Nephrology 21 (2016) 729–735

Review Article

Community-acquired acute kidney injury: A challenge and

opportunity for primary care in kidney health
PAUL DER MESROPIAN,1 JENNIFER OTHERSEN,2 DARIUS MASON,3,4,5 JEFFREY WANG,5,6 ARIF ASIF7 and
ROY O MATHEW2
1
Division of Nephrology, Department of Medicine, Stratton Veterans Affairs Medical Center, 3Department of Research Stratton Veterans Affairs Medical Center,
4
Department of Pharmacy Practice, Albany College of Pharmacy and Health Sciences, and 5Division of Nephrology and Hypertension, Albany Medical College, Albany,
New York, 2Division of Nephrology, Department of Medicine, William Jennings Bryan Dorn Veterans Affairs Medical Center, Columbia, South Carolina; and 6Division of
Nephrology and Hypertension, Department of Medicine, Hennepin County Medical Center, Minneapolis, Minnesota, USA; and 7Department of Medicine, Jersey
Shore University Medical Center, Meridian Health, Neptune, NJ

KEY WORDS: ABSTRACT:

acute kidney injury, adverse events, community
acquired, epidemiology, renal prognosis.
Correspondence
Dr Roy O Mathew, Division of Nephrology,
Department of Medicine, William Jennings Bryan
Dorn Veterans Affairs Medical Center, 6439
Garners Ferry Road, Columbia, SC 29209, USA.
Email: roy.mathew@va.gov
Accepted for publication 11 February 2016.
Accepted manuscript online 17 February 2016.
doi: 10.1111/nep.12751
Community-acquired acute kidney injury (CA-AKI) has been found to be a
common event in the population. Current incidence estimates are not avail-
able, but evaluations of severe elevations in serum creatinine indicate that
incidence can be as high as 989 cases per million population in those older than
80 years. Data on risk factors are limited, but older age and higher comorbid ill-
ness burden, especially diabetes and cardiovascular disease, seem to be more
common in patients who suffer CA-AKI. In addition to being more common
than hospital-acquired AKI, the long-term sequelae of CA-AKI seem to be just
as severe, including renal disease progression and mortality. Efforts to better
understand the aetiology of CA-AKI and how ultimately to prevent the
development of this condition will need to be taken. In the meantime, a
concerted effort by general internists and nephrologists will be needed to
prevent CA-AKI in the highest risk patients and thus limit the poor outcomes
associated with this entity.

SUMMARY AT A GLANCE
In this review, the authors show that
community acquired acute kidney injury is
common, severe and can have important
long term adverse consequences.

Acute kidney injury (AKI), even when mild, is a well-known
contributor to increased mortality and morbidity in hospitalized
patients.1 AKI occurring outside of the hospital setting – so
called community-acquired AKI (CA-AKI) – has gained in-
creased attention over the last 2–3 years. Hospital-acquired
AKI (HA-AKI) has been the focus of research over the last
two decades. A definition that maximally uses the available
clinical information (serum creatinine and urine output) has
been developed in this setting (summarized in Table 1). The
most recent definition for AKI has been organized by the
Kidney Disease – Improving Global Outcomes initiative.2 This
review will focus on CA-AKI endured in developed countries,
despite the fact that CA-AKI is more common in developing na-
tions including those in tropical zones. This distinction is impor-
tant because the usual aetiologic spectrum of AKI endured in
developing countries, especially the tropical setting, is unique,
ranging from plant or animal toxin ingestions or infections such
as malaria or Hantavirus to obstetric complications.3–5 A sum-
mary of CA-AKI as witnessed in the western, non-tropical
countries has not been conducted to date. In addition, this en-
tity has particular relevance to the broad medical community
including general internist and nephrologist, as many of these
patients will be managed in the primary care setting and often
by the hospitalist when they are admitted with AKI.
EPIDEMIOLOGY
Prevalence and incidence of CA-AKI
Community-acquired AKI is not a new concept. Some of the
earliest case reports of AKI described persons with severe trau-
matic muscle injuries and subsequent rhabdomyolysis from the

© 2016 Asian Pacific Society of Nephrology 729

PD Mesropian et al.

