scholarly journals Furosemide reverses medullary tissue hypoxia in ovine septic acute kidney injury

2019 ◽  
Vol 317 (2) ◽  
pp. R232-R239 ◽  
Author(s):  
Naoya Iguchi ◽  
Yugeesh R. Lankadeva ◽  
Trevor A. Mori ◽  
Eduardo A. Osawa ◽  
Salvatore L. Cutuli ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Oxygen Consumption ◽  
Oxygen Delivery ◽  
Rapid Development ◽  
Kidney Injury ◽  
Experimental Sepsis ◽  
Thick Ascending Limb ◽  
Medullary Tissue ◽  
Fractional Excretion Of Sodium ◽  
Renal Oxygen

In experimental sepsis, the rapid development of renal medullary hypoxia precedes the development of acute kidney injury (AKI) and may contribute to its pathogenesis. We investigated whether inhibiting active sodium transport and oxygen consumption in the medullary thick ascending limb with furosemide attenuates the medullary hypoxia in experimental septic AKI. Sheep were instrumented with flow probes on the pulmonary and renal arteries and fiber optic probes to measure renal cortical and medullary perfusion and oxygen tension (Po2). Sepsis and AKI were induced by infusion of live Escherichia coli. At 24 h of sepsis there were significant decreases in renal medullary tissue perfusion (1,332 ± 233 to 698 ± 159 blood perfusion units) and Po2 (44 ± 6 to 19 ± 6 mmHg) (both P < 0.05). By 5 min after intravenous administration of furosemide (20 mg), renal medullary Po2 increased to 43 ± 6 mmHg and remained at this normal level for 8 h. Furosemide caused transient increases in fractional excretion of sodium and creatinine clearance, but medullary perfusion, renal blood flow, and renal oxygen delivery were unchanged. Urinary F2-isoprostanes, an index of oxidative stress, were not significantly changed at 24 h of sepsis but tended to transiently decrease after furosemide treatment. In septic AKI, furosemide rapidly restored medullary Po2 to preseptic levels. This effect was not accompanied by changes in medullary perfusion or renal oxygen delivery but was accompanied by a transient increase in fractional sodium excretion, implying decreased oxygen consumption as a mechanism.

scholarly journals Renal Tubular Cell Mitochondrial Dysfunction Occurs Despite Preserved Renal Oxygen Delivery in Experimental Septic Acute Kidney Injury

2018 ◽  
Vol 46 (4) ◽  
pp. e318-e325 ◽  
Author(s):  
Nishkantha Arulkumaran ◽  
Sean Pollen ◽  
Elisabetta Greco ◽  
Holly Courtneidge ◽  
Andrew M. Hall ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Mitochondrial Dysfunction ◽  
Oxygen Delivery ◽  
Kidney Injury ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Septic Acute Kidney Injury ◽  
Renal Tubular ◽  
Renal Oxygen

scholarly journals The Relevance of Renal Oxygen Saturation Over Other Markers in Cardiac Surgery–Associated Acute Kidney Injury

2019 ◽  
Vol 33 (10) ◽  
pp. 2622-2623 ◽  
Author(s):  
Christian Ortega-Loubon ◽  
Manuel Fernández-Molina ◽  
Pablo Jorge-Monjas ◽  
Inmaculada Fierro ◽  
Gonzalo Herrera-Calvo ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Oxygen Saturation ◽  
Kidney Injury ◽  
Renal Oxygen

scholarly journals Time–dose response of oxygen delivery during cardiopulmonary bypass predicts acute kidney injury

2019 ◽  
Vol 158 (2) ◽  
pp. 492-499 ◽  
Author(s):  
Hiroshi Mukaida ◽  
Satoshi Matsushita ◽  
Kenji Kuwaki ◽  
Takahiro Inotani ◽  
Yuki Minami ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiopulmonary Bypass ◽  
Dose Response ◽  
Oxygen Delivery ◽  
Kidney Injury ◽  
Time Dose

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

scholarly journals Duration of critically low oxygen delivery is associated with acute kidney injury after cardiac surgery

2019 ◽  
Vol 63 (10) ◽  
pp. 1290-1297 ◽  
Author(s):  
Sebastian R. Rasmussen ◽  
Kristian Kandler ◽  
Rikke V. Nielsen ◽  
Peter Cornelius Jakobsen ◽  
Nikoline N. Knudsen ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Oxygen Delivery ◽  
Kidney Injury ◽  
Low Oxygen

scholarly journals Comparison of serum creatinine and serum cystatin C as biomarkers to detect sepsis-induced acute kidney injury and to predict mortality in CD-1 mice

2014 ◽  
Vol 307 (8) ◽  
pp. F939-F948 ◽  
Author(s):  
Asada Leelahavanichkul ◽  
Ana Carolina P. Souza ◽  
Jonathan M. Street ◽  
Victor Hsu ◽  
Takayuki Tsuji ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Cystatin C ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Organ Damage ◽  
Experimental Sepsis ◽  
Sepsis Mortality ◽  
Serum Cystatin C ◽  
Serum Cystatin

Acute kidney injury (AKI) dramatically increases sepsis mortality, but AKI diagnosis is delayed when based on serum creatinine (SCr) changes, due in part, to decreased creatinine production. During experimental sepsis, we compared serum cystatin C (sCysC), SCr, and blood urea nitrogen (BUN) to inulin glomerular filtration rate (iGFR) before or 3–18 h after cecal ligation and puncture (CLP)-induced sepsis in CD-1 mice. sCysC had a faster increase and reached peak levels more rapidly than SCr in both sepsis and bilateral nephrectomy (BiNx) models. sCysC was a better surrogate of iGFR than SCr during sepsis. Combining sCysC with SCr values into a composite biomarker improved correlation with iGFR better than any biomarker alone or any other combination. We determined the renal contribution to sCysC handling with BiNx. sCysC and SCr were lower post-BiNx/CLP than post-BiNx alone, despite increased inflammatory and nonrenal organ damage biomarkers. Sepsis decreased CysC production in nephrectomized mice without changing body weight or CysC space. Sepsis decreased sCysC production and increased nonrenal clearance, similar to effects of sepsis on SCr. sCysC, SCr, and BUN were measured 6 h postsepsis to link AKI with mortality. Mice with above-median sCysC, BUN, or SCr values 6 h postsepsis died earlier than mice with below-median values, corresponding to a substantial AKI association with sepsis mortality in this model. sCysC performs similarly to SCr in classifying mice at risk for early mortality. We conclude that sCysC detects AKI early and better reflects iGFR in CLP-induced sepsis. This study shows that renal biomarkers need to be evaluated in specific contexts.

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 PPARαcontributes to protection against metabolic and inflammatory derangements associated with acute kidney injury in experimental sepsis

2019 ◽  
Vol 7 (10) ◽  
pp. e14078 ◽  
Author(s):  
Takuma Iwaki ◽  
Brock G. Bennion ◽  
Erin K. Stenson ◽  
Jared C. Lynn ◽  
Cynthia Otinga ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Experimental Sepsis
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