REVIEW ARTICLE

Acute kidney injury, its definition, and

treatment in adults: guidelines and reality
Joanna Matuszkiewicz­‑Rowińska, Jolanta Małyszko
Department of Nephrology, Dialysis and Internal Diseases, Medical University of Warsaw, Warsaw, Poland

Key words Abstract

acute kidney injury, In the last decades, a lot of research has been done to improve our understanding of acute kidney injury
creatinine, glomerular (AKI) as well to standardize its diagnostic criteria. As a result of many years of work of intensivists and
filtration rate, renal nephrologists, consensus definitions were established, finally unified in 2012 by the Kidney Disease:
replacement therapy Improving Global Outcomes (KDIGO) group. These criteria refer to the time of AKI development and are
based on serum creatinine level increase and / or urine output decrease. Acute kidney injury is defined
as an increase in serum creatinine levels by at least 0.3 mg/dl within 48 hours or 1.5­‑fold the baseline,
which is known or presumed to have occurred within the preceding 7 days, or—according to the urine
output criterion—urine volume less than 0.5 ml/kg/hour for at least 6 hours. The present review covers is‑
sues discussed during the KDIGO controversy conference, devoted to AKI. Here, we attempted to answer
3 main questions: Is the KDIGO definition of AKI valuable in clinical research and global epidemiology?
Is it helpful in everyday clinical practice? Is it useful in the treatment of critically ill patients with AKI?

Introduction Over the past decades, there has dysfunction syndrome. Therefore, in the 1970s
been a significant increase in the incidence of and 1980s, patients with severe AKI were treat­
acute kidney injury (AKI),1 especially in the old­ ed mainly in general wards. Today, most of them
er population (>65 years). The number of AKI are referred to intensive care units (ICUs). Such
cases in the hospitalized population have more a change in the spectrum of AKI must have in­
than doubled; it also concerns AKI requiring di­ fluenced patients’ survival; that is why mortality
alysis.2 At the same time, in high­‑income coun­ in severe AKI remains very high, despite several
tries, we have witnessed a profound change in treatment improvements. In patients requiring
the disease spectrum (Figure 1). It is a consequence renal replacement therapy (RRT), the overall 90­
of the spectacular progress in medicine, leading ‑day mortality ranges between 44% and 60%.5 -7
to a considerable life extension. In high­‑income Moreover, those who survive the hospitalization
countries, AKI develops in up to 20% of hospi­ period are at risk of developing long­‑term com­
talized patients, which is approximately 50% of plications associated with a substantial cost bur­
adult patients receiving intensive care, and in 1 den. Recent studies have consistently shown that,
Correspondence to:
in 4 pediatric patients receiving intensive care.3,4 in both adults and children, AKI and its stage is
Prof. Joanna Matuszkiewicz­ In adults, it has become a disease of the older, a strong, independent risk factor for CKD devel­
‑Rowińska, MD, PhD, FERA, who, with many comorbidities and chronic de­ opment.8,9 The mechanisms of progression from
Department of Nephrology, generative organ changes, are much more vul­ AKI to CKD have been partially elucidated in ex­
Dialysis and Internal Diseases,
Medical University of Warsaw,
nerable to acute insults. Many of them have al­ perimental studies. They include maladaptive re­
ul. Banacha 1a, 02-097 Warszawa, ready had some form of chronic kidney disease pair and endothelial injury, which result in neph­
Poland, phone: +48 22 599 26 58, (CKD), called “AKI on CKD.” Patients who sur­ ron and capillary dropout, interstitial fibrosis,
email: jrowinska@gmail.com
Received: February 29, 2020.
vive extensive, high­‑risk cardiovascular or ab­ and the progressive decline of glomerular filtra­
Revision accepted: May 13, 2020. dominal surgery, extensive trauma, or burns and tion rate (GFR).10 -12 In those with already existing
Published online: May 19, 2020. those after hematopoietic stem cell or solid organ CKD, AKI may significantly accelerate its progres­
Pol Arch Intern Med. 2020;
transplant often develop sepsis and other com­ sion to the end­‑stage disease. Patients who recov­
130 (12): 1074-1080
doi:10.20452/pamw.15373 plications. In many of them, AKI occurs as a late er from AKI also remain at higher risk of develop­
Copyright by the Author(s), 2020 event, often as a manifestation of multiorgan ing hypertension and cardiovascular events.10,13,14

