scholarly journals Terlipressin Attenuates Hemorrhagic Shock-Induced Acute Kidney Injury in Rats

2022 ◽  
Author(s):  
Leticia Urbano Cardoso Castro ◽  
Denise Aya Otsuki ◽  
Talita Rojas Sanches ◽  
Felipe Lima Souza ◽  
Mirela Aparecida Rodrigues Santinho ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Body Weight ◽  
Hemorrhagic Shock ◽  
Fluid Resuscitation ◽  
Kidney Injury ◽  
Fractional Excretion ◽  
Organ Damage ◽  
Receptor Expression ◽  
Control Group ◽  
Fractional Excretion Of Sodium

Abstract Hemorrhagic shock (HS), a major cause of trauma-related mortality, is mainly treated by crystalloid fluid administration, typically with lactated Ringer’s (LR). Despite beneficial hemodynamic effects, such as the restoration of mean arterial pressure (MAP), LR administration has major side effects, including organ damage due to edema. One strategy to avoid such effects is pre-hospitalization intravenous administration of the potent vasoconstrictor terlipressin, which can restore hemodynamic stability/homeostasis and has anti-inflammatory effects. Wistar rats were subjected to HS for 60 min, at a target MAP of 30–40 mmHg, thereafter being allocated to receive LR infusion at 3 times the volume of the blood withdrawn; at 2 times the volume, plus terlipressin (10 µg/100 g body weight); and at an equal volume, plus terlipressin (10 µg/100 g body weight). A control group comprised rats not subjected to HS and receiving no fluid resuscitation or treatment. At 15 min after fluid resuscitation/treatment, the blood previously withdrawn was reinfused. At 24 h after HS, MAP was higher among the terlipressin-treated animals. Terlipressin also improved post-HS survival and provided significant improvements in glomerular/tubular function (creatinine clearance), neutrophil gelatinase-associated lipocalin expression, fractional excretion of sodium, aquaporin 2 expression, tubular injury, macrophage infiltration, IL-6 levels, IL-18 levels, and NF-κB expression. In terlipressin-treated animals, there was also significantly higher ANG II type 1 receptor expression and normalization of AVP 1a receptor expression. Terlipressin could be a viable therapy for HS-induced acute kidney injury, likely attenuating such injury by modulating the inflammatory response via the AVP 1a receptor.

Fractional excretion of sodium or urea as prognostic indicators for acute kidney injury in the emergency department

2021 ◽  
Vol 29 (1) ◽  
pp. 82-84
Author(s):  
Gregor Lindner ◽  
Adrian Wolfensberger ◽  
Aristomenis K. Exadaktylos ◽  
Christoph Schwarz ◽  
Georg-Christian Funk ◽  
...  
Keyword(s):  
Emergency Department ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Fractional Excretion ◽  
Prognostic Indicators ◽  
Fractional Excretion Of Sodium

Clinical approach to the patient with acute kidney injury

2018 ◽  
Author(s):  
Norbert Lameire ◽  
Raymond Vanholder ◽  
Wim Van Biesen
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Urinary Tract ◽  
Physical Examination ◽  
Kidney Injury ◽  
Fractional Excretion ◽  
Clinical Approach ◽  
Volume Depletion ◽  
Number Of Patients ◽  
Fractional Excretion Of Sodium

