Electrolyte and acid–base disorders in AKI

2015 ◽  
Author(s):  
Achim Jörres ◽  
Dietrich Hasper ◽  
Michael Oppert
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Renal Replacement Therapy ◽  
Sodium Bicarbonate ◽  
Kidney Injury ◽  
Medical Emergency ◽  
Acid Base ◽  
Compensatory Mechanisms ◽  
Electrolyte Disturbances ◽  
Underlying Pathology

Electrolyte disturbances are common in patients with acute kidney injury (AKI) and should be corrected. In particular, hyperkalaemia above 6–6.5 mmol/L (especially with electrocardiogram changes) constitutes a medical emergency and warrants immediate intervention. Both hypo- and hypernatraemia may occur during AKI. Chronic changes in serum sodium need to be corrected bearing in mind the underlying pathology; however, when severe and evolving rapidly they should be corrected faster, irrespective of the cause. Acid–base disorders are also common in AKI and need to be treated in the context of underlying problems and physiological compensatory mechanisms. In metabolic acidosis, a bicarbonate deficit may be corrected by sodium bicarbonate administration. Of note, whilst patients with AKI tend to retain electrolytes such as potassium and phosphate, this might be reversed during renal replacement therapy and even substitution of these losses may be required.

Sodium Bicarbonate and Renal Function after Cardiac Surgery

2015 ◽  
Vol 122 (2) ◽  
pp. 294-306 ◽  
Author(s):  
Michael Bailey ◽  
Shay McGuinness ◽  
Michael Haase ◽  
Anja Haase-Fielitz ◽  
Rachael Parke ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Serum Creatinine ◽  
Sodium Bicarbonate ◽  
Replacement Therapy ◽  
Primary Outcome ◽  
Artery Bypass ◽  
Kidney Injury ◽  
Acute Kidney Injury Network ◽  
Double Blind

Abstract Background: The effect of urinary alkalinization in cardiac surgery patients at risk of acute kidney injury (AKI) is controversial and trial findings conflicting. Accordingly, the authors performed a prospectively planned individual patient data meta-analysis of the double-blind randomized trials in this field. Methods: The authors studied 877 patients from three double-blind, randomized controlled trials enrolled to receive either 24 h of intravenous infusion of sodium bicarbonate or sodium chloride. The primary outcome measure was a postoperative increase in serum creatinine concentration of greater than 25% or 0.5 mg/dl (> 44 μm/L) within the first five postoperative days. Secondary outcomes included the raw change in serum creatinine, greater than 50% and greater than 100% rises in serum creatinine, developing AKI (Acute Kidney Injury Network criteria), initiation of renal replacement therapy, morbidity, and mortality. Results: Patients were similar in demographics, comorbidities, and cardiac procedures. Sodium bicarbonate increased plasma bicarbonate (P < 0.001) and urine pH (P < 0.001). There were no differences in the development of the primary outcome (Bicarbonate 45% [39–51%] vs. Saline 42% [36–48%], P = 0.29). This result remained unchanged when controlling for study and covariates (odds ratio [OR], 99% confidence interval [CI]: Bicarbonate vs. Control, 1.11 [0.77–1.60], P = 0.45). There was, however, a significant study-adjusted benefit in elective coronary artery bypass surgery patients in terms of renal replacement therapy (Bicarbonate vs. Control, OR: 0.38 [99% CI: 0.25–0.58], P < 0.0001) and the development of an Acute Kidney Injury Network grade = 3 (Bicarbonate vs. Control, OR: 0.45 [99% CI: 0.43–0.48], P < 0.0001). Conclusions: Urinary alkalinization using sodium bicarbonate infusion is not associated with an overall lower incidence of AKI; however, it reduces severe AKI and need for renal replacement therapy in elective coronary artery bypass patients.

scholarly journals Sodium bicarbonate versus isotonic saline solution to prevent contrast-induced nephropathy : a systematic review and meta-analysis

2015 ◽  
pp. 90-103 ◽  
Author(s):  
Carlos Andres Zapata Chica ◽  
Lina Maria Serna Higuita ◽  
John Fredy Nieto Ríos ◽  
Fabian David Casas Arroyave ◽  
Jorge Hernando Donado Gómez
Keyword(s):  
Systematic Review ◽  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Sodium Bicarbonate ◽  
Replacement Therapy ◽  
Saline Solution ◽  
Isotonic Saline ◽  
Kidney Injury ◽  
Contrast Induced Nephropathy ◽  
Randomized Controlled Studies