1074 POLISH ARCHIVES OF INTERNAL MEDICINE 2020; 130 (12)

 Multiorgan dysfunction syndrome allowed for the standardization of entry crite­
Isolated ria and endpoints in the clinical trials of AKI, al­
Severe sepsis acute kidney injury though there have been numerous studies that
and septic shock used classification systems other than the KDIGO
Drugs criteria.23 -28
Cardiac surgery
Contrast media However, the question remains as to whether
Multiple traumatic injuries it is a reliable tool for the estimation of AKI glob­
Other nephrotoxins
Severe burns
al epidemiology? This issue has been a matter of
Rhabdomyolysis and a heated debate. Probably, the highest controver­
Extensive abdominal surgery hemolysis sy is related to the possibility of diagnosing AKI
Acute hepatic failure Other based on the increase in serum creatinine lev­
els ≥0.3 mg/dl within 48 hours. It was criticized
Hematopoietic stem cell
and solid organ
by many as a too small alteration to eliminate lab­
transplant oratory errors or physiologic fluctuations, which
may misclassify healthy patients as well as pa­
tients with CKD and baseline serum creatinine
levels ≥1.5 mg/dl,29 in whom such small increas­
Figure 1 The changing spectrum of acute kidney injury in hospitalized patients es may represent normal daily variations. Anoth­
er limitation of the KDIGO definition is the de­
termination of a baseline creatinine level when
In the last decades, much research has been the true value is unknown. None of the proposed
conducted to improve our understanding of AKI methods seems to be reliable, and all of them may
as well to standardize its definition and diagnos­ be the source of substantial errors. The incorpo­
tic criteria. It was necessary, since there had been ration of RRT initiation as a possible definition
more than 35 definitions in use, based on various of stage 3 disease is maybe even more unfavor­
serum creatinine levels or its clearances obtained able, since this criterion is subjective.
using different methods, precluding any data or The diuresis criterion, although reported to in­
study comparisons in the field. The first consensus crease early AKI detection rates, has raised many
definition of AKI, the Risk, Injury, Failure, Loss doubts. Urine output is easy and inexpensive to
of kidney function, and End­‑stage kidney disease determine, but it can be significantly changed by
(RIFLE) criteria, were published in 2003, as a joint the use of diuretics, fluid therapy, and hemody­
work of intensivists and nephrologists,15 subse­ namic status. Therefore, it may increase diagnos­
quently changed by the same group to the Acute tic false­‑positive rates. Of note, in patients who
Kidney Injury Network (AKIN) criteria 3 years have undergone major surgical procedures, oligu­
later,16 and finally unified by the Kidney Disease: ria may be an appropriate physiological response
Improving Global Outcomes (KDIGO) group and to stress related to surgery. Also, the proposed
published in 201217 (Table 1 ). The KDIGO criteria, threshold is controversial. As rightly pointed out
or classification, refer to the time of AKI devel­ by Erdbruegger and Okusa,30 in a 70­‑kg adult
opment and are based on serum creatinine level man, diuresis ≤0.5 ml/kg/hour for 6 hours would
increase and / or urine output decrease. It is de­ represent a urine volume as high as 840 ml/d,
fined as an increase in serum creatinine levels which seems to be an adequate response to lim­
at least by 0.3 mg/dl within 48 hours or 1.5­‑fold ited fluid intake. Last but not least, what about
the baseline, which is known or presumed to have nonoliguric AKI?
occurred within the preceding 7 days, or—accord­ However, in our opinion, the greatest uncer­
ing to the urine output criterion—as urine vol­ tainty about the value of the KDIGO classifica­
ume below 0.5 ml/kg/hour for at least 6 hours. tion in clinical research is the fact that the defi­
The KDIGO definition has been developed to nition does not differentiate between 2 extreme
achieve several objectives: to unify terminology, forms of AKI: the functional one, formerly called
to facilitate research and comparability among prerenal azotemia, and structural tubular inju­
studies, to raise the awareness of AKI among gen­ ry. Prerenal kidney injury is not clearly defined
eral practitioners and non­‑nephrologists, to en­ by the KDIGO classification and seems often to
able its earlier detection and, possibly, preven­ be a neglected issue. Unfortunately, this may be
tion, and, ultimately, to improve patient out­ a serious obstacle in the accurate estimation of
comes. Let us have a quick look at how it has ful­ AKI global epidemiology and should be overcome.
filled these goals. Many shortcomings of the KDIGO definition
result from the fact that it is based on serum
Question 1: is the KDIGO definition of acute kidney creatinine levels, which are imperfect biomark­
injury valuable in clinical research and global epide- ers of AKI, being affected by numerous factors.
miology? The answer is equivocal. From 2012, In their excellent review, Thomas et al31 delin­
when it was introduced, the classification has eated as many as 14 various acute or chronic
been evaluated and validated in several studies factors that may alter serum creatinine levels,
and claimed by many as useful in comparing out­ making it difficult to establish an accurate di­
comes between AKI studies and interventions.18-22 agnosis. The serum creatinine level is a func­
The adoption of the KDIGO staging system also tional marker, and its rise does not necessarily

