Differentiate Study on Urine Creatinine and Plasma Creatinine of Acute Kidney Injury in Eastern State of Jharkhand, Ranchi, India

Abstract Background Vancomycin and piperacillin–tazobactam (VAN+TZP) are two of the most commonly utilized antibiotics in the hospital setting and are reported in clinical studies to increase acute kidney injury (AKI). However, no clinical study has demonstrated that synergistic AKI occurs, only that serum creatinine increases with VAN+TZP. Previous preclinical work demonstrated that novel urinary biomarkers and histopathologic scores were not increased in the VAN+TZP group compared with VAN alone. The purpose of this study was to assess changes in urinary output and plasma creatinine between VAN, TZP, and VAN+TZP treatments. Methods Male Sprague–Dawley rats (n = 32) received either saline, VAN 150 mg/kg/day intravenously, TZP 1,400 mg/kg/day intraperitoneally, or VAN+TZP for 3 days. Animals were placed in metabolic cages pre-study and on drug dosing days 1–3. Urinary output, plasma creatinine, urinary biomarkers were compared daily and kidney histopathology was compared at the end of therapy between the groups. Mixed-effects, repeated-measures models were employed to assess differences between the groups. Results In the VAN-treated rats, urinary output was increased on days 1, 2 and 3 compared with baseline and saline (P < 0.01 for all), whereas it increased later for VAN+TZP (i.e., day 2 and 3 compared with saline, P < 0.001). No changes in urinary output were observed with saline and TZP alone. Plasma creatinine rose for VAN on days 1, 2, and 3 from baseline and VAN+TZP on day 3 (P < 0.02 for all), but no treatment group was different from saline. In the VAN-treated rats, urinary KIM-1 and clusterin were increased on days 1, 2, and 3 compared with controls (P < 0.001). Elevations were seen only after 3 days of treatment with VAN+TZP (P < 0.001 KIM-1, P < 0.05 clusterin). No changes in urinary biomarkers output were observed with saline and TZP alone. Histopathology was only elevated in the VAN group compared with saline (P < 0.002). No histopathology changes were noted with VAN+TZP. Conclusion All groups with VAN demonstrated kidney injury; however, VAN+TZP did not cause more kidney injury than VAN alone in a rat model of VIKI when using plasma creatinine, urinary output, or urinary biomarkers as outcomes. Histopathology data suggest that adding TZP did not worsen VAN-induced AKI and may even be protective. Disclosures Kevin J. Downes, MD, Merck: Grant/Research Support, Research Grant; Pfizer: Grant/Research Support.

Download Full-text

P0544INHIBITION OF 15-HYDROXYPROSTAGLANDIN DEHYDROGENASE (15-PGDH) PROTECTS MICE AGAINST CONTRAST-INDUCED ACUTE KIDNEY INJURY

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa142.p0544 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Byeong Woo KIm ◽

Sun hee Kim ◽

Ki beom Bae

Keyword(s):

Acute Kidney Injury ◽

Blood Flow ◽

Protective Effect ◽

Renal Blood Flow ◽

Smooth Muscle Actin ◽

Kidney Injury ◽

Plasma Creatinine ◽

Histological Evaluation ◽

Vehicle Group ◽

Before And After

Abstract Background and Aims Although the mechanism of contrast-induced acute kidney injury (CI-AKI) is not fully known, the imbalance of vasoconstrictive and vasodilative mediators plays a major role. Prostaglandin E2 (PGE2) is one of the vasodilators involved in this process. Inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) causes elevation of PGE2 level in tissue by delaying the rapid degradation of PGE2 by the enzyme. We tested the hypothesis that the 15-PGE2 inhibitor would protect against CI-AKI in a mouse model and attempted to elucidate the mechanism involved. Method 10-week aged male C57/BL6 Mice were injected with 10gI/kg of iodixanol by tail vein. Renal blood flow measurement, right nephrectomy, and blood sampling were taken at 48 hours after iodixanol injection. The 15-PGDH inhibitor was injected before and after iodixanol administration. Plasma creatinine, NGAL, KIM-1 were measured as biomarkers for renal function. Histological evaluation was analyzed by the necrosis scoring system and TUNEL assay. Arteriolar area of outer medulla was analyzed by α-smooth muscle actin stain. Renal blood flow was measured by the non-invasive laser doppler. Results Plasma creatinine (1.94±0.75 vs 1.11±0.44 mg/dL, p=0.005), NGAL (299.7±115.87 vs 140.4±76.56 ng/mL, p=0.004), and KIM-1 (2.09±2.34 vs 0.43±0.89 ng/mL, p=0.024) levels were significantly lower when the 15-PGDH inhibitor was injected before and after iodixanol administration than the vehicle group. But no significant renal protective effect was shown when the 15-PGDH inhibitor was injected before or after iodixanol administration. The 15-PGDH inhibitor administration before and after iodixanol injection showed a significantly wider renal arteriolar area (683.63±248.46 vs 1132.97±357.46 μm2, p=0.039) and larger renal blood flow (360.0±49.72 vs 635.1±27.20, p=0.011) than vehicle administration. Conclusion The 15-PGDH inhibitor has a renal protective effect against CI-AKI in mice by increasing renal blood flow when injected intravenously before and after iodine contrast media administration.