The prognosis of acute kidney injury (AKI) depends on early diagnosis and therapy. A multitude of causes are classified according to their origin as prerenal, intrinsic (intrarenal), and post-renal.Prerenal AKI means a loss of renal function despite intact nephrons, for example, because of volume depletion and/or hypotension.There is a broad spectrum of intrinsic causes of AKI including acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. Evaluation includes careful review of the patient’s history, physical examination, urinalysis, selected urine chemistries, imaging of the urinary tree, and eventual kidney biopsy. The history should focus on the tempo of loss of function (if known), associated systemic diseases, and symptoms related to the urinary tract (especially those that suggest obstruction). In addition, a review of the medications looking for potentially nephrotoxic drugs is essential. The physical examination is directed towards the identification of findings of a systemic disease and a detailed assessment of the patient’s haemodynamic status. This latter goal may require invasive monitoring, especially in the oliguric patient with conflicting clinical findings, where the physical examination has limited accuracy.Excluding urinary tract obstruction is necessary in all cases and may be established easily by renal ultrasound.Distinction between the two most common causes of AKI (prerenal AKI and ATN) is sometimes difficult, especially because the clinical examination is often misleading in the setting of mild volume depletion or overload. Urinary chemistries, like calculation of the fractional excretion of sodium (FENa), may be used to help in this distinction. In contrast to FENa, the fractional excretion of urea has the advantage of being rather independent of diuretic therapy. Response to fluid repletion is still regarded as the gold standard in the differentiation between prerenal and intrinsic AKI. Return of renal function to baseline or resuming of diuresis within 24 to 72 hours is considered to indicate ‘transient, mostly prerenal AKI’, whereas persistent renal failure usually indicates intrinsic disease. Transient AKI may, however, also occur in short-lived ATN. Furthermore, rapid fluid application is contraindicated in a substantial number of patients, such as those with congestive heart failure.‘Muddy brown’ casts and/or tubular epithelial cell casts in the urine sediment are typically seen in patients with ATN. Their presence is an important tool in the distinction between ATN and prerenal AKI, which is characterized by a normal sediment, or by occasional hyaline casts. There is a possible role for new serum and/or urinary biomarkers in the diagnosis and prognosis of the patient with AKI, including the differential diagnosis between pre-renal AKI and ATN. Further studies are needed before their routine determination can be recommended.When a diagnosis cannot be made with reasonable certainty through this evaluation, renal biopsy should be considered; when intrarenal causes such as crescentic glomerulonephritis or vasculitis are suspected, immediate biopsy to avoid delay in the initiation of therapy is mandatory.

scholarly journals Assessment of Urinary Kidney Injury Molecule-1 as an Indicator of Early Renal Insult in Children with Cystic Fibrosis

2020 ◽  
Vol 8 (B) ◽  
pp. 262-267
Author(s):  
Walaa Shahin ◽  
Ahmed Bader ◽  
Rawdah Ahmed ◽  
Mona Alattar ◽  
Mona Alfalaki ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Urine Analysis ◽  
Kidney Injury ◽  
Fractional Excretion ◽  
Control Group ◽  
Renal Ultrasound ◽  
Fractional Excretion Of Sodium ◽  
Beta 2 ◽  
Renal Tubular ◽  
Kidney Injury Molecule 1

BACKGROUND: The risk of acute kidney injury in cystic fibrosis (CF) patients is due to renal tubular affection by CFTR gene. AIM: Our study aimed at early detection of renal impairment in CF patients, to enable careful monitoring and adjustment of nephrotoxic medications. METHODS: Fifty patients with CF were enrolled in our study; they were age- and sex-matched to 40 healthy control children. All subjects were screened by urine analysis, measurements of kidney function tests, fractional excretion of sodium, β2-microglobulin (beta-2-M) excretion, and renal ultrasound examination. Urinary kidney injury molecule-1 (KIM-1) was assayed using ELISA technique. RESULTS: Both urinary beta-2-M and KIM-1 concentrations were significantly higher in CF patients compared to the control group (p < 0.001). The duration of the disease was significantly positively correlated with the urinary beta-2-M and KIM-1 levels (r = 0.6 and 0.7, respectively; p < 0.01). CONCLUSIONS: Our results showed that urinary KIM-1 can be considered as a sensitive early indicator of acute renal injury.

Comparative Study between Fractional Excretion of Sodium and Fractional Excretion of Urea in Differentiating Prerenal From Renal Acute Kidney Injury in ICU Patients with Circulatory Shock

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
S W N Sargious ◽  
M H M Hassan ◽  
S A R Mostafa ◽  
G S R Saad
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Fractional Excretion ◽  
Multiple Organ ◽  
Circulatory Shock ◽  
University Hospital ◽  
Shock State ◽  
Mild Renal Impairment ◽  
Fractional Excretion Of Sodium ◽  
Point Calculation