REVIEW ARTICLE The definition of acute kidney injury 1075

TABLE 1 Acute kidney disease staging according to the Kidney Disease: Improving Unfortunately, despite extensive research, the
Global Outcomes classification8 uphill battle to find reliable structural biomarkers
Stage Serum creatinine levels Urine output of AKI may last longer than we expect, provided
they can ever be found. Therefore, we agree that
1 1.5–1.9­‑fold higher than baseline or <0.5 ml/kg/hr for 6–12 hrs
increase ≥0.3 mg/dl the AKI definition endorsed by the KDIGO guide­
lines, with serum creatinine levels as the main pa­
2 2–2.9­‑fold higher than baseline <0.5 ml/kg/hr for ≥12 hrs
rameter, remains the best option for clinical re­
3 3­‑fold higher than baseline or <0.3 ml/kg/hr for ≥24 hrs search. However, we should be aware of its weak­
increase ≥4 mg/dl, or initiation of RRT or anuria for ≥12 hrs
ness in the estimation of AKI global epidemiolo­
Abbreviations: RRT, renal replacement therapy
gy, since it may be a potent source of mainly false­
‑positive results.
Considering epidemiological studies, one can­
represent kidney injury. There are numerous ex­ not forget that many of them use large adminis­
amples of hemodynamically driven, transient se­ trative databases based on the International Clas‑
rum creatinine elevations, like in patients with sification of Diseases, Tenth Revision (ICD­‑10) cod­
prerenal azotemia and hepatorenal or cardiore­ ing, which neither accounts for the current AKI
nal syndrome. In a number of these clinical sit­ definition nor distinguishes between various AKI
uations, the kidney is not injured, and its re­ stages. Moreover, as stressed by several research­
sponse to reduced intravascular volume is ho­ ers, changes in discharge coding practices, driv­
meostatic, thus, absolutely normal and can be en by reimbursement systems, may, in part, ex­
life­‑saving. However, tubular damage can oc­ plain the dramatic rises in the incidence of AKI
cur in some situations, but it is insufficient to observed in some countries over the past 2 de­
considerably change serum creatinine levels in cades.37-39 The International Classification of Dis‑
the volume­‑overloaded patient. The incorpora­ eases, Eleventh Revision is on its way and is ex­
tion of structural biomarkers that directly in­ pected to replace ICD­‑10 on January 1, 2022. It
dicate tubular damage could improve the diag­ will be integrated with the KDIGO classification,
nostic value of the AKI definition. including the current definition and differentia­
Several recent cardiologic studies have advo­ tion between AKI stages. If and to what extent it
cated the need to redefine AKI, which is often will improve AKI identification remains unclear.
replaced in cardiology with the term “worsen­
ing renal function (WRF)” in patients with acute Question 2: is the KDIGO definition of acute kidney
heart failure (HF), linking biochemical changes injury helpful in everyday clinical practice? We do
with clinical status.32-36 Worsening renal func­ not think so. There are at least 3 crucial ques­
tion that has occurred in the setting of acute tions, which a clinician facing a patient with
HF is classified into 2 categories, ie, true and an abrupt worsening of kidney function should
pseudo­‑worsening renal function, by the exten­ ask. Is the patient in a life­‑threatening condition?
sion of the RIFLE / AKIN criteria and combining What is (are) the most probable cause(s) of AKI?
them with the presence or absence of worsening How should they manage the patient? The KDIGO
HF.13,14,33,36 True WRF is diagnosed in patients definition leaves us without any answer to these
with the simultaneous presence of worsening issues. The reason for that is its complete lack of
HF, defined as the deterioration or no improve­ the clinical context, which can vary a lot, with en­
ment of HF that requires intensified therapy tirely different forms of worsened kidney func­
during the first 3 days of hospitalization. Those tion such as hemodynamic AKI, blockage of urine
who demonstrate only isolated alterations in cre­ flow, and a decrease in renal secretion due to tu­
atinine levels or eGFR are classified as having bular damage.
pseudo­‑WRF. The rationale behind this distinc­ For this reason, in our practice, we prefer to use
tion is that not every increase in serum creati­ the old pathophysiological classification, which
nine levels in acute HF indicates kidney injury categorizes the causes of AKI into 3 groups: pre­
or dysfunction with unfavorable consequences, renal (renal hypoperfusion), postrenal (obstruc­
and an increase in creatinine levels with simulta­ tion of the urinary tract), and intrinsic (structur­
neous effective decongestion and hemoconcen­ al damage to the kidney), which can be related to
tration is often related to better outcomes.33 -35 ischemia, nephrotoxins, or inflammatory process­
Recently, Sokolski et al36 investigated the defi­ es. The strengths of this old approach lie in what
nition of true WRF in relation to clinical char­ remains the weakness of the RIFLE, AKIN, and
acteristics and outcomes in patients with acute KDIGO classifications, namely, limited complex­
HF. They found that while 14% of patients de­ ity, memorability, and the relation to the etiolo­
veloped WRF during hospitalization, a change gy and pathophysiology of the condition. It de­
in creatinine or eGFR was associated with un­ termines the appropriate diagnostic steps and
favorable clinical settings only in 4%. In the re­ provides us with vital therapeutic suggestions.
maining 10%, the clinical course was unevent­ Therefore, when keeping in mind that this old
ful and did not differ from that observed in pa­ classification simplifies a highly complex clinical
tients without WRF. It may be of interest to com­ syndrome and, in many cases, the pathogenesis
pare WRF with the AKI definition proposed by of AKI is multifactorial, we still recommend its
the KDIGO group. use to our students and trainees.

