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Table of Contents
REVIEW ARTICLE
Year : 2019  |  Volume : 5  |  Issue : 1  |  Page : 17-22

Prevention of acute kidney injury in the clinical practice: The whole at a glance


1 Director, Department of Nephrology, 404 General Military Hospital, Larissa, Greece
2 Chief Nurse, Department of Neurosurgery, Faculty of Medicine, School of Health Sciences, University of Thessaly Larissa, Greece
3 Assistant Professor, Department of Cardiothoracic Surgery, Faculty of Medicine, School of Health Sciences, AHEPA Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece
4 Professor, Department of Neurosurgery Cardiovascular and Thoracic Surgery, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa, Greece
5 Professor, Department of Nephrology, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa, Greece

Date of Web Publication15-Nov-2019

Correspondence Address:
Dr. Dimitrios C Karathanasis
Andrea Papandreou 49, 41500 Terpsithea-Larisa
Greece
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrnm.jrnm_20_19

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  Abstract 


The gradual formation and the final acceptance of a definition of acute kidney injury highlighted the importance of prevention as it contributed to the recording of its impact on the parameters of mortality, the economic burden on health systems, and the progression to chronic kidney disease. Prevention could be separated into general principles and specific clinical cases. The general principles include early diagnosis with the identification of predisposing factors and use of electronic warning and biomarker systems, adequate renal perfusion by administering fiuid and vasomotor drugs, and finally avoidance of nephrotoxicity and administration of nephroprotective drugs. More frequent clinical cases are the postoperative, and also contrast-induced acute kidney injury, which implies both assessments of contrast need and hydration depending on the level of renal function. Despite the ongoing acute kidney injury research, prevention remains the main parameter to address it and needs the utmost attention and application in clinical practice.

Keywords: Acute kidney injury, acute renal failure, prevention


How to cite this article:
Karathanasis DC, Karaolia AC, Tagarakis GI, Tsilimingas NB, Stefanidis I. Prevention of acute kidney injury in the clinical practice: The whole at a glance. J Renal Nutr Metab 2019;5:17-22

How to cite this URL:
Karathanasis DC, Karaolia AC, Tagarakis GI, Tsilimingas NB, Stefanidis I. Prevention of acute kidney injury in the clinical practice: The whole at a glance. J Renal Nutr Metab [serial online] 2019 [cited 2019 Dec 11];5:17-22. Available from: http://www.jrnm.in/text.asp?2019/5/1/17/271039




  Introduction Top


The term acute kidney injury (AKI) entered the nephrological terminology in 2004, replacing the oldest term of Acute Renal Failure which was focused only on the clinical-laboratory effect of the reduction of renal function by neglecting the fact that it is the result of a renal injury that begins much earlier with extensive etiology and pathophysiology.[1],[2] On the contrary, the term AKI essentially refiects the shift of interest from clinical to molecular level with the ultimate goal of early and valid prevention.[3] According to today's commonly accepted Kidney Disease Improving Global Outcomes (KDIGO) definition, the minimum requirement for the characterization of AKI is the existence of at least one of the three criteria: (i) Increase in serum creatinine ≥0.3 mg/dl within 2 days; (ii) increase in serum creatinine at least 1.5 times within 7 days; and (iii) urine volume <0.5 ml/kg/h for 6 h.[4]


  Significance of Acute Kidney Injury Prevention Top


Incidence

The absence for many years of a commonly accepted definition of AKI led to the creation of varied criteria for determining it. As a result, initial studies of AKI appeared a wide range of incidence from 1% to 25%, with rates of 0.02% in the general population levels.[5] Following the gradual formulation of an acceptable definition,[1],[3],[4] a common feature of the studies was the finding of a gradual increase in the incidence of AKI worldwide.[6] An analysis of 312 studies including 49 million patients determined the overall incidence of AKI at 21.6%.[7] Other studies recorded the incidence in hospitalized patients at 10.7%–18.3%,[8],[9],[10] in intensive care units (ICUs) at 35.8%–67%,[11],[12],[13] and in cardiac surgery at 6.9%–43%.[14],[15]