Abstract Background The incidence of acute renal injury (AKI) in ICU is 5%. The mortality rate increases up to 50% if AKI is a part of multiple organ dysfunction syndrome. Aim of the Work Comparison between FENa and FEurea in differentiating renal from prerenal acute kidney injury in circulatory shock, and the effect of diuretics on their handling. Patients and Methods This retrospective study was conducted on 45 Egyptian patients with AKI complicating circulatory shock admitted to the ICUs of AIN SHAMS University Hospital, from August 2018 to February 2019. Consents were taken from all of them according to the local ethics committee approval. Results The cutoff points of both FENa and FEurea as a predictor of mortality were not statistically justified. This is explained as all our patients had circulatory shock, and so patients with mild renal impairment may die from their severe shock state, and patients with severe renal affection may survive if their shock could be rapidly corrected. This cutoff point calculation is recommended only in patients with AKI without other organ affections or shock that may affect the mortality. Conclusion Although both fractional excretion of urea (FEurea) and fractional excretion of sodium (FENa) are feasible, reproducible, and inexpensive markers used in differentiating renal from prerenal azotemia, in our study FEurea showed higher sensitivity and specificity than FENa, not only in differentiating renal from prerenal azotemia in critically ill patients complicating circulatory shock, but also its values were not affected by the use of diuretics like FENa in the same group of patients.

scholarly journals Urinary output and fractional excretion of sodium and urea as indicators of transient versus intrinsic acute kidney injury during early sepsis

Critical Care ◽  
2013 ◽  
Vol 17 (5) ◽  
pp. R234 ◽  
Author(s):  
Jill Vanmassenhove ◽  
Griet Glorieux ◽  
Eric Hoste ◽  
Annemieke Dhondt ◽  
Raymond Vanholder ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Fractional Excretion ◽  
Urinary Output ◽  
Fractional Excretion Of Sodium ◽  
Early Sepsis

scholarly journals 5-aminoisoquinoline improves renal function and fibrosis during recovery phase of cisplatin-induced acute kidney injury in rats

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Andrés Quesada ◽  
Francisco O’Valle ◽  
Sebastián Montoro-Molina ◽  
Mercedes Gómez-Morales ◽  
Mercedes Caba-Molina ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Body Weight ◽  
Renal Dysfunction ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Kidney Injury ◽  
Body Weight Loss ◽  
Recovery Phase ◽  
The Body ◽  
Control Group

The aim of the present study is to analyze the effects of 5-aminoisoquinoline (5-AIQ), a poly(ADP-ribose) polymerase-1 (PARP1) inhibitor, over renal dysfunction and fibrosis during recovery phase of cisplatin (CisPt)-induced acute kidney injury (AKI) in rats. Male Wistar rats were distributed in three groups (n=8 each group): control, CisPt, and CisPt + 5-AIQ. Control and CisPt groups received a subcutaneous injection of either saline or 7 mg/kg CisPt, respectively. CisPt + 5-AIQ group received two intraperitoneal injections of 10 mg/kg 5-AIQ 2 h before and 24 h after CisPt treatment. Thirteen days after the treatment, rats were housed in metabolic cages and 24-h urine collection was made. At day 14, CisPt-treated rats showed increased diuresis, N-acetyl-β-d-glucosaminidase (NAG) excretion, glucosuria and sodium fractional excretion (NaFE), and decreased creatinine clearance (CrCl). 5-AIQ significantly increased CrCl and decreased NAG excretion, glucosuria, and NaFE. In plasma, CisPt increased sodium, urea, and creatinine concentrations, while 5-AIQ treatment decreased these variables to the levels of control group. 5-AIQ completely prevented the body weight loss evoked by CisPt treatment. CisPt also induced an increased renal expression of PAR polymer, α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), and collagen-IV. These variables were decreased in CisPt + 5-AIQ group. Tubular lesions and renal fibrosis were also decreased by 5-AIQ treatment. We conclude that inhibition of PARP1 with 5-AIQ can attenuate long-term nephrotoxic effects associated with the CisPt treatment, preventing renal dysfunction and body weight decrease and ameliorating tubular lesions and collagen deposition.

scholarly journals Anticoagulant Related Nephropathy Induced by Dabigatran

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Nazia Sharfuddin ◽  
Mahra Nourbakhsh ◽  
Alan Box ◽  
Hallgrimur Benediktsson ◽  
Daniel A. Muruve
Keyword(s):  
Acute Kidney Injury ◽  
Iga Nephropathy ◽  
Kidney Injury ◽  
Volume Overload ◽  
Fractional Excretion ◽  
Bleeding Risk ◽  
Renal Ultrasound ◽  
Nonvalvular Atrial Fibrillation ◽  
Fractional Excretion Of Sodium ◽  
Ultrasound Findings