1076 POLISH ARCHIVES OF INTERNAL MEDICINE 2020; 130 (12)

 Although we do not find the KDIGO criteria creatinine levels. The Sequential Organ Failure
much helpful in the everyday care of patients with Assessment (SOFA) renal score was the most
AKI, we do recognize that there are some positive commonly used system to define and quantify
consequences of introducing them to clinical prac­ the frequency of AKI (43.5% of studies), while the
tice. Most importantly, it raised the awareness of RIFLE / AKIN / KDIGO criteria were used only in
AKI among physicians. The adoption of the con­ 5 trials (10.9%). The authors stated that their find­
sensus definition has enabled us to build electron­ ings may raise concerns about the evidence­‑based
ic AKI alerts, similar to other healthcare informa­ use of these classification systems in the clinical
tion technology systems, coupled with hospital­ management of critically ill patients.
‑wide AKI guidelines and educational programs,
warning clinicians of possible AKI and supporting Initiation of renal replacement therapy Classic in­
them in implementing appropriate nephroprotec­ dications for dialysis in AKI are well known; they
tive measures. These include the discontinuation are based mainly on the development of refrac­
of nephrotoxic agents, avoidance of diuretics and tory to diuretics, life­‑threatening fluid overload
radiocontrast media, ensuring an adequate vol­ and severe solute imbalances, accompanied by
ume status, hemodynamic management in pa­ hyperkalemia and acidosis. However, in the ab­
tients with hypotension, monitoring urine output sence of these clearly urgent indications, the deci­
and serum creatinine levels, as well as addition­ sion when to initiate RRT in critically ill patients
al diagnostic workup (ie, urinalysis, kidney ultra­ with AKI is often much more difficult and—de­
sound). In numerous alert systems, when the pa­ spite a remarkable progress in intensive care med­
tient is diagnosed with AKI, a request for nephrol­ icine during the last decades—remains a sub­
ogy consultation is automatically generated. Fi­ ject of controversy. Notably, although RRT is in­
nally, these systems may identify candidates for evitable and life­‑saving in many cases of severe
appropriate outpatient follow­‑up and monitoring AKI, it may also negatively impact the outcomes
for long­‑term renal recovery after AKI. It remains of these patients. Dialysis exposes them to (or
unclear whether these systems will meet the ex­ aggravates the already present) hemodynamic
pectations. The results of some studies, most­ instability with deleterious intradialytic hypo­
ly from the United Kingdom, are inconsistent, tension, anticoagulation­‑induced bleeding, vas­
with some of them showing an improvement in cular access–related bacteremia, and inflamma­
the care of patients with AKI, and others demon­ tory stress due to bioincompatibility of an ex­
strating no substantial benefit, the increased use tracorporeal circuit. One of the key untoward ef­
of resources, and higher hospitalization rates.40 - 42 fects of RRT is a not entirely predictable change
in the pharmacokinetics of various therapeutic
Question 3: is the KDIGO definition of acute kidney inju- agents, especially antibiotics, posing a substan­
ry helpful in the treatment of critically ill patients with tial risk of underdosing them.