Table 1 Definitions proposed for the identification and staging of acute kidney injury (reviewed in the work of the Group KDIGOKAKIW2)

Risk injury failure loss Acute kidney injury Kidney Disease – Improving
and end stage network Global Outcomes

Creatinine Urine output Creatinine Urine output Creatinine Urine output

Risk (>1.5× the <0.5 mL/kg Stage 1 (greater <0.5 mL/kg Stage 1 (greater than <0.5 mL/kg
baseline creatinine) per h for 6 than 26.4 μmol/L – per h for 6 26.4 μmol/L – 0.3 mg/dL per h for 6–12 h
0.3 mg/dl – rise in –rise in 48 h or >1.5–1.9×
48 h or >1.5× baseline)
baseline)
Injury (2–3× greater <0.5 mL/kg Stage 2 (2–3× <0.5 mL/kg Stage 2 (2–2.9× <0.5 mL/kg
than the baseline per h for 12 h baseline creatinine) per h for 12 h baseline creatinine) per h for >12 h
creatinine
Failure (>3× greater <0.3 mL/kg Stage 3 (>3× <0.3 mL/kg Stage 3 (>3× <0.3 mL/kg per h
than the baseline per h for 24 h baseline creatinine) per h for 24 h or baseline creatinine) for >24 h or anuria
creatinine or anuria for 12 h anuria for 12 h for >12 h

battlefield or areas of natural disaster.6–8 Despite the preface
community acquired, most of the data on this entity have been
derived from hospitalized patients. Kaufman and colleagues
performed the first formal analysis of CA-AKI.9 They prospec-
tively identified patients admitted to a single Veteran Affairs
hospital over a 17 month period. The definition of AKI was
derived from a schema for hospital-acquired acute renal failure
used by Hou et al.10 Kaufman et al. found that the prevalence of
CA-AKI was 1% of hospital admissions, whereas HA-AKI was
4%. This is in contrast to later reports. For example, in the
Liano et al. study that explored the population level epidemiol-
ogy of hospital-detected AKI (at or during admission), the
major proportion of cases were identified on admission
(60%).11
In studies that specifically examined the epidemiology of CA-
AKI as compared with HA-AKI, CA-AKI has been found to be
2–3× more prevalent than HA-AKI (Table 2). In these studies,
the cases of AKI were identified by international classification di-
agnostic (ICD) codes for ARF, thereby possibly underestimating
the true prevalence of both CA-AKI and HA-AKI in hospital.
Only one study from China, by Wang and colleagues, found a
smaller (1.5× greater) difference between CA-AKI and HA-
AKI.12
Population-wide incidence of CA-AKI was investigated by
two separate groups. Liano and colleagues noted that of the to-
tal AKI identified in the hospital setting, 60.4% were identified
on admission; however, this study did not distinguish the inci-
dence of CA-AKI from HA-AKI in their final analysis.11 Feest

Table 2 Epidemiologic characteristics of CA-AKI compared with HA-AKI from selected studies

Talabani
Study AKI Schissler 201316 Wonnacott Der Mesropian 201414
definition Liano11 custom Obialo 200015 custom RIFLE 201429 AKIN 201417 RIFLE KDIGO

