scholarly journals Intravenous Fluids and Acute Kidney Injury

2017 ◽  
Vol 43 (1-3) ◽  
pp. 163-172 ◽  
Author(s):  
Xiaoqiang Ding ◽  
Zhen Cheng ◽  
Qi Qian

Over 50% of the human body is comprised of fluids that are distributed in defined compartments. Although compartmentalized, these fluids are dynamically connected. Fluids, electrolytes, and acid-base balance in each compartment are tightly regulated, mostly in an energy-dependent manner to achieve their designed functions. For over a century, our understanding of the microvascular fluid homeostasis has evolved from hypothesized Ernest Starling principle to evidence-based and the revised Starling principle, incorporating the functional endothelial surface layer. The kidney is a highly vascular and encapsulated organ that is exquisitely sensitive to inadequate (insufficient or excess) blood flow. The kidney is particularly sensitive to venous congestion, and studies show that reduced venous return triggers a greater degree of kidney damage than that from lacking arterial flow. Thus, fluid overload can induce severe and sustained kidney injury. In the setting of established acute kidney injury, fluid management can be challenging. Impaired capacity of urine output and urine concentration and dilution should be taken into consideration when designing fluid therapy. Video Journal Club ‘Cappuccino with Claudio Ronco' at http://www.karger.com/?doi=452702.

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Marios Papasotiriou ◽  
Adamantia Mpratsiakou ◽  
Georgia Georgopoulou ◽  
Lamprini Balta ◽  
Paraskevi Pavlakou ◽  
...  

Abstract Background and Aims Crystalline solutions, such as normal saline 0.9% (N/S 0.9%) and Ringer's Lactate (L/R), are readily administered for increasing plasma volume. Despite the utility of administering N/S 0.9% to hypovolemic patients, the dose of 154 mmol of sodium (Na) contained in 1 L exceeds the recommended daily dose increasing the risk of sodium overload and hyperchloremic metabolic acidosis. In contrast, L/R solution has the advantage of lower Na content, significantly less chlorine and contains lactates which may be advantageous in patients with significant acidemia such as patients with acute kidney injury (AKI) and chronic kidney disease (CKD). The aim of the present study is to investigate the safety and efficacy of administration of L/R versus N/S 0.9% in patients with prerenal AKI and established CKD. Method The study included adult patients with known CKD stage II to V without need for dialysis, with prerenal AKI (AKIN Stage I to III Criteria). Patients with other forms of AKI as well as hypervolemia, heart congestion or hyperkalemia (serum K>5.5 meq/l) were excluded from the study. Patients were randomized in 1:1 ratio to receive intravenously either N/S 0.9% or L/R solution at a dose of 20 ml/kg body weight/day. We studied kidney function (eGFR: CKD-EPI) and response to treatment at discharge and at 30 days after discharge, duration of hospitalization, improvement in serum bicarbonate levels (HCO3), acid-base balance, serum potassium levels and the need for dialysis. Results The study included 26 patients (17 males) with a mean age of 59.1 ± 16.1 years. Thirteen patients received treatment with N/S 0.9% and the rest with L/R solution. Baseline demographic and clinical characteristics at hospital admission and historical data did not show any significant differences in both groups of patients. Renal function at the onset of AKI did not show significant differences between the two groups (16.4 ± 5.8 vs 16.9 ± 5.7 ml/min/1.73 m2, p=ns, treatment with N/S and L/R respectively). The mean volume of solutions received by the two groups (N/S 0.9% 1119 ± 374 vs L/R 1338 ± 364 ml/day, p=ns) as well as the mean total volume of liquids received per day, did not differ significantly (2888 ± 821 vs 3069 ± 728 ml/d, p=ns). Patients treated with L/R were discharged 1 day earlier than patients treated with N/S (5.2 ± 3.2 vs 6.2 ± 4.9 days of hospitalization, p=ns). Renal function improvement during hospitalization and 30 days after discharge did not differ significantly between the two groups. Patients that received L/R showed a higher increase in plasma HCO3 (ΔHCO3) concentration at discharge than those that received N/S 0.9% (4.9 ± 4.1 vs 2.46 ± 3.7 meq/l, p=ns) and pH increase (ΔpH) was slightly higher in those that received L/R solution (0.052 ± 0.066 vs 0.023 ± 0.071, p=ns). Patients treated with N/S 0.9% showed a greater decrease in serum potassium (ΔK) at discharge compared to those treated with L/R (-0.39 ± 1.03 vs -0.17 ± 0.43 meq/l, p=ns, respectively). No patient received acute dialysis treatment. Conclusion Administration of L/R solution as a hydration treatment to patients with prerenal AKI and established CKD is not inferior concerning safety and efficacy to N/S 0.9% solution. In addition, L/R administration seems to marginally improve acid-base balance in this specific group of patients.