Mortality

Overall mortality was recorded at 23.9%[7] while in hospitalized patients from 5.3% for KDIGO stage I[10] to 50%–60% for patients requiring dialysis.[16],[17] In ICUs, it was estimated at 25.6%.[12] About 300,000 deaths per year are reported in the United States due to AKI.[18]

Financial burden

The financial burden is presented as an increase of 7500 $ in the cost of hospitalization with an extension of the duration of hospitalization by 3.5 days.[18] Another study in 2012, on a sample of about 30 million hospitalizations showed an increase of 7933 $ in hospitalization cost and 3.2 days in the hospital stay.[19] A similar study in Canada estimated the increase in hospitalization cost at 3779 Canada $ and in the length of hospitalization at 2.8 days.[20] AKI is a significant annual burden affecting the health systems economy.[21] For the United Kingdom National Health System, it was estimated at 1.02 billion £, which corresponds to about 1% of its annual funding[22] and for the United States of America at 24 billion $.[21]

Evolution to chronic kidney disease

Patients with a history of AKI are eight times more likely to develop chronic kidney disease (CKD).[23] The more advanced the AKI stage, the greater the probability of progression to CKD.[24] Hypertrophy of residual kidneys, peritubular capillary loss, arterial hypertension, disturbance of tubular epithelial repair with subsequent tubular atrophy, and tubular fibrosis are recognized as more likely mechanisms.[25],[26],[27] Prevention of AKI can be divided into the general principles of prevention and those relating to specific clinical cases.


  General Prevention of Acute Kidney Injury Top


Principles of general prevention of acute kidney injury

It has been determined that about one-third of the AKI incidents could have been prevented.[28] Prevention is not only aimed at deterring the appearance of AKI but also hindering it from developing further. The main pillars of general prevention are the identification of predisposing factors, the ensuring of early diagnosis, the maintaining of adequate renal perfusion, the avoidance of nephrotoxic drugs, and the parallel administration of nephroprotective ones.

Identification of predisposing factors

Prerequisite of prevention is the identification of predisposing factors and knowledge of the causal. In addition to advanced age and female sex, chronic heart, lung, liver, and kidney diseases, as well as diseases such as diabetes mellitus and neoplasms, offer the conditions for AKI manifestation.[27],[29] Given that dehydration is an important predisposing factor, the assessment of the patient's hydration status becomes crucial.

Ensure of early diagnosis

Early diagnosis is achieved by electronic early warning systems and biomarkers.

Electronic early warning systems

Thefirst electronic systems began a decade ago based on the risk, injury, failure, loss of kidney function, and end-stage kidney disease criteria.[30] These are programs that retrieve a real-time database of parameters such as serum creatinine value and urine volume and promptly inform the physician of the forthcoming AKI by E-mail.[31] Later on, electronic systems were introduced at the hospital level[32] and incorporated the acute kidney injury network criteria.[9] A recent KDIGO-based application detected 91.2% of AKI incidents, demonstrating the large scope for future use of these systems.[33]

Biomarkers

Biomarkers are substances that originate from the kidney tissue and are released from the kidneys or are derived from other tissues and are filtered, absorbed, or excreted by the kidneys in response to renal damage, highlighting the nature, size, and location of the lesion.[34],[35] Although they have not yet been applied to the clinical practice, they monopolize the research interest in the field of prevention.[36]

The ideal biomarker must meet a set of features ranging from application speed, reliability, sensitivity, and specificity to the cost of application.[37],[38]

The long-term absence of renal lesion biomarker is evident in relation to the progression of biomarkers to another tissue damage such as acute ischemic heart damage. Over the past 50 years, while the biomarkers of heart lesion have an evolutionary course, the only essential marker of renal impairment remains serum creatinine over the same period. This results in a decrease in mortality from myocardial infarction, while the corresponding mortality from acute renal damage remains high.[39],[40]