HA-AKI CA-AKI HA-AKI CA-AKI HA-AKI CA-AKI HA-AKI CA-AKI HA-AKI CA-AKI CA-AKI

% of N/A N/A N/A N/A (0.17) (0.6) 2.1 4.3 N/A N/A 54% were
Hospitalized hospitalized
% of AKI cases 40 60 21 79* 20.6 79.4* 32.8 67.3* 22 78* 100
% baseline CKD Exclusion Exclusion Exclusion Exclusion 48.9 43.2 28.4 33.2 51.9 42.3* 37.8
Peak serum N/A N/A 4.7 5.9 3.53 3.75 N/A N/A 3.6 4.2 N/A
creatinine
(mg/dL)
% in highest AKI N/A N/A N/A N/A 20.7 31.6 20.7 27.3 29.1 43.8 8.3
stage
Dialysis 36% of all AKI 36% of all AKI 14 7 9.9 5.5 1.8 3.5 5.1 3.6 Only told of
requirement (%) patients patients 8/11 patients
admitted to a
renal unit
In-hospital Overall 45% - Overall 45% - N/A N/A 33.7 11.5 42.8 19.6* 26.6 19.6 3.4
mortality (%) HA-AKI patients HA-AKI patients
20% higher than 20% higher than
CA-AKI CA-AKI

*P < 0.05 AKI, acute kidney injury; AKIN, acute kidney injury network; CA-AKI, community-acquired AKI; CKD, chronic kidney disease; HA-AKI, hospital-acquired AKI;
RIFLE: risk injury failure loss end-stage.

730 © 2016 Asian Pacific Society of Nephrology


et al, on the other hand, specifically looked at creatinine values
from measurements made in the outpatient setting.13 Their in-
clusion criteria for AKI only included those with severe injury
(serum creatinine of 500 μmol/L; 5.6 mg/dL); in addition, pa-
tients with chronic kidney disease (CKD) or malignancy were
excluded. The annual incidence of this severe AKI was
dependent on age, with an incidence of 17.1 cases per million
population in those under 50 years and 949 cases per million
per year in the 80 to 89 age group. There appeared to be differ-
ences in gender-related incidence as well: males demonstrating
259.4 cases per million adult males, and females demonstrating
92.6 cases per million adult females.
Talabani and colleagues conducted the first population-wide
analysis of changes in serum creatinine values specifically
examining all variety of CA-AKI.14 Of the patients who had
creatinine measurements in an outpatient laboratory during a
1 month period, 0.7% were identified as meeting the criteria
for CA-AKI (50% rise from baseline serum creatinine – which
was measured in the 6 months prior to the index creatinine
value. As compared with a random subset of the population
who did not suffer CA-AKI, the CA-AKI individuals were older
(70 vs 57 years.) and more likely to have pre-existing CKD
(37.8% vs 27.7%, P = 0.023). Unfortunately, incidence esti-
mates were not provided.
Aetiology and severity of CA-AKI
Understanding the causes of CA-AKI is important so that
preventive interventions can be devised. Both Kaufman et al.
and Obialo et al. examined aetiologies in a prospective manner
(Table 3). In the study by Kaufman and colleagues, the majority
Table 3 Risk factors and aetiology of community-acquired acute kidney
injury (CA-AKI)
Identified risk factors for CA-AKI
Older age
Presence of diabetes mellitus
Presence of coronary artery disease
Presence of congestive heart failure
Presence of baseline chronic kidney disease
Co-existent acute illness such as community-acquired pneumonia
HIV infection
Identified aetiology of CA-AKI
Pre-renal
Gastrointestinal illness
Poor oral intake
Angiotensin converting enzyme inhibitor use
Non-steroidal anti-inflammatory drug use
Diuretics
Intrinsic
Postoperative acute tubular injury
Acute tubular necrosis
Primary glomerular disease
Various drug induced tubulointerstitial nephritis
Pigment or crystal induced tubular injury
Obstructive uropathy
© 2016 Asian Pacific Society of Nephrology
Challenge of CA-AKI in primary care
of CA-AKI was classified as pre-renal (70 of 98 classified pa-
tients).9 Looking at both obstruction and pre-renal disease, 88
of 98 patients demonstrated one of these aetiologies and the
remainder being some form of intrinsic renal disease. Analysis
of specific causes of pre-renal disease found gastrointestinal
illness or poor oral intake in the majority of cases. Drugs were
implicated in pre-renal cases as well, the majority being angio-
tensin converting enzyme inhibitors (ACEI) and diuretics.
Intrinsic causes included a mix of primary glomerular diseases
and drug induced tubular injury. In contrast to the study by
Kaufman et al., Obialo et al. found that intrinsic renal disease
constituted the majority (55%) of CA-AKI cases.15 The cases
of intrinsic disease included: acute tubular necrosis, postopera-
tive, drug toxicity and pigment or crystal induced; this classifi-
cation may have had some overlap in categories thereby
possibly underestimating cases of pre-renal disease. Among
the patients with CA-AKI, 35% had a diagnosis of pre-renal
disease, and 10% of cases were considered to be post-renal.
Differences in inclusion criteria and age of populations may
have accounted for some of the variation in findings.
The introduction of the new staging schemas for HA-AKI has
also allowed the exploration of the severity of AKI in CA-AKI.
All recent analyses have staged the identified cases of CA-AKI
based on one of the available schemas listed in Table 1. In the
analysis of Schissler et al., 37.3% of CA-AKI cases were in the
RIFLE Risk category.16 Der Mesropian et al. found that 22.5%
of CA-AKI cases were in the RIFLE Risk category. Aside from
the analysis by Der Mesropian et al., which found a higher
percentage of Failure criteria among patients with CA-AKI as
compared with HA-AKI, the percentage of patients achieving
the highest stage of AKI was similar between HA-AKI and
CA-AKI groups (Table 2). This suggests that despite the seem-
ingly more benign causes (pre-renal and post-renal) seen in
CA-AKI, at least that which presents to the hospital, the actual
severity of injury is no different between CA-AKI and HA-AKI.
Risk Factors for the development of CA-AKI
There is little information available on the risk factors (Table 3) of
CA-AKI. Ideal studies would compare patients with CA-AKI
with those who had not developed AKI. Der Mesropian et al.
compared baseline characteristics among US Veterans with CA-
AKI, HA-AKI and no AKI.17 Patients with any form of AKI were
at least 20 year older and a higher proportion had diabetes (DM),
coronary artery disease (CAD) and congestive heart failure
(CHF) and underlying CKD. These conditions were similar be-
tween AKI groups. The prevalence of comorbidities between
AKI groups is not perfectly consistent between studies. For in-
stance, Schissler and colleagues examined characteristics and in
hospital outcomes of patients with CA-AKI and HA-AKI.16 Med-
ical conditions noted to be more frequent among patients with
HA-AKI as compared with CA-AKI included CAD, CHF and DM.
Risk factors for CA-AKI likely include other disease processes
such as community-acquired pneumonia (CAP). Akram and
colleagues examined the relationship between CA-AKI and
731
PD Mesropian et al.