Download Full-text

Monitoring of plasma creatinine and urinary γ-glutamyl transpeptidase improves detection of acute kidney injury by more than 20%*

Critical Care Medicine ◽

10.1097/ccm.0b013e3181fa431a ◽

2011 ◽

Vol 39 (1) ◽

pp. 52-56 ◽

Cited By ~ 8

Author(s):

Valéry Blasco ◽

Sandrine Wiramus ◽

Julien Textoris ◽

François Antonini ◽

Carole Bechis ◽

...

Keyword(s):

Acute Kidney Injury ◽

Kidney Injury ◽

Plasma Creatinine ◽

Glutamyl Transpeptidase

Download Full-text

Reduced urinary levels of angiotensin-converting enzyme 2 activity predict acute kidney injury in critically ill patients

Critical Care and Resuscitation ◽

10.51893/2020.4.oa7 ◽

2020 ◽

Vol 22 (4) ◽

pp. 344-354

Author(s):

Laurent Bitker ◽

◽

Sheila K Patel ◽

Intissar Bittar ◽

Glenn M Eastwood ◽

...

Keyword(s):

Intensive Care Unit ◽

Acute Kidney Injury ◽

Angiotensin Converting Enzyme ◽

Kidney Injury ◽

Renin Angiotensin System ◽

Urine Collection ◽

Converting Enzyme ◽

Angiotensin System ◽

Angiotensin Converting Enzyme 2 ◽

Urine Creatinine

Objective: Angiotensin-converting enzyme 2 activity reflects non-classical renin–angiotensin system upregulation. We assessed the association of urinary angiotensin-converting enzyme 2 (uACE2) activity with acute kidney injury (AKI). Design, setting and participants: A prospective observational study in which we measured uACE2 activity in 105 critically ill patients at risk of AKI. We report AKI stage 2 or 3 at 12 hours of urine collection (AKI12h) and AKI stage 2 or 3 at any time during intensive care unit stay in patients free from any stage of AKI at inclusion (AKIICU). AKI prediction was assessed using area under the receiver-operating characteristics curve (AUROC) and net reclassification indices (NRIs). Main outcome measure: AKI stage 2 or 3 at 12 hours of urine collection. Results: Within 12 hours of inclusion, 32 of 105 patients (30%) had developed AKI12h. Corrected uACE2 activity was significantly higher in patients without AKI12h compared with those with AKI12h (median [interquartile range], 13 [6–24] v 7 [4–10] pmol/min/mL per mmol/L of urine creatinine; P < 0.01). A 10-unit increase in uACE2 was associated with a 28% decrease in AKI12h risk (odds ratio [95% CI], 0.72 [0.46–0.97]). During intensive care unit admission, 39 of 76 patients (51%) developed AKIICU. uACE2 had an AUROC for the prediction of AKI12h of 0.68 (95% CI, 0.57–0.79), and correctly reclassified 28% of patients (positive NRI) to AKI12h. Patients with uACE2 > 8.7 pmol/min/mL per mmol/L of urine creatinine had a significantly lower risk of AKIICU on log-rank analysis (52% v 84%; P < 0.01). Conclusions: Higher uACE2 activity was associated with a decreased risk of AKI stage 2 or 3. Our findings support future evaluations of the role of the non-classical renin–angiotensin system during AKI.

Download Full-text

Nephrocheck after cardiac surgery: Does it play a role in daily practice? A sequel of “Nephrocheck results should be corrected for dilution”

The International Journal of Artificial Organs ◽

10.1177/0391398819852958 ◽

2019 ◽

Vol 42 (11) ◽

pp. 665-667 ◽

Cited By ~ 2

Author(s):

Camilla L’Acqua ◽

Erminio Sisillo ◽

Luca Salvi ◽

Giovanni Introcaso ◽

Maria Luisa Biondi

Keyword(s):

Acute Kidney Injury ◽

Cardiac Surgery ◽

Kidney Injury ◽

Daily Practice ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Inclusion Criteria ◽