In recent years, interest has been focused on cellular damage biomarkers due to the early indication of AKI, and essentially, the term AKI biomarker is now identical to that class.[35] Neutrophil Gelatinase Associated Lipocalin (NGAL) has been more extensively investigated, and since 2013, the research interest has attracted from the earliest promising cell cycle inhibitors, TIMP2 and IGFBP7. They are involved in the inhibition of the cell cycle G1 phase. They simply refiect a “stressful” condition of the epithelial cells of the renal tubule rather than permanent damage. The former is higher in postoperative patients, while the latter in septicemic patients.[41],[42]

Maintenance of adequate renal perfusion

Maintaining euvolemia should strike a balance between treating hypovolemia and avoiding overhydration. Sufficient renal perfusion is achieved through the administration of fiuid and vasomotor drugs.

Administration

The administration of fiuids is aimed at replacing the lost volume without patient overhydration and maintaining the active circulating volume. The indicated fiuid solutions are crystalloids. The exceptions are the hemorrhagic shock with an indication of blood transfusion and cirrhosis where albumin solutions are indicated.[43],[44]

Colloids of albumin or semi-synthetics are currently contraindicated on the one hand because their excellency has not been proved and on the other hand because they increase both mortality and need of dialysis.[45],[46]

Ideal crystalloids are mainly balanced Ringer's lactate solutions. The term “balanced” designates solutions where the anion of chlorine has been replaced by another metabolized anion.[47],[48]

Normal saline due to increased chlorine content, after administration of at least 2 l, leads to hyperchloremic acidosis with a risk of thrombosis and hyperkalemia, increases fiuid retention, decreases renal blood perfusion through swelling of the interstitial tissue, and reduces glomerular filtration by vasoconstriction of the afferent arteriole. On the contrary, normal saline is indicated in cases of acute central nervous system diseases and metabolic alkalosis resulting from upper gastrointestinal injuries.[44]

Administration of vasoactive agents


  Vasoconstrictors Top


Both the KDIGO team in 2012 and the European Society of Intensive Care Medicine (ESICM) AKI prevention team in 2017 recommend the administration of vasoconstrictors against septic shock after correction of any underlying disease. Median blood pressure goal is set at 65–70 mmHg or 80–85 mmHg in chronic arterial hypertension. Higher blood pressure was associated with an increased need for dialysis and increased mortality. Noradrenaline is recommended by both groups as thefirst choice. Its administration in thefirst 6–8 h is advantageous over other vasoconstrictors due to reduced arrhythmia events, reduced need for dialysis in thefirst 28 days, and decreased mortality. Vasopressin is recommended in cases of heart surgery.[43],[49],[50]


  Vasodilators Top


The KDIGO and the ESICM teams give a negative recommendation or suggestion for the use of vasodilators. Dopamine, although at low doses, causes renal vasodilation and an increase in glomerular filtration rate (GFR), at the same time may lead to many side effects. Fenoldopam as a dopamine receptor agonist, atrial natriuretic peptide as a vasodilator of the afferent arteriole, and levosimendan as an inotropic vasodilator cause side effects without clinical benefit in AKI prevention. The suggestions for fenoldopam and atrial natriuretic peptide were strengthened in 2017 from 2C to 2B.[43],[49]


  Diuretics Top


The previously established use of diuretics was based on the concept of converting an oliguric to nonoliguric AKI with a better prognosis, decreasing oxygen consumption in the renal medulla, removing necrotic tubule content, and reducing renal vascular resistance by inhibiting prostaglandin dehydrogenase. Nowadays, with the exception of the treatment of overhydration, the administration of diuretics and especially loop ones are contraindicated in the prevention of AKI not only because they affect the intravascular volume but also mainly because their benefit in preventing AKI has not been documented so far in mortality and need of dialysis.[43],[49],[51],[52]

Avoiding nephrotoxic drugs

The most important nephrotoxic or potential nephrotoxic drugs in clinical practice are nonsteroidal anti-infiammatory drugs, angiotensin-converting-enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), aminoglycosides, and contrast agents. Additional factors of toxicity are the duration of treatment, the dosage, and the pharmacodynamic and pharmacokinetic interactions. The most dangerous and most common clinical combination includes the triad of a nonsteroidal anti-infiammatory drug, an ACEI or ARB and a diuretic.