acute kidney injury? In the treatment of critical­ The ongoing discussion entitled “early versus
ly ill patients, the clinical context matters most. late”43 - 49 seems to be as passionate as a bit point­
The presence of sepsis, failure of other organs, and less, since what is early for one patient may be
malnutrition may dramatically influence the out­ too late for another one. Recently, as a result of
come. The sequence of clinical events is also essen­ the Acute Disease Quality Initiative (ADQI) 17th
tial. In the case when AKI develops late, after ICU Conference on Continuous RRT, an individualized
admission, as a manifestation of multiple organ approach based on the demand–capacity balance
failure, the prognosis seems to be much worse. was proposed.50 According to the consensus, acute
Since these patients are often in a highly catabol­ RRT should be considered when metabolic and flu­
ic state, the development of metabolic disorders id demands exceed the patient’s total kidney ca­
may rapidly progress and be accompanied by se­ pacity. This “watchful waiting” strategy requires
vere acidosis and hyperkalemia, while extensive a careful ongoing recognition of the clinical con­
fluid resuscitation and parenteral nutrition pose text (causes, the clinical course, the AKI trajecto­
a risk of severe fluid overload. Of note, in critical­ ry, nonrenal organ dysfunction, the degree of fluid
ly ill patients, the severity of AKI can be under­ overload, chronic comorbidities, accommodation
estimated due to dilution of serum creatinine by of nutritional and medication needs and other or­
fluid accumulation, increased or decreased creat­ gan support therapies) by the experienced, opti­
inine production, and loss of muscle mass, and mally multidisciplinary, treatment team.
may delay therapeutic decisions. Recently, the idea of rapid response teams com­
In ICU practice, the severity of renal fail­ posed of different healthcare professionals (phy­
ure is often evaluated by combining the func­ sicians, nurses, and paramedics) was conceived to
tional parameters of the kidneys and other or­ bring ICU­‑level skills such as the intensification of
gans. In their recently published systematic re­ fluid resuscitation, an appropriate antimicrobial
view, da Hora Passos et al24 evaluated the criteria therapy in previously unrecognized septic shock,
used to determine the severity and progression and care outside of the ICU.51 It also appears that
of kidney injury in multicenter randomized clin­ this approach may not only reduce the incidence
ical trials conducted in ICUs, with mortality re­ of AKI but also decrease in­‑hospital and long­
garded as a primary outcome. Out of 46 studies, ‑term mortality. However, an increased work­
only 7 (15.2%) included mean or median serum load of active team members has been the major

REVIEW ARTICLE The definition of acute kidney injury 1077

 STEP 1. Prerenal AKI? (RBF decrease)
Fluid resuscitation / treatment
Volume depletion, hypotension, sepsis, Yes
of heart failure or sepsis
liver failure

No
STEP 2. Prerenal or renal toxic AKI?
Drugs that influence renal hemodynamics Discontinuation of suspicious
Yes
(NSAIDs, ACEIs, ARBs) drug(s), fluid therapy
Other drugs, contrast agents

No
STEP 3. Postrenal AKI?
USG: urinary Removing or bypassing
Prostate disease, nephrolithiasis, pelvic malignancies, Yes
tract obstruction the obstruction
anticholinergic drugs, RPF
AKI
No

STEP 4. Renal inflammatory AKI?