Ventricular Ejection Fraction ◽

Cycle Arrest ◽

Urine Creatinine

Acute kidney injury is a well-recognized complication after cardiac surgery and significantly affects morbidity and mortality. Although the mechanisms of acute kidney injury are not fully understood, Nephrocheck (Astute Medical, San Diego, CA, USA) is a meter for early detection of acute kidney injury based on bedside urinalysis of two cell-cycle arrest biomarkers. However, considerable overlap in the AKIRiskTM score of different RIFLE groups makes interpretation of the score uncertain. A possible reason for the overlap in the AKIRisk score between different RIFLE groups could be that the score is not corrected for dilution. We performed a pilot study to explore the applicability of the test in our daily practice. A total of 68 patients electively scheduled for cardiac surgery with at least two of the following inclusion criteria: age > 70 years, glomerular filtration rate <60 mL/min, left ventricular ejection fraction <41%, redo procedure and combined procedures have been enrolled in the study, and 25 of them developed acute kidney injury. We described the correlation between urine creatinine and Nephrocheck, all the samples with low Nephrocheck (<0.2) also have low urine creatinine, less than 50 mg/dL, detecting a potential diluted sample. In conclusion, in our daily practice AKIRisk score, together with an assessment of whether urine is diluted or concentrated can better discriminate between various degrees of acute kidney injury.

Download Full-text

Point of care measurement of plasma creatinine in critically ill patients with acute kidney injury

Anaesthesia ◽

10.1111/j.1365-2044.2008.05818.x ◽

2009 ◽

Vol 64 (4) ◽

pp. 403-407 ◽

Cited By ~ 28

Author(s):

A. Udy ◽

S. O’Donoghue ◽

V. D’Intini ◽

H. Healy ◽

J. Lipman

Keyword(s):

Acute Kidney Injury ◽

Critically Ill ◽

Critically Ill Patients ◽

Point Of Care ◽

Kidney Injury ◽

Plasma Creatinine

Download Full-text

Early Diabetes Aggravates Renal Ischemia/reperfusion-induced Acute Kidney Injury

10.21203/rs.3.rs-145880/v1 ◽

2021 ◽

Author(s):

Mariana de Ponte ◽

Vanessa Cardoso ◽

Juliana Costa-Pessoa ◽

Maria Oliveira-Souza

Keyword(s):

Acute Kidney Injury ◽

Risk Factor ◽

Mrna Expression ◽

Ischemia Reperfusion ◽

Kidney Tissue ◽

Kidney Injury ◽

Plasma Creatinine ◽

Ki 67 ◽

Early Diabetes ◽

The Impact

Abstract Acute kidney injury (AKI) due to ischemia and reperfusion (IR) can be associated with the progression of chronic kidney injury. In addition, studies suggest that chronic diabetes is an independent risk factor for AKI; however, the impact of early diabetes on the severity of AKI remains unknown. We investigated the effects of early diabetes on the pathophysiology of renal IR-induced AKI. C57BL/6J mice were randomly assigned into the following groups: 1) sham-operated; 2) renal IR; 3) streptozotocin (STZ - 55 mg/kg/day) and sham-operated; and 4) STZ and renal IR. On the 12th day after treatments, the animals were subjected to bilateral IR for 30 minutes followed by reperfusion for 48 hours, and the mice were euthanized by exsanguination. Renal function was assessed by analyzing the plasma creatinine and urea concentrations with biochemical methods. Proteinuria was evaluated using a commercial kit. Kidney tissue was used to evaluate the morphology, gene expression by qPCR, and protein expression by Western blotting. Compared to the sham operated, renal IR resulted in increased plasma creatinine and urea levels, decreased nephrin mRNA expression, increased tubular cast formation, and Kim-1, Ki-67, pro-inflammatory and pro-fibrotic factor mRNA expression. Compared with the sham treatment, STZ treatment resulted in hyperglycemia, but did not induce changes in kidney function or pro-inflammatory or pro-fibrotic factors. However, STZ treatment aggravated renal IR-induced AKI by exacerbating glomerular and tubular injury, inflammation, and the profibrotic response. Early diabetes constitutes a relevant risk factor for renal IR-induced AKI.

Download Full-text

Plasma creatinine below limit of quantification in a patient with acute kidney injury

Clinica Chimica Acta ◽

10.1016/j.cca.2021.12.001 ◽

2022 ◽

Vol 524 ◽

pp. 101-105

Author(s):

Arthur Orieux ◽

Julien Brunier ◽

Claire Rigothier ◽

Benoit Pinson ◽

Sandrine Dabernat ◽

...