Introduction: Contrast-induced nephropathy is one of the main causes of acute kidney injury and increased hospital-acquired morbidity and mortality. The use of sodium bicarbonate for nephroprotection has emerged as a preventative strategy; however, its efficacy is controversial compared to other strategies, such as hydration using 0.9% saline solution. Objective: To compare the effectiveness of sodium bicarbonate vs. hydration using 0.9% saline solution to prevent contrast-induced acute kidney injury. Methods: A systematic review of studies registered in the Cochrane, Pubmed, Medline, Lilacs, ScielO and Embase databases was conducted. Randomized controlled studies that evaluated the use of 0.9% saline solution vs. sodium bicarbonate to prevent contrast-induced nephropathy were included. Results: A total of 22 studies (5,686 patients) were included. Sodium bicarbonate did not decrease the risk of contrast-induced nephropathy (RD= 0.00; 95% CI= -0.02 to 0.03; p= 0.83; I2= 0%). No significant differences were found in the demand for renal replacement therapy (RD= 0.00; 95% CI= -0.01 to 0-01; I2= 0%; p= 0.99) or in mortality (RD= -0.00; 95% CI= -0.001 to 0.001; I2= 0%; p= 0.51). Conclusions: Sodium bicarbonate administration is not superior to the use of 0.9% saline solution for preventing contrast-induced nephropathy in patients with risk factors, nor is it better at reducing mortality or the need for renal replacement therapy.

The Use of Sodium Bicarbonate for Metabolic Acidosis in Patients With Acute Kidney Injury

2020 ◽  
Vol 48 (3) ◽  
pp. e251-e252 ◽  
Author(s):  
Hiroshi Yonekura ◽  
Yohei Kawasaki ◽  
Yuki Nakamori ◽  
Masataka Kamei
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Kidney Injury

scholarly journals Automobile Paint Reducer Induced Acute Kidney Injury

2021 ◽  
Vol 5 (2) ◽  
pp. 10-13
Author(s):  
Muzamil Latief ◽  
Zhahid Hassan ◽  
Mohd Latief Wani ◽  
Farhat Abbas ◽  
Summyia Farooq
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Organic Solvents ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Solvent Exposure ◽  
The Third ◽  
Tubular Necrosis

The various aspects of the automobile industry also carry with it the risk for occupational health hazards with it. Toluene has also evolved as a commonly used drug by substance abusers. Accidental exposure or self-poisoning with these substances has been reported in literature. These substances can also cause distal renal tubular acidosis (RTA), acute tubular necrosis, glomerulonephritis and interstitial nephritis, rhabdomyolysis and myoglobinemia.In this series, we report about three patients who developed renal manifestations because of organic solvents. Two of the three patients had ingested the paint reducer substance and the third one was addicted to sniffing the toluene based paint reducer. All the patients had in taken these substances with suicidal intent and developed acute kidney injury (AKI) and severe metabolic acidosis. One of the patients had features of rhabdomyolysis as well. The third patient was a substance abuser and had inhaled higher than usual dose and developed severe and refractory acidosis and mild kidney injury and required Renal Replacement Therapy (RRT) for acidosis. All the patients eventually recovered their kidney functions and were doing well during their follow-up.Toluene based organic solvents lead to acute neurological symptoms, accompanied by severe metabolic alterations, organ injury and dysfunc-tion. An association of the development of hypokalemic paralysis and metabolic acidosis with toluene intoxication has been observed. The management of acute toluene toxicity is mainly conservative, consisting of electrolytes correction, acid-base and fluid abnormalities and renal replacement therapy in severe AKI.Organic solvent exposure may result in acute tubular necrosis, rhabdomyolysis, RTA and AKI irrespective of the intake route. Clinical suspicion of organ dysfunction and failure and timely induction of supportive care leads to a good outcome.

scholarly journals Reversal of acute kidney injury after peritoneal dialysis in a dog: a case report

2016 ◽  
Vol 61 (No. 7) ◽  
pp. 399-403
Author(s):  
PTC Guimaraes-Okamoto ◽  
SS Geraldes ◽  
JFA Ribeiro ◽  
ANLS Vieira ◽  
LP Porto ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Peritoneal Dialysis ◽  
Metabolic Acidosis ◽  
Drug Therapy ◽  
Small Animal ◽  
Kidney Injury ◽  
Clinical Results ◽  
Endocrine Function ◽  
Prolonged Treatment ◽  
Electrolyte Disturbances