Rash, fever, Discontinuation of the drug(s),
Acute interstitial nephritis: drugs, infection Yes antibiotics
eosinophilia
Glomerular: primary or secondary Nephritic / Specific treatment:
glomerulonephritis Yes
nephrotic GCS, immunosupression,
syndrome, immunomodulation.
Vascular: vasculitis, HUS / TTP-accelerated disease of
hypertension, renal artery embolism Yes Dialysis may be necessary.
other organs
No

STEP 5. Renal noninflammatory AKI

Supportive treatment,
Ischemic: different types of shock, discontinuation of nephrotoxic
prolonged prerenal AKI Yes drug(s), close clinical monitoring
Dialysis often necessary
Toxic, endogenous: rhabdomyolysis, hemolysis,
TLS, uric acid crystals, myeloma light chains

Figure 2 A stepwise approach for the recognition and management of acute kidney injury
Abbreviations: ACEIs, angiotensin­‑converting enzyme inhibitors; ARBs, angiotensin II receptor blockers; GCS, glucocorticosteroids; HUS, hemolytic
uremic syndrome; NSAIDs, nonsteroidal anti­‑inflammatory drugs; RBF, renal blood flow; RPF, retroperitoneal fibrosis; TLS, tumor lysis syndrome;
TTP, thrombotic thrombocytopenic purpura; USG, ultrasonography

concern about implementing this system in Pol­ metabolic and fluid demands exceed the total kid­
ish hospitals.51 ney capacity.
The prognosis in hospital­‑acquired AKI is gen­
Key messages for everyday practice The current erally poor and is associated with high in­‑hospital
approach to AKI includes: 1) identification and and long­‑term mortality. However, since AKI is
treatment of the underlying causes such as vol­ not a single disease yet a complex, heterogeneous
ume depletion, hypotension, use of selected syndrome being a collection of entirely different
drugs, or urinary tract obstruction; 2) removal entities, ranging from those relatively benign such
of any potential insults to minimize additional as pre- and postrenal AKI to multiorgan failure,
injury; and 3) supportive measures to maintain the prognosis widely varies among patients. In ad­
optimal fluid, acid–base, and electrolyte balanc­ dition to the cause, the risk of poor outcomes is
es. In patients with severe AKI, RRT is initiated determined by a variety of clinical factors includ­
when these measures fail to provide an adequate ing patients’ age, underlying CKD, baseline renal
and safe control of homeostasis. A stepwise ap­ function, failure of other organs, sepsis, chron­
proach for the recognition and management of ic comorbidities, stage and length of an AKI epi­
AKI is presented in Figure 2 . The timing of dialy­ sode, and the degree of renal recovery.
sis initiation as well as its optimal dose remains It is suggested that AKI survivors, especially
controversial. It should be related to the general those who develop AKI in the hospital, should be
condition of the patient, capacity of the cardio­ closely followed up, since they are at substantial
vascular system and other organs, as well as ob­ risk of relapse and the subsequent development
served or predicted dynamics of serum potassium of end­‑stage CKD as well as other adverse out­
and acid–base alterations. In recent years, a con­ comes including hypertension and cardiovascu­
cept of the differentiated and individualized ap­ lar disease. According to the 2012 KDIGO guide­
proach has been increasingly appreciated,50 ac­ lines, patients discharged from the hospital with
cording to which RRT should be considered when a diagnosis of AKI should be evaluated within 90

1078 POLISH ARCHIVES OF INTERNAL MEDICINE 2020; 130 (12)

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Conflict of interest None declared. ed urinary levels of kidney injury molecule type 1 and adverse cardiovascu‑
lar events at 12 months in patients with coronary artery disease. Pol Arch
Open access This is an Open Access article distributed under the terms
Intern Med. 2018; 128: 301-309.
of the Creative Commons Attribution­‑NonCommercial­‑ShareAlike 4.0 Inter‑
national License (CC BY­‑NC­‑SA 4.0), allowing third parties to copy and re‑ 26 Walther CP, Winkelmayer WC, Deswal A, et al. Readmissions after
distribute the material in any medium or format and to remix, transform, and acute kidney injury during left ventricular assist device implantation hospi‑
build upon the material, provided the original work is properly cited, distrib‑ talization. Am J Nephrol. 2020; 21: 1-10. 
uted under the same license, and used for noncommercial purposes only. For 27 Gilligan LA, Davenport MS, Trout AT, et al. Risk of acute kidney injury
commercial use, please contact the journal office at pamw@mp.pl. following contrast­‑enhanced CT in hospitalized pediatric patients: a propen‑
How to cite Matuszkiewicz­‑Rowińska J, Małyszko J. Acute kidney inju‑ sity score analysis. Radiology. 2020; 294: 548-556. 
ry, its definition, and treatment in adults: guidelines and reality. Pol Arch In‑ 28 Bassegoda O, Huelin P, Ariza X, et al. Development of chronic kidney
tern Med. 2020; 130: 1074-1080. doi:10.20452/pamw.15373 disease after acute kidney injury in patients with cirrhosis is common and
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