outcomes in patients admitted with CAP.18 In their analysis,
they found that approximately 18% of patients admitted with
CAP had CA-AKI on admission. Of these, nearly 14% had met
RIFLE category F. Patients with CAP who also had CA-AKI were
more likely to have had pre-existing CKD as compared with
those who did not develop CA-AKI, and they were more likely
to be on an ACEI or angiotensin receptor type II blocker (ARB).
The presence of CA-AKI on admission resulted in a higher inci-
dence of the need for mechanical ventilation, pressor support
and longer hospital stays. Patients with CA-AKI had higher
30 day mortality than those patients without CA-AKI, and the
mortality risk increased with increasing stage of AKI.
Medications that negatively affect kidney hemodynamics
increase the risk for AKI (Table 4). Non-steroidal anti-
inflammatory drugs (NSAIDs) including cyclo-oxygenase
(COX) 2 enzyme inhibitors, loop diuretics, ACEI, and ARBs
modify kidney perfusion and increase the risk for AKI.19–21
Patients with concurrent comorbidities that impede renal perfu-
sion such as pre-existing CKD, heart failure, cirrhosis or renal
vessel disease can increase the likelihood of a patient experienc-
ing AKI from these medications. Several studies have illustrated
the role of medications in AKI; however, parsing the medication
related associations between CA-AKI versus HA-AKI is rarely
evaluated. Schissler et al. revealed higher NSAIDs and
ACEI/ARB use in a CA-AKI cohort versus HA-AKI (NSAIDS,
19.6% vs 11%; ACEI/ARB, 54.3% vs 45.7%, respectively).16
Similarly, Dreischulte and colleagues demonstrated an in-
creased risk of AKI when NSAIDs were combined with renin-
angiotensin aldosterone system antagonists, as well as when
loop diuretics were combined with aldosterone antagonists.21
This was especially pronounced in those over 75 with pre-
existing CKD. With the association of age and CA-AKI and the
increased use of NSAIDS in the elderly population, future CA-
AKI studies are warranted to provide greater analysis of nephro-
toxic medication usage.22 A topic of particular relevance to the
general medicine community is the finding of increased AKI
with statin use.23 The risk of rhabdomyolysis with resultant
pigment induced AKI is a real concern with statin use. Although
these earlier observational studies have suggested an increased
risk of AKI with the use of statins, further studies have failed
to confirm this risk.24,25 Murugan and colleagues examined
the use of statins and the association with the development of
AKI in the setting of CAP.26 They identified that the risk of
AKI seen with statin use was explained by the indication for
therapy with statin. Patients requiring statin therapy were gen-
erally older and with greater comorbid condition burden than
those not on therapy; all the conditions currently indicated as
risk factors for CA-AKI (Table 3).
The risk of age is likely, in part, related to a number of inter-
related factors. The presence of severe disease, even in young
individuals, equally places these individuals at risk for AKI.
Franceschini et al. examined a prospectively collected cohort
of individuals with HIV for any AKI.27 Of all, the 754 patients
in this cohort, 71 (9.4%) suffered AKI and 71% of the AKI
episodes were community acquired. The majority of patients,
98%, were <60 years old. The patients who suffered AKI were
more likely to have acquired immunodeficiency syndrome,
lower CD4 counts and higher HIV viral load.
An examination of Table 3 highlights an important distinc-
tion between the aetiology of CA-AKI encountered in tropical
and non-tropical countries; there is a much lower incidence
of infection-related CA-AKI in the latter.3 Infection-related
CA-AKI is not unheard of in western, non-tropical countries.
Outinen et al. describe 556 cases of Puumala hantavirus
infection treated, over a 31 year period, an academic medical
centre in Finland.28 Eighty-three per cent of patients were
found to have a creatinine that was elevated (>100 μmol/L or
1.14 mg/dl), and 34% were found to have a severe elevation
(>356.5 μmol/L or 4 mg/dL).
Outcomes related to CA-AKI
Given that most causes of CA-AKI are reversible, it would be
expected that long-term renal and patient outcomes would be