2012 ◽  
Vol 302 (11) ◽  
pp. C1569-C1587 ◽  
Author(s):  
Adriana C. C. Girardi ◽  
Francesca Di Sole

The Na+/H+ exchanger-3 (NHE3) belongs to the mammalian NHE protein family and catalyzes the electro-neutral exchange of extracellular sodium for intracellular proton across cellular membranes. Its transport function is of essential importance for the maintenance of the body's salt and water homeostasis as well as acid-base balance. Indeed, NHE3 activity is finely regulated by a variety of stimuli, both acutely and chronically, and its transport function is fundamental for a multiplicity of severe and world-wide infection-pathological conditions. This review aims to provide a concise overview of NHE3 physiology and discusses the role of NHE3 in clinical conditions of prominent importance, specifically in hypertension, diabetic nephropathy, heart failure, acute kidney injury, and diarrhea. Study of NHE3 function in models of these diseases has contributed to the deciphering of mechanisms that control the delicate ion balance disrupted in these disorders. The majority of the findings indicate that NHE3 transport function is activated before the onset of hypertension and inhibited thereafter; NHE3 transport function is also upregulated in diabetic nephropathy and heart failure, while it is reported to be downregulated in acute kidney injury and in diarrhea. The molecular mechanisms activated during these pathological conditions to regulate NHE3 transport function are examined with the aim of linking NHE3 dysfunction to the analyzed clinical disorders.


2016 ◽  
Vol 37 (2) ◽  
pp. 277-288 ◽  
Author(s):  
Paul D. Weyker ◽  
Xosé L. Pérez ◽  
Kathleen D. Liu

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Lei Lei ◽  
Liangping Li ◽  
Hu Zhang

Liver cirrhosis is a common progressive and chronic clinical liver disease. Due to the strong compensation ability of the liver, no obvious symptoms develop in the early stage. However, multiple systems are involved in decompensation of the liver. Acute kidney injury (AKI) is one of the most serious complications, characterized by a sharp drop in the glomerular filtration rate (GFR); a rapid increase in Scr and BUN, as well as sodium and water storage; and a disturbance of acid-base balance. The mortality rate is high, and the prognosis is very poor. Thus, it is important to make a definite diagnosis and initiate treatment in the early stage to decrease mortality and improve the prognosis. Although diagnosing liver cirrhosis with serum creatinine has many shortcomings, a dynamic change in this marker is still the main diagnostic criterion for AKI. Identifying new markers of kidney injury with clinical value has also become an increasing focus of research. In this text, we review recent changes regarding categorization of AKI diagnostic criteria as well as new markers of AKI and treatments for cirrhosis-related AKI.


2008 ◽  
Vol 31 (2) ◽  
pp. 96-110 ◽  
Author(s):  
J. A. Kellum ◽  
J. Cerda ◽  
L. J. Kaplan ◽  
M. K. Nadim ◽  
P. M. Palevsky

Fluids are the only known method of attenuating renal injury. Furthermore, whether for hydration, resuscitation or renal replacement therapy, fluid prescriptions must be tailored to the fluid and electrolyte, cardiovascular status and residual renal function of the patient. Different fluids have significantly different effects both on volume expansion as well as on the electrolyte and acid-base balance; while controversial, different fluids may even influence renal function differently. This systematic review focuses on fluids for prevention and management of acute kidney injury. We have reviewed the available evidence and have made recommendations for clinical practice and future studies.


2017 ◽  
Vol 44 (2) ◽  
pp. 140-155 ◽  
Author(s):  
William R. Clark ◽  
Martine Leblanc ◽  
Zaccaria Ricci ◽  
Claudio Ronco

Background/Aims: Delivered dialysis therapy is routinely measured in the management of patients with end-stage renal disease; yet, the quantification of renal replacement prescription and delivery in acute kidney injury (AKI) is less established. While continuous renal replacement therapy (CRRT) is widely understood to have greater solute clearance capabilities relative to intermittent therapies, neither urea nor any other solute is specifically employed for CRRT dose assessments in clinical practice at present. Instead, the normalized effluent rate is the gold standard for CRRT dosing, although this parameter does not provide an accurate estimation of actual solute clearance for different modalities. Methods: Because this situation has created confusion among clinicians, we reappraise dose prescription and delivery for CRRT. Results: A critical review of RRT quantification in AKI is provided. Conclusion: We propose an adaptation of a maintenance dialysis parameter (standard Kt/V) as a benchmark to supplement effluent-based dosing of CRRT. Video Journal Club “Cappuccino with Claudio Ronco” at http://www.karger.com/?doi=475457


Author(s):  
Maura Scott ◽  
Grace McCall

Acute kidney injury (AKI) is under-recognised in children and neonates. It is associated with increased mortality and morbidity along with an increased incidence of chronic kidney disease in adulthood. It is important that paediatricians are able to recognise AKI quickly, enabling prompt treatment of reversible causes. In this article, we demonstrate an approach to recognising paediatric AKI, cessation of nephrotoxic medication, appropriate investigations and the importance of accurately assessing fluid status. The mainstay of treatment is attempting to mimic the kidneys ability to provide electrolyte and fluid homeostasis; this requires close observation and careful fluid management. We discuss referral to paediatric nephrology and the importance of long-term follow-up. We present an approach to AKI through case-presentation.


