(1) Read” Acute kidney injury: Challenges and opportunities “article then the two additional articles (  Challenges of targeting vascular stability in acute kidney injury  & The importance of early detection in stopping  acute kidney injury)

2. After you’ve read the 3 articles (attached) provide an un plagiarized summation of at least 500 words. Include all 3 references. Use APA format throughout the document. 

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44 l Nursing2020 l Volume 50, Number 9 www.Nursing2020.com

Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.










Acute kidney injury:
Challenges and


Abstract: Acute kidney injury (AKI) can be a devastating diagnosis for any patient and can
increase mortality during hospitalization. There can be long-term consequences for those who
survive the initial insult. This article discusses AKI and its implications for nurses.

Keywords: acute kidney injury, Acute Kidney Injury Network, AKI, chronic kidney disease,
CKD, community-acquired acute kidney injury, hospital-acquired acute kidney injury, KDIGO,
Kidney Disease Improving Global Outcomes, Nephrotoxic Injury Negated by Just-in-time
Action, sick day rule

heterogeneous kidney disorder that
increases in-hospital morbidity and
mortality. In 2016 data, the inci-
dence of AKI was 20% for Medicare
patients with both chronic kidney
disease (CKD) and diabetes.1 Based
on Veterans Affairs (VA) 2016 data,
AKI occurred in more than 25% of
hospitalized veterans over age 22,
but less than 50% of those with
lab-documented AKI were coded as
such.1 The chief concern here is a
missed opportunity for intervention.
AKI increases long-term risk of CKD,
but if clinicians do not recognize
the diagnosis, they cannot follow up
or intervene. An AKI diagnosis also
increases the chance of another AKI
episode, with a 30% risk of a recur-
rent AKI episode within 1 year.1

Mortality is increased with an AKI
episode. Medicare data from 2016

shows in-hospital mortality of 8.2%,
but this increases to over 13% when
including patients who were dis-
charged to hospice.1 The in- hospital
mortality for patients without AKI
was only 1.8% (3.8% if including
patients discharged to hospice).1 Pa-
tients with AKI also were more likely
to be referred to a long-term-care
facility. (See Hospital discharge status of
first hospitalization for Medicare patients
ages 66+, 2016.)

AKI defined
AKI was previously known as acute
renal failure.2 However, many pa-
tients with kidney injury did not
progress to renal failure, yet still had
significant, often permanent, loss of
kidney function. Researchers worked
to better define AKI and noted that
it is a potential but often reversible
rapid deterioration of kidney func-

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JULY 2017 M L O – O N L I N E .C O M 38


The importance of early detection in stopping
acute kidney injury
By Salvatore Di Somma, MD

cute kidney injury (AKI) is as serious and common as a
heart attack, and it can strike without any warning signs
or symptoms. It affects as many one in fi ve hospital pa-

tients in the United States1 and can rapidly develop into chronic
kidney disease (CKD) or kidney failure, leading in more severe
cases to the need for permanent dialysis treatment with com-
promised quality of life or even to death. Sometimes called a
silent killer, AKI is often overlooked as the true cause of mortal-
ity. AKI is also one of the costliest health issues both in the U.S.
and around the world.

Compounding the problem is that the medical community
has been slow to recognize the disease and implement a stan-
dard of care. However, recent developments and research have
led to new testing that can detect AKI much earlier than other
commonly used tests and is expected to improve clinical and
economic outcomes for patients and hospitals.

What is AKI?
AKI is the rapid deterioration of kidney function within hours
or days. It is often diagnosed in the context of other acute ill-
nesses.2 It indicates initial subclinical kidney cell injury that can
be reversible if the condition is detected early, before dysfunc-
tion. AKI is most commonly brought on by an infl ux of drugs
or toxins or contrast-induced substances, a blockage of urine,
serious infection, trauma, acute heart failure, major surgery,
or chronic illness. Up to 50 percent of critically ill patients will
develop some stage of AKI.3 Patients most at risk are those in
intensive care, as well as the elderly and diabetic patients.

AKI can cause the accumulation of waste products, electro-
lytes, and fl uid in the body as well as reduced immunity and
dysfunction of other organs.2 Prevention through proper test-
ing is the best measure to address AKI. Treatment of AKI can
include many different therapeutic strategies such as reducing
the intake of antibiotics or other drugs, managing fl uids and
diuretic dosages, and monitoring urine output. Other treat-
ments or surgeries could be delayed until the kidneys are
functioning normally. If detection of the risks of AKI occurs
early enough and changes to treatment are made, the kid-
neys can sometimes normalize themselves; consequently, it is
crucial to immediately recognize all phases of AKI occurrence.

More cases, more costs
While AKI is a preventable disease, it is a growing problem
around the world. A 2014 report by the National Confi den-
tial Enquiry into Patient Outcome and Death (NCEPOD), a
London-based nonprofi t that reviews the management of pa-
tients through research and surveys, found that 30 percent of
AKI cases that occurred during hospital admission

Kidney International (2008) 74 257

commentar yhttp://www.kidney-international.org

© 2008 International Society of Nephrology

The compromise of renal microvascular
structure has received considerable atten-
tion as a central and possibly causative
feature of the development of chronic
fibrotic kidney diseases. The reduction
in capillary number has been reported
in a number of chronic diseases and has
been suggested to promote fibrosis in a
variety of different ways, including the
exacerbation of hypoxia.1,2 However, in
the case of chronic kidney disease, the
reduction of renal microvessels repre-
sents a chicken-and-egg dilemma: does
microvessel dropout contribute to renal
fibrosis, or does developing renal fibro-
sis impinge on renal capillary stability?
The answer to this is not known, but data
derived from acute or subtle injury mod-
els (folate, ischemia, nephrotoxin, tran-
sient angiotensin II) demonstrate a loss
of capillaries that typically precedes the
development of prominent fibrosis.3–5

These observations suggest that pres-
ervation or reversal of microvascular loss
in a reversible injury model represents
a sound strategy for ameliorating the

Challenges of targeting vascular
stability in acute kidney injury
David P. Basile1

Acute kidney injury following folate administration is characterized by
a vascular remodeling that is initially proliferative but subsequently
results in vascular endothelial loss. Interventions directed toward
promoting endothelial growth may preserve vascular structure and
therefore renal function. However, angiopoietin-1 therapy in the setting
of folate-induced acute kidney injury resulted in an expanded fibrotic
response despite apparent preservation of the vasculature, indicating
that renal repair responses are complex and vascular-directed therapies
should be approached with caution.
Kidney International (2008) 74, 257–258. doi:10.1038/ki.2008.243

development of renal interstitial fibrosis,
as well as addressing the role of vascular
dropout as an antecedent event in pro-
gressing disease. We and others have dem-
onstrated that a number of factors with
potential to influence vascular growth are
altered in the early course of renal injury
(in our experience using ischemia/reper-
fusion) and have argued that replacement
or enhancement of these factors should
maintain blood vessel structure and influ-
ence long-term outcome.1,6,7

Angiopoietin-1 is a potent angiogenic
factor that interacts with the Tie-2 recep-
tor on endothelial cells. Angiopoietin-1
has little or no proliferative potential but
is a potent inhibitor of endothelial apop-
tosis.8 Angiopoietin-1 has promigratory
effects on endothelial cells, and this may
relate to its important activity facilitat-
ing tube formation during angiogenesis.
Angiopoietin-1 stimulation also tightens
endothelial junctio