Keyword(s):

Acute Kidney Injury ◽

Kidney Injury ◽

Plasma Creatinine ◽

Limit Of Quantification

Download Full-text

A Simple Method to Detect Recovery of Glomerular Filtration Rate following Acute Kidney Injury

BioMed Research International ◽

10.1155/2014/542069 ◽

2014 ◽

Vol 2014 ◽

pp. 1-8 ◽

Cited By ~ 6

Author(s):

John W. Pickering ◽

John Mellas

Keyword(s):

Acute Kidney Injury ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Filtration Rate ◽

Kidney Injury ◽

Plasma Creatinine ◽

Creatinine Concentration ◽

Simple Method ◽

Creatinine Excretion ◽

Excretion Rates

In acute kidney injury (AKI), elevated plasma creatinine is diagnostic of an earlier loss of glomerular filtration rate (GFR) but not of the concomitant GFR. Only subsequent creatinine changes will inform if GFR had already recovered or not. We hypothesized that the creatinine excretion rate to production rate ratio would provide this information. A retrospective analysis of 482 critically ill patients from two intensive care units (ICU) is shown. Plasma creatinine was measured on ICU entry and 12 hours later. Four-hour creatinine excretion rates (E) were measured on entry. Creatinine production rates were estimated (eG). The ability of the ratioE/eGto predict a decrease in plasma creatinine concentration, identify recovered AKI (≥0.3 mg/dL decrease), and predict AKI (≥0.3 mg/dL increase) was assessed by the area under the receiver operator characteristic curves (AUC). There was a linear relationship between reduced creatinine concentration andE/eG(r2=0.15;P<0.0001).E/eGpredicted a decrease in creatinine (AUC 0.70 (0.65 to 0.74)), identified recovered AKI (0.75 (0.67 to 0.84)), and predicted AKI (0.80 (0.73 to 0.86)). A ratio of the rates of creatinine excretion to estimated production much less than 1 indicated a concomitant GFR below baseline, whereas a ratio much more than 1 indicated a recovering or recovered GFR.

Download Full-text

Urinary Mitochondrial DNA Identifies Renal Dysfunction and Mitochondrial Damage in Sepsis-Induced Acute Kidney Injury

Oxidative Medicine and Cellular Longevity ◽

10.1155/2018/8074936 ◽

2018 ◽

Vol 2018 ◽

pp. 1-14 ◽

Cited By ~ 16

Author(s):

Qiongyuan Hu ◽

Jianan Ren ◽

Huajian Ren ◽

Jie Wu ◽

Xiuwen Wu ◽

...

Keyword(s):

Acute Kidney Injury ◽

Mitochondrial Dna ◽

Mitochondrial Dysfunction ◽

Renal Dysfunction ◽

Renal Injury ◽

Cecal Ligation ◽

Surrogate Marker ◽

Kidney Injury ◽

Plasma Creatinine ◽

Acute Renal Dysfunction

Background. Recent animal studies have shown that mitochondrial dysfunction initiates and accelerates renal injury in sepsis, but its role in sepsis remains unknown. Mitochondrial stress or dying cells can lead to fragmentation of the mitochondrial genome, which is considered a surrogate marker of mitochondrial dysfunction. Therefore, we evaluated the efficiency of urinary mitochondrial DNA (UmtDNA) as a marker of renal dysfunction during sepsis-induced acute kidney injury (AKI). Methods. We isolated DNA from plasma and urine of patients. mtDNA levels were quantified by quantitative PCR. Sepsis patients were divided into no AKI, mild AKI, and severe AKI groups according to RIFLE criteria. Additionally, cecal ligation and puncture (CLP) was established in rats to evaluate the association between UmtDNA and mitochondrial function. Results. A total of 52 (49.5%) developed AKI among enrolled sepsis patients. Increased systemic mtDNA did not correlate with systemic inflammation or acute renal dysfunction in sepsis patients, while AKI did not have an additional effect on circulating mtDNA levels. In contrast, UmtDNA was significantly enriched in severe AKI patients compared with that in the mild AKI or no AKI group, positively correlated with plasma creatinine, urinary neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1, and inversely with the estimated glomerular filtration rate. Additionally, UmtDNA increased in rats following CLP-induced sepsis. UmtDNA was predictive of AKI development and correlated with plasma creatinine and blood urea nitrogen in the rat sepsis model. Finally, the UmtDNA level was inversely correlated with the cortical mtDNA copy number and relative expression of mitochondrial gene in the kidney. Conclusion. An elevated UmtDNA level correlates with mitochondrial dysfunction and renal injury in sepsis patients, indicating renal mitochondrial injury induced by sepsis. Therefore, UmtDNA may be regarded as a valuable biomarker for the occurrence of AKI and the development of mitochondria-targeted therapies following sepsis-induced AKI.

Download Full-text