Table 4 Effects of several medications on renal hemodynamics and function

Afferent arteriolar resistance Efferent arteriolar resistance Renal blood flow GFR

Renal sympathetic nerves ↑↑ ↑ ↓ ↓

Epinephrine ↑ ↑ ↓ ↓
Adenosine ↑ → ↓ ↓
Cyclosporine ↑ → ↓ ↓
NSAIDs ↑↑ ↑ ↓ ↓
Angiotensin II ↑ ↑↑ ↓ ↓→
Endothelin-1 ↑ ↑↑ ↓ ↓
High-protein diet ↓ → ↑ ↑
Nitric oxide ↓ ↓ ↑ ↑(?)
ANP (high dose) ↓ → ↑ ↑
PGE2/PGI2 ↓ ↓(?) ↑ ↑
Calcium channel blockers ↓ → ↑ ↑
ACE inhibitors, ARBs ↓ ↓↓ ↑ ?†

†Barring critical renal artery stenosis, renin-angiotensin-aldosterone system inhibitors generally produce an initial decrease in glomerular filtration that then manifests as
a reduction in the decline in glomerular filtration rate as compared with not taking this class of medications. ACE, angiotensin converting enzyme; ANP, atrial natriuretic
peptide; ARBs, angiotensin receptor blockers; GFR, glomerular filtration rate; NSAIDs, non-steroidal anti-inflammatory drugs; PGE, prostaglandin E; PGI, prostaglandin I.