We describe a case of biopsy-proven dabigatran related nephropathy in a patient without underlying IgA nephropathy. To date, dabigatran related nephropathy was only reported in patients with concurrent or undiagnosed IgA nephropathy, suggesting that it may predispose patients to dabigatran associated injury. The patient is an 81-year-old woman with multiple medical comorbidities, including nonvalvular atrial fibrillation, who was anticoagulated with dabigatran. She presented to hospital with acute kidney injury in the setting of volume overload. Her estimated glomerular filtration rate decreased from a baseline of 57 mL/min/1.73 m2 to 4 mL/min/1.73 m2, necessitating hemodialysis. Renal ultrasound findings, fractional excretion of sodium, and urinalysis suggested acute kidney injury. Renal biopsy showed acute tubular injury, tubular red blood cell casts, and an absence of active glomerulonephritis, similar to the pathological findings of warfarin related nephropathy. A diagnosis of anticoagulant related nephropathy secondary to dabigatran was therefore established. This case demonstrates that dabigatran, like warfarin, may increase tubular bleeding risk in patients, irrespective of underlying kidney or glomerular disease.

scholarly journals A Metabolic Profiling Study of Realgar-Induced Acute Kidney Injury in Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Sheng Zhang ◽  
Chao Li ◽  
Tingting Feng ◽  
Shuai Cao ◽  
Heng Zhou ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Body Weight ◽  
Correlation Analysis ◽  
Metabolic Profiling ◽  
Kidney Injury ◽  
Control Group ◽  
Dependent Manner ◽  
Kidney Weight ◽  
Dose Dependent ◽  
Metabolomic Approach

Realgar has been used as a type of mineral drug that contains arsenic for thousands of years. Previous studies have shown that Realgar-induced acute kidney injury is associated with abnormal metabolism, but the underlying mechanism is poorly understood. The aim of this study is to investigate the metabolic changes in serum and kidney tissues of mice exposed to Realgar by using a metabolomic approach and explore the molecular mechanisms of acute kidney injury induced by Realgar. Forty mice were randomly divided into four groups: Control group, 0.5-, 1.0, and 2.0 g/kg Realgar group. After 1 week, the body weight and kidney weight of the mice were measured. The serum and kidney samples were used for LC-MS spectroscopic metabolic profiling. Principal component analysis (PCA), correlation analysis, and pathway analysis were used to detect the nephrotoxic effects of Realgar. Body weight decreased significantly in the 2.0 g/kg group, and the kidney weight index also showed a dose-dependent increase in Realgar. The PCA score plot showed the serum and kidney tissue metabolic profile of mice exposed to 2.0 g/kg Realgar separated from the control group, while the lower-doses of 0.5 g/kg and 1.0 g/kg Realgar shown a similar view to the Control group. Thirty-three metabolites and seventeen metabolites were screened and identified in the serum and kidney of mice in a dose-dependent manner. respectively. Correlation analysis showed a strong correlation among these metabolites. Amino acid metabolism, lipid metabolism, glutathione metabolism, and purine metabolism pathways were found to be mainly associated with Realgar nephrotoxicity. This work illustrated the metabolic alterations in Realgar-induced nephrotoxic mice through a metabolomic approach.

scholarly journals Volume Management in the Critically Ill Patient with Acute Kidney Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Mary Labib ◽  
Raeesa Khalid ◽  
Akram Khan ◽  
Supriya Khan
Keyword(s):  
Acute Kidney Injury ◽  
Fluid Management ◽  
Kidney Injury ◽  
Volume Overload ◽  
Fractional Excretion ◽  
Current Evidence ◽  
Critically Ill Patient ◽  
Negative Effects ◽  
Volume Depletion ◽  
Fractional Excretion Of Sodium

Acute kidney injury (AKI) frequently occurs in the setting of critical illness and its management poses a challenge for the intensivist. Optimal management of volume status is critical in the setting of AKI in the ICU patient. The use of urine sodium, the fractional excretion of sodium (FeNa), and the fractional excretion of urea (FeUrea) are common clinical tools used to help guide fluid management especially further volume expansion but should be used in the context of the patient’s overall clinical scenario as they are not completely sensitive or specific for the finding of volume depletion and can be misleading. In the case of oliguric or anuric AKI, diuretics are often utilized to increase the urine output although current evidence suggests that they are best reserved for the treatment of volume overload and hyperkalemia in patients who are likely to respond to them. Management of volume overload in ICU patients with AKI is especially important as volume overload has several negative effects on organ function and overall morbidity and mortality.

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