Aminoglycosides act adversely on the proximal tubule by acute damage with subsequent apoptosis and necrosis, on the mesangium by contraction resulting in a reduction in GFR and on the renal vasculature by vasoconstriction leading to a reduction in renal perfusion. Prevention includes avoidance of administration whenever there is an alternative and increasing the once-daily dose to maintain the trough levels (18–24 h postdose) ≤1 μg/ml.[43]

Administration of nephroprotective medication

N-acetyl cysteine

In the past, acetylcysteine as a factor of potent antioxidant and vasodilatory action has been extensively used to prevent AKI. From 2012, the KDIGO team deters N-acetyl cysteine (NAC) use with a negative recommendation for postoperative AKI and a negative recommendation for severely ill patients with hypotension.[43],[49]

Statins

Statins were tested against AKI due to their anti-infiammatory action (by inhibiting infiltration of infiammatory cells and reducing the expression of infiammatory mediators) and their antioxidant effect on endothelial function (through increased expression of nitrate acid). The hitherto poor results have led ESICM in 2017 to make a negative recommendation for preventing AKI in heart surgery.[49],[53]

Lipoic acid – spermidine – magnolol - EDL peptide

Recently, antioxidant agents such as lipoic acid, spermidine, magnolol, and the synthetic peptide glutamyl-aspartyl-leucin have been proposed and supported by published results which require further research.[54],[55],[56],[57]


  Prevention of Specific Clinical Cases of Acute Kidney Injury Top


Specific clinical cases are the postoperative AKI and the contrast-induced AKI (CI-AKI).

Postoperative acute kidney injury

There are not any other specific preventive measures than those mentioned above. However, identification of risk factors such as age over 65 years, preexisting CKD, heart failure, liver disease, diabetes mellitus, nephrotoxic medication, and intraperitoneal surgery is of paramount importance.[58],[59]

Contrast-induced-acute kidney injury

Although the general definition of AKI by the KDIGO group is valid without exception, CI-AKI is recognized as an increase in serum creatinine ≥0.5 mg/dl or at least 25%, within 48 h of contrast administration.[44] The incidence in nonhospitalized and hospitalized patients is 2% and 5%, respectively, whereas in special groups such as coronary angioplasty 8.2%, coronary intervention 32.6%, and ICU 16.3%.[43],[60],[61]

Pathophysiologically, contrast agents cause a reduction of glomerular filtration due to vascular and tubular endothelial damage. Main mechanisms are the reduction of renal fiow, the increase in renal oxygen consumption, and the production of free radicals.[62]

Contrast agents are substances that show increased contrasting ability due to their iodine content. According to their chemical formula, they are divided into monomers or dimers while according to their osmolality, they are divided into hyperosmolar which are no longer used, hypoosmolar (compared to the former ones) and iso-osmolar with the representative of iodixanol.[63]

Of primary importance for the prevention of CI-AKI is the identification of risk factors through the patient's medical record. Most important factors are age over 75 years, preexisting CKD with or without diabetes mellitus, heart failure, obesity, kidney transplantation, increased contrast volume, and arterial administration.[58],[59]

Although gadolinium and its derivatives do not show the nephrotoxicity of iodinated contrast agents, cases of gadolinium-related CI-AKI have been described in patients suffering from CKD and diabetes mellitus who received an increased amount of contrast agent.[43] Furthermore in a study published in 2016, it was mentioned that in patients with normal renal function the administration of gadolinium was followed by a transient increase of IL18 and N-acetyl-β-D-glucosaminidase biomarkers demonstrating toxic damage to the tubular epithelial cells.[64]

