection on days 7 and 70. The method of redoximetric titration with a KMnO4 solution was adopted to evaluate total ODA in fecal microbiota; the results were expressed as % of oxalate degradation per 0.01 g of feces. Renal injury was assessed by histopathological examination, serum creatinine and daily proteinuria levels after removing the animals from the experiment on day 70. Cortical interstitial fibrosis was measured by computerized image analysis on sections stained with picrosirius red. The median (Me) and the interquartile ranges (Q25; Q75) were calculated and compared using the nonparametric Mann-Whitney test. The Spearman correlation coefficient was used to evaluate association between the examined parameters. Results The obtained results demonstrated: 1) after glycerol injection on day 7, no differences were found in the numbers of ODB and total fecal ODA between the experimental and control groups: 5.9 (5.4-6.0) vs 6.0 (5.4-6.4) CFU/g, p=0.65 and 2.0 (0.1-5.0) vs 2.5 (2.0-9.0) %/0.01g, p=0.24, respectively; 2) after AKI initiation on day 70, the numbers of ODB and total fecal ODA were significantly lower in Group I compared with control Group II (Fig. 1); 3) the higher percentage of renal interstitial fibrosis was, the higher total fecal ODA occurred in the experimental rats (Fig. 2). In addition, the number of ODB in feces in Group 1 had an inverse association with serum creatinine (r=-0.52, p=0.006) and 24-h proteinuria levels (r=-0.86, p<0.0001). Conclusion AKI had the long-term negative effects on the quantitative and qualitative characteristics of ODB in fecal microbiota in rats. Moreover, the results of our study confirmed an increasing trend in total fecal ODA according to the aggravation of renal interstitial fibrosis in rats.


2017 ◽  
Vol 43 (1) ◽  
pp. 15-21 ◽  
Author(s):  
Nakhshab Choudhry ◽  
Amna Ihsan ◽  
Sadia Mahmood ◽  
Fahim Ul Haq ◽  
Aamir Jamal Gondal

AbstractObjectives:This study was designed to find the reliability of serum NGAL as an early and better diagnostic biomarker than that of serum creatinine for acute kidney injury after percutaneous coronary intervention in Pakistani population.Materials and methods:One hundred and fifty-one patients undergoing elective percutaneous coronary intervention were included and demographic data were recorded. Blood was drawn by venipuncture in clot activator vacutainers and serum was separated and stored at 4°C. Sample was drawn before the percutaneous procedure and subsequently sampling was done serially for 5 days.Results:The mean±SD serum NGAL pre-PCI (39.92± 10.35 μg/L) and 4 h post-PCI (100.42±26.07 μg/L) showed highly significant difference (p<0.001). The mean±SD serum creatinine pre-PCI (70.1±11.8 μmol/L) and post-PCI (71.2±11.6 μmol/L) showed significant difference (p=0.005) on day 2 onwards but mean microalbumin showed insignificant results (p=0.533). The serum NGAL predicted CI-AKI with sensitivity of 95.8% and specificity of 97.6% for a cut off value of 118 μg/L.Conclusion:Our results suggest that NGAL is an excellent early diagnostic biomarker for acute kidney injury in patients undergoing elective percutaneous coronary intervention.


PLoS ONE ◽  
2018 ◽  
Vol 13 (11) ◽  
pp. e0205791 ◽  
Author(s):  
Tania C. Spada ◽  
José M. R. D. Silva ◽  
Lucila S. Francisco ◽  
Lia J. Marçal ◽  
Leila Antonangelo ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Abdulmuttalip Simsek ◽  
Volkan Tugcu ◽  
Ali Ihsan Tasci

Acute kidney injury (AKI) is a common and strong problem in the diagnosis of which based on measurement of BUN and serum creatinine. These traditional methods are not sensitive and specific for the diagnosis of AKI. AKI is associated with increased morbidity and mortality in critically ill patients and a quick detection is impossible with BUN and serum creatinine. A number of serum and urinary proteins have been identified that may messenger AKI prior to a rise in BUN and serum creatinine. New biomarkers of AKI, including NGAL, KIM-1, cystatin-C, IL-18, and L-FABP, are more favourable tests than creatinine which have been identified and studied in several experimental and clinical training. This paper will discuss some of these new biomarkers and their potential as useful signs of AKI. We searched the literature using PubMed and MEDLINE with acute kidney injury, urine, and serum new biomarkers and the articles were selected only from publication types in English.


2020 ◽  
Vol 92 (12) ◽  
pp. 48-52
Author(s):  
O. Iu. Mironova ◽  
A. D. Deev ◽  
P. G. Lakotka ◽  
V. V. Fomin

Aim.The aim of our study was to assess the role of anemia as a risk factor of contrast-associated acute kidney injury (CA-AKI) in patients with stable coronary artery disease. Materials and methods.1023 patients with chronic coronary artery disease were enrolled in a prospective, open, cohort study (ClinicalTrials.gov ID NCT04014153). 83 patients had anemia. CA-AKI was defined as an increase of 25% or more, or an absolute increase of 0.5 mg/dl or more in serum creatinine from baseline value, assessed at 48 hours following the administration of the contrast. The primary endpoint of the study was the development of CA-AKI according to KDIGO criteria. Results.CA-AKI developed in 12 (14.5%) patients with anemia according to the relative increase of the level of serum creatinine (25% and more from the baseline). With using the absolute increase of the level of serum creatinine the prevalence of CA-AKI was 2 (2.4%) patients. Patients with anemia had higher rate of CA-AKI than the overall population of the study (14.4% versus 12.7%). Although our results were not statistically significant (р=0.61, odds ratio 1.19, 95% confidence interval 0.632.24). Conclusion.The prevalence of CA-AKI was higher in the group of patients with anemia, but didnt meet statistical significance and needs further evaluation in larger studies.


2021 ◽  
Author(s):  
Titik Setyawati ◽  
Ricky Aditya ◽  
Tinni Trihartini Maskoen

AKI is a syndrome consisting of several clinical conditions, due to sudden kidney dysfunction. Sepsis and septic shock are the causes of AKI and are known as Sepsis-Associated AKI (SA-AKI) and accounted for more than 50% of cases of AKI in the ICU, with poor prognosis. Acute Kidney Injury (AKI) is characterized by a sudden decline in kidney function for several hours/day, which results in the accumulation of creatinine, urea and other waste products. The most recent definition was formulated in the Kidney Disease consensus: Improving Global Outcome (KDIGO), published in 2012, where the AKI was established if the patient’s current clinical manifestation met several criteria: an increase in serum creatinine levels ≥0.3 mg/dL (26.5 μmol/L) within 48 hours, an increase in serum creatinine for at least 1.5 times the baseline value within the previous 7 days; or urine volume ≤ 0.5 ml/kg body weight for 6 hours. The AKI pathophysiology includes ischemic vasodilation, endothelial leakage, necrosis in nephrons and microtrombus in capillaries. The management of sepsis associated with AKI consisted of fluid therapy, vasopressors, antibiotics and nephrotoxic substances, Renal Replacement Therapy (RRT) and diuretics. In the analysis of the BEST Kidney trial subgroup, the likelihood of hospital death was 50% higher in AKI sepsis compared to non-sepsis AKI. Understanding of sepsis and endotoxins that can cause SA-AKI is not yet fully known. Some evidence suggests that renal microcirculation hypoperfusion, lack of energy for cells, mitochondrial dysfunction, endothelial injury and cycle cell arrest can cause SA-AKI. Rapid identification of SA-AKI events, antibiotics and appropriate fluid therapy are crucial in the management of SA-AKI.


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