732 © 2016 Asian Pacific Society of Nephrology


better for CA-AKI as compared with HA-AKI. Der Mesropian
et al. examined renal outcomes of patients with either CA-
AKI or HA-AKI as compared with patients who had no
AKI.17 Twelve per cent and 6.1% of those with CA-AKI devel-
oped a doubling of serum creatinine or end-stage renal disease
at 3 years, respectively. These estimates were similar in patients
with HA-AKI. Mortality was also very common among patients
with any AKI and not different between the two groups. This
was different from the findings of Wonnacott et al. who looked
at mortality at 14 months following CA-AKI. As compared with
HA-AKI, patients with CA-AKI demonstrated a higher survival
rate (55% vs 36.9%, P < 0.001).29 However, a closer look at
their rate, which included all in-hospital deaths into their
long-term outcomes, the observed longer term mortality rate,
after the initial post-hospitalization period, was similar for the
14 months for both groups.
Talabani et al. paint a picture of a problem that is far larger in
scope than what has been understood from the hospital-based
studies.14 The majority of subjects with AKI in hospitals have
suffered CA-AKI. However, based on the findings of Talabani
et al., 46% of patients with CA-AKI in the community are never
admitted to the hospital. The analysed outcomes, both short
(3 months) and long (3 years) term, were found to be worse
among patients who had CA-AKI. Of patients with CA-AKI,
only 58% demonstrated complete recovery by 3 months follow-
ing the CA-AKI episode. Interestingly, patients with CA-AKI
who were admitted to the hospital had higher proportion of
complete renal recovery (69%) as compared with those ‘man-
aged’ as outpatients (44.6%). Three month mortality was de-
pendent on the severity of AKI suffered. Of those patients who
died within 3 months, 69% had AKI stage 2 or 3; whereas of
those who lived past 3 months, only 39% had AKI stages 2 or 3.
Long-term (3 years) outcomes, as compared with age and
gender matched control subjects without CA-AKI, were signifi-
cantly worse among patients with CA-AKI. Progressive CKD
(decline in renal function >3 mL/min per year) was seen in
83% CA-AKI patients with pre-existing CKD compared with
49% in those without pre-existing CKD. Among age and gender
matched control subjects, the respective proportions were
32.7% and 4.1%. This would suggest two things: AKI is a strong
risk factor for progression of CKD and it is an important risk fac-
tor for the development of CKD in elderly individuals. As would
be expected, a higher proportion of those with no or incomplete
recovery had progressive CKD (88%) as compared with those
with complete recovery (46%). The finding that those with
‘complete’ recovery did not have a lower level of progressive
CKD has important practical implications. This would suggest
that even if an episode of CA-AKI recovers in terms of creatinine
measurements, there may be underlying structural injury that
requires regular follow-up of renal function. Mortality was also
increased among patients with CA-AKI as compared with age
and gender matched control subjects without AKI.
The available data suggest that long-term outcomes are very
similar between CA-AKI and HA-AKI. This has stark clinical
and financial implications, especially if it is confirmed that the
© 2016 Asian Pacific Society of Nephrology
Challenge of CA-AKI in primary care
prevalence and incidence of CA-AKI truly exceeds HA-AKI.
The economic burden of HA-AKI has been well described.1,30,31
Using the current evidence, it will be important to estimate the
economic burden imposed by CA-AKI and allocate resources
accordingly.
Management recommendations based on available
evidence (Table 5)
The highest risk individuals seem to be those who have multi-
ple medical problems and are on medications that influence
the renal hemodynamics (a summary of the effects on renal he-
modynamics is provided in Table 3) Directly educating patients
at the point of care of the risks of AKI with the use of NSAIDs
may be another means of reducing the incidence of CA-
AKI.32 Another measure that has been advised is the tempo-
rary discontinuation of anti-hypertensives and NSAIDs during
inter-current illnesses such as upper respiratory infections and