Nonpharmaceutical prevention

In this category, a number of risk factors are taken into consideration, such as the need for contrast, the nephrotoxic medication, the adequate hydration, and the administration of hypo-osmolar or iso-osmolar contrast agent. The benefit that some researchers have been proposed from the withdrawal of potentially nephrotoxic drugs such as ACEI and ARB at least 2 days before contrast implementation has not been documented. It remains as a general rule to administer the smallest possible volume of a hypo-osmolar or iso-osmolar contrast agent, bearing in mind that if something needs attention in relation to GFR, this is not the volume of the contrast but essentially the amount of iodine administered in grams.[65],[66]

Hydration

The benefit of hydration is achievedfirst by reducing the direct toxic effect of the contrast agent on the tubular epithelial cells due to a decrease in tubular concentration and an increase in diuresis. Second, by a reduction in the vasoconstrictive action of the contrast medium on the renal medulla due to a decrease in the secretion of the anti-diuretic hormone, inhibition of the renin–angiotensin–aldosterone axis and an increment in renal prostaglandin synthesis.[62],[67]

According to the KDIGO guidelines, the recommended hydration must be achieved by an isotonic solution of saline or sodium bicarbonate intravenously. Although there is not any recommendation for a particular hydration rate, the advisable form is 1 to 1.5 ml/kg/h for 3-–12 h before and 6–12 h after contrast administration. Till date, neither the superiority of sodium bicarbonate solution nor the oral hydration has been documented.[43],[60],[68],[69],[70]

Depending on the GFR, patients can be divided into a low, medium, and high risk for contrast-induced nephropathy with adjustment of hydration depending on the severity of the risk.[71],[72]


  Low Risk Top


It is defined as: Estimated glomerular filtration rate (eGFR) >60 mL/min/1.73 m2.


  Average Risk Top


It is defined as eGFR: 30–45 mL/min/1.73 m2 (without diabetes mellitus or heart failure) or eGFR: 45–60 mL/min/1.73 m2 (with diabetes mellitus or heart failure).


  High Risk Top


High risk is defined as eGFR <30 mL/min/1.73 m2

(no diabetes mellitus or heart failure) or eGFR: 30–45 mL/min/1.73 m2 (with diabetes mellitus or heart failure) or monoclonal gammopathy.

Drug prevention

A variety of drugs have been tested such as NAC, statins, calcium channel blockers, Vitamin C, Vitamin E, trimetazidine, Na/K citrate, synthetic prostacyclin, fenoldopam, theophylline as well as the implementation of preventive dialysis.

Some choices such as fenoldopam and theophylline have so far received a negative recommendation or suggestion while others such as hemodialysis or hemofiltration have been proved to be ineffective.[43],[73]

Some other options, such as statins.[74],[75],[76] calcium channel blockers,[77] Vitamins C[78] and E,[79] trimetazidine,[80] Na/K Citrate,[81] and synthetic prostacyclins,[82] need further studies to justify their benefit.

N-acetyl cysteine

Administration of acetylcysteine was tested in a number of studies either alone or in combination with bicarbonates. The loose positive KDIGO recommendation for oral administration is based on its poorly documented benefit, very few side effects, and low cost.[43]


  Conclusion Top


AKI, in particular following its widely accepted definition, is recognized as a clinical entity with increased incidence, mortality, and financial burden on health systems. These factors highlight the importance of shifting treatment to the level of prevention. In addition to parallel research efforts, the main pillars of prevention remain the early recognition of predisposing factors, the adequate hydration using balanced solutions and the avoidance of nephrotoxic drugs while in cases of contrast need always should be given as little amount as possible. However, the utmost measure of AKI prevention in clinical practice is the vigilance of the physician for both the early recognition of increased risk cases and the timely implementation of preventive mechanisms.

Financial support and sponsorship

Nil.

Confiicts of interest

There are no confiicts of interest.



 
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