2015 ◽  
Vol 13 (1) ◽  
pp. 39-41
Author(s):  
Emma Aitken ◽  
Alex Vesey ◽  
Julie Glen ◽  
Mark Steven ◽  
Marc Clancy

Abstract Perioperative insults, including hypotension, hypovolaemia and pneumoperitoneum may occur during laparoscopic live donor nephrectomy. These may have deleterious effects to both donor and recipient. The extent and significance of these insults is poorly understood and difficult to quantify. The aim of this study was to evaluate acute kidney injury (AKI) in the donor using the novel biomarker neutrophil-gelatinase associated lipocalin (N-GAL). We report the results of a pilot study of 20 patients undergoing hand-assisted live donor nephrectomy. eGFR and serum NGAL measurements (Triage CardioRenal Panel, Alere) were obtained preoperatively, immediately post-operatively, day 1 and 6 weeks post-operatively. Mean pre-operative eGFR was 105.6+/-10.1ml/min/1.73m2. Mean eGFR 6 weeks postoperatively demonstrated a 29.4+/-8.8% reduction from baseline. Serum N-GAL increased by 34.1+/-16.7% following an overnight fast pre-operatively (day 0) (ΔNGAL 45.1+/-36.0ng/ml), by a further 14.9+/-7.2% following surgery (immediate post-op). The largest ΔNGAL was observed during the pre-operative fasting period. ΔNGAL [day -1 to day 0] and [day -1 to post-op] were found to correlate inversely with eGFR at 6 weeks (p<0.05, r2=0.47 and p<0.001, r2=0.52 respectively). We conclude that clinically significant AKI does occur in the donor following live donor nephrectomy. Optimisation of perioperative fluid management is likely to have a protective role.


2020 ◽  
Vol 10 (1) ◽  
pp. 42-50 ◽  
Author(s):  
Yuko Oyama ◽  
Yoichi Iwafuchi ◽  
Tetsuo Morioka ◽  
Ichiei Narita

Oliguric acute kidney injury (AKI) with minimal change nephrotic syndrome (MCNS) has long been recognized. Several mechanisms such as hypovolemia due to hypoalbuminemia and the nephrosarca hypothesis have been proposed. However, the precise mechanism by which MCNS causes AKI has not been fully elucidated. Herein, we describe an elderly patient with AKI caused by MCNS who fully recovered after aggressive volume withdrawal by hemodialysis and administration of a glucocorticoid. A 75-year-old woman presented with diarrhea and oliguria, and laboratory examination revealed nephrotic syndrome (NS) and severe azotemia. Fluid administration had no effect on renal dysfunction, and hemodialysis was initiated. Her renal function improved upon aggressive fluid removal through hemodialysis. Renal pathological findings revealed minimal change disease with faint mesangial deposits of IgA. After administration of methylprednisolone pulse therapy followed by oral prednisolone, she achieved complete remission from NS. The clinical course of this case supports the nephrosarca hypothesis regarding the mechanism of AKI caused by MCNS. Furthermore, appropriate fluid management and kidney biopsy are also important in elderly patients with AKI caused by NS.


2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Wei Li ◽  
Yuanyuan Yang ◽  
You Li ◽  
Yueyue Zhao ◽  
Hong Jiang

Cisplatin- (CDDP) induced acute kidney injury (AKI) limits the clinical use of cisplatin. Several sirtuin (SIRT) family proteins are involved in AKI, while the roles of Sirt5 in cisplatin-induced AKI remain unknown. In the present study, we characterized the role and mechanism of Sirt5 in cisplatin-induced apoptosis using the human kidney 2 (HK-2) cell line. CDDP treatment decreased Sirt5 expression of HK-2 cells in a dose-dependent manner. In addition, Sirt5 overexpression enhanced the metabolic activity in CDDP-treated HK-2 cells while Sirt5 siRNA attenuated it. Forced expression of Sirt5 inhibited CDDP-induced apoptosis while Sirt5 siRNA showed the opposite effects. Accordingly, Sirt5 overexpression inhibited the level of caspase 3 cleavage and cytochrome c levels. Furthermore, we found that Sirt5 increased mitochondrial membrane potentials and ameliorated intracellular ROS production. Mitotracker Red staining indicated that Sirt5 overexpression was able to maintain the mitochondrial density during CDDP treatment. We also investigated possible downstream targets of Sirt5 and found that Sirt5 increased Nrf2, HO-1, and Bcl-2 while it decreased Bax protein expression. Sirt5 siRNA showed the opposite effect on these proteins. The levels of Nrf2, HO-1, and Bcl-2 proteins in HK-2 cells were also decreased after CDDP treatment. Moreover, Nrf2 and Bcl-2 siRNA partly abolished the protecting effect of Sirt5 on CDDP-induced apoptosis and cytochrome c release. Catalase inhibitor 3-AT also abolished the cytoprotective effect of Sirt5. Together, the results demonstrated that Sirt5 attenuated cisplatin-induced apoptosis and mitochondrial injury in human kidney HK-2 cells, possibly through the regulation of Nrf2/HO-1 and Bcl-2.


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