Acute kidney injury is characterised by a sudden injury to the renal parenchyma and causes defects in its excretory, metabolic and endocrine function. Dialysis therapy has been instituted in small animal clinics with the aim of removing the metabolic waste and correcting the electrolyte disturbances stemming from renal dysfunction. Peritoneal dialysis is a therapy based on the use of the peritoneum as a semipermeable membrane through which solutes and fluids are exchanged between blood from the peritoneal capillaries and the dialysis solution. This report describes a case of acute kidney injury stemming from drug therapy in a 13-year-old female mongrel canine. The patient exhibited anorexia, emesis, prostration and anuria and had a history of prolonged treatment with meloxicam. The patient also presented with azotaemia and metabolic acidosis. When anuria continued to persist after drug therapy (volume restoration, chemical and osmotic diuresis and renal vasodilation), peritoneal dialysis was instituted. Three cycles of peritoneal dialysis were performed; during the second cycle, the patient’s anuria was reversed, and at the end of the third cycle she showed a significant reduction in azotaemia, hyperkalaemia and an improved metabolic acidosis. Therefore, peritoneal dialysis showed satisfactory clinical results and reversed anuria, reduced azotaemia and electrolyte disturbances, thereby providing clinical improvement.

scholarly journals Renal Replacement Therapy in Critically Ill: Current Trend and New Direction

2015 ◽  
Vol 3 (1) ◽  
pp. 17-21
Author(s):  
Sarwar Iqbal ◽  
Mohammad Omar Faruq
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Serum Creatinine ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Early Identification ◽  
Kidney Injury ◽  
Hemodynamic Instability ◽  
Acid Base ◽  
Icu Patients

Critically ill patients often present with renal dysfunction. Acute kidney injury (AKI) is common in intensive care unit (ICU) patients and is often a component of multiple organ dysfunction syndrome (MODS). Renal replacement therapy (RRT) plays a significant role in management of acute and chronic renal failure in ICU. During the last decade RRT has made remarkable progress in management of renal dysfunction of critically ill. The Acute Dialysis Quality Initiative conceived in 2002 proposed RIFLE classification for AKI (risk, injury, failure, loss, end-stage kidney disease) using serum creatinine and urine output in critically ill patients. More recently, the Acute Kidney Injury Network (AKIN) has been introduced for staging AKI. Studies have shown that mortality increases proportionately with increasing severity of AKI. In patients with severe AKI requiring RRT mortality is approximately 50% to 70% according to one study and even a small changes in serum creatinine are associated with increased mortality. The most common causes of AKI in ICU are sepsis, hypovolemia, low cardiac output and drugs. The various techniques of RRT used in ICU include intermittent hemodialysis (IHD), continuous RRT (CRRT), sustained low efficiency dialysis (SLED) and peritoneal dialysis (PD). It is preferable to use RRT at either RIFLE injury type or at AKIN stage II in critically ill patients. IHD is commonly used in hemodynamically stable ICU patients. Because of high dialysate (500ml/min) IHD may cause hypotension in some patients. Solute removal may be episodic and often result in inferior uraemic control and acid base control. CRRT is usually initiated with a blood flow of 100 to 200 ml/min. and thus hemodynamic instability associated with IHD is avoided. Major advantages of CRRT include continuous control of fluid status, hemodynamic stability and control of acid base status. It is expensive and there is high risk of bleeding because of use of high dose of IV heparin. SLED has been found to be safe and effective in critically ill patients with hemodynamic instability. It uses the same dialysis machine of IHD and combines the effectiveness of CRRT in unstable patients and easy operability of IHD. It is also cost effective. PD is initiated in ICU for AKI patients when bedside IHD is not available. It is good for hemodynamically unstable patients when IHD or CRRT is difficult. In patients on mechanical ventilator, PD interferes with function of diaphragm causing decrease in lung compliance. Early identification of AKI with bio markers is an important step in improving outcomes of AKI. These bio markers help early detection of AKI before the onset of rise in serum creatinine. Serum cystatin C is one of the sensitive bio markers of small changes in Glomerular filtration rate (GFR) and has been found to be useful. AKI in the ICU most commonly results from multiple insults. Therefore appropriate and early identification of patients at risk of AKI provides an opportunity to prevent subsequent renal insults. This strategy will influence overall ICU morbidity and mortality.Bangladesh Crit Care J March 2015; 3 (1): 17-21

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