especially acute gastrointestinal illnesses that limit fluid and
food intake.33 The International Society of Nephrology has
put forward the ‘0 by 25’ campaign to highlight the importance
of AKI in preventable causes of death in the community.34
Such an effort can only be accomplished through the strong in-
volvement of the general medical community, and the
methods highlighted earlier may be important in achieving this
noble goal of 0 preventable deaths related to AKI by 2025.
Table 5 Management/prevention recommendations and evidence level
Evidence level (based on Oxford
Recommendations to prevent CA-AKI classification of evidence)†
Identify high-risk individuals (age, pre- 2b
existing CKD, pre-existing cardiovascular
disease) for targeting of risk reduction
measures
Directly educating patients at point of 2b
purchase of OTC medications that can
place patients at risk for AKI such as NSAIDs
Educating patients to either contact 5
physician’s office or temporarily
discontinue anti-hypertensives and/or
diuretics during times of acute illness such
as gastrointestinal illness.
No recommendation for routine NA
hospitalization for CA-AKI found on
outpatient testing (i.e. use clinical
judgement)
†(http://www.cebm.net/oxford-centre-evidence-based-medicine-levels-evi-
dence-march-20:39/; accessed 21 January 2016 at 20:39 )1a, based on systemic
reviews with homogeneity of effects; 1b, based on single randomized controlled
trial (RCT) with narrow confidence intervals; 1c, less well designed RCT; 2a, sys-
tematic review (SR) of cohort studies with homogenous effect; 2b, single cohort
or poorly designed RCTs; 2c, outcomes research or ecological studies; 3a, SR of
case–control studies; 3b, individual case–control study; 4, case series and poorly
designed cohort studies; 5, expert opinion. CA-AKI, community-acquired acute
kidney injury; CKD, chronic kidney disease; NSAIDs, non-steroidal anti-inflamma-
tory drugs.
733
PD Mesropian et al.
Future directions in understanding CA-AKI
Biomarkers (biologic compounds that can serve as an indicator
of disease, its outcome, or both) that can identify true paren-
chymal injury have been identified and are being studied in
various settings where AKI is encountered. The authors refers
the reader to a recent review on the various biomarkers avail-
able for AKI.35 The major limitation of the current application
of biomarkers of AKI for the evaluation of CA-AKI is that these
biomarkers have been primarily validated in homogenous pop-
ulations (such as patients undergoing coronary artery bypass
grafting), which is very different than the CA-AKI population
as described. When Nikolas and colleagues examined urinary
neutrophil gelatinase-associated lipocalin (uNGAL) in all pa-
tients presenting to a major metropolitan university–hospital-
based ED36}, a single measurement of uNGAL provided no
greater discrimination than presenting serum creatinine for
predicting the incidence of AKI. There was only slightly greater
distinction between AKI severity grades based on RIFLE Criteria
than serum creatinine, relegating the use of biomarkers, as un-
derstood currently, to possibly research analysis of CA-AKI.
CONCLUSION
Community-acquired AKI appears to be the most common
form of AKI encountered in the clinical setting and with similar
poor long-term outcomes as with HA-AKI. Patients with high
comorbidity on multiple medications appear to be at highest
risk. Involvement of the general medicine community will be
critical in reducing the incidence of this disorder by early recog-
nition of high-risk individuals and risk modification where pos-
sible. Liano and colleagues identified this as an important
feature of CA-AKI in their original report.11 They identified
that ‘Our work illustrates the fact that ARF is a universal prob-
lem in medical practice…As a result, any physician may face a
patient with an ARF episode independently of his/her specialty
or working place’.11 Thus, further study will be needed to better
understand the epidemiology of CA-AKI and the efficacy of
preventive measures, and estimate its cost to society.
CONFLICTS OF INTEREST
The authors attest to having no conflicts of interest in relation
to this review.
FUNDING
No funding for this review.
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