ACUTE KIDNEY INJURY
The renal system stands at nearly the top of the
list of organ systems most often impacted by
the course of a critical illness. The kidneys are
extremely susceptible to even subtle changes
In the acute phases of a patient’s illness,
this decrease in kidney function is known as
AKI, formally called acute renal failure. The
name change was necessitated by the fact that
a decrease in the kidneys’ ability to clear waste
didn’t equate to absolute organ failure. In addition, most cases of AKI are transient if the
reversible causes are treated early.
The diagnosis of AKI is made when the
kidneys are unable to clear the buildup of
nitrogenous waste from the body at a nor-
mal rate. The buildup of these waste prod-
ucts is best observed by the measurement of
a patient’s serum creatinine. The criteria for
diagnosis is having at least one of the follow-
ing: 1) A rise in serum creatinine of at least 0.3
mg/dL over the baseline in a 48-hour period;
or 2) A rise in serum creatinine of at least 1. 5
times the baseline creatinine over the previous
seven days. 1 A third criterion that utilizes urine
output as a diagnostic trigger isn’t often used
because certain circumstances can confound its
reliability. 2 That said, a sudden or progressive
decline in urine output should still warrant
the suspicion of renal impairment.
Classically, renal dysfunction is categorized
based on where the causative injury to the kid-ney(s) originated and which part of renal anatomy is most directly impacted. The causes of
AKI are categorized into three groups:
1. Pre-renal. Pre-renal insults primarily
focus on disease processes that affect renal
perfusion. The pathogenesis of pre-renal AKI
can include true volume depletion (e.g., excessive vomiting/diarrhea or diuretic overdose),
hypovolemia from hemorrhage, other shock
states, cardiorenal syndrome (i.e., heart failure),
and hepatorenal syndrome (i.e., liver failure).
Volume depletion and hypovolemia inhibit
renal perfusion due to an overall lack of circulating blood volume. Conversely, other forms of
shock, cardiorenal syndrome and hepatorenal
syndrome cause decreases in the kidney’s pulsatile perfusion due to impaired blood circulation. In nonhemorrhagic shock and cardiorenal
syndrome, blood isn’t able to be effectively
propelled through the kidney’s vasculature.
In hepatorenal syndrome, the kidneys become
bogged down by an inability to clear venous
blood volume due to portal vein hypertension.
2. Intra-renal. AKI from intra-renal pathol-ogies lead to renal impairment by injuring the
renal tissue directly. The intra-renal processes
that lead to AKI are differentiated based on
which parenchymal tissue is affected: renal
vasculature (e.g., malignant hypertensive crisis, hemolytic uremia), glomeruli (e.g., IgA
nephropathy, lupus), and renal tubules (e.g.,
nephrotoxin exposure, sepsis).
3. Post-renal. Post-renal causes are due to
obstructive urinary stasis that ultimately results
in hydronephrosis. The obstruction is usually
a result of progressive prostate diseases (e.g.,
benign prostatic hyperplasia or malignancy)
or other metastatic disease.
It’s important to note that, despite how
a particular cause of AKI is categorized, its
effects can progress to another component of
the renal anatomy. For instance, prolonged
hypotension, which is pre-renal in origin, can
cause acute tubular necrosis, which is intra-renal. This crossing of etiologies demands
astute clinical attention to the root cause.
Although the majority of AKIs are revers-
ible, the longer an AKI persists and progresses,
the greater the likelihood the injury will lead
to permanent damage. 3
Given the wide range of causative factors
that can lead to the development of an AKI,
it’s not surprising that AKI is one of the more
common complications of critical illness. Of all
patients hospitalized, nearly 10% will develop
some degree of AKI. 4 The incidence soars to
more than 50% for intensive care patients. 5
For nearly 70% of these patients, the etio-
logical category is pre-renal and/or acute tubu-
lar necrosis (ATN). 6 This is likely due to the
prevalence of sepsis in this patient population.
Among critically ill and injured patients,
the most common cause of AKI is sepsis. 7.
There are several reasons for this, many of
which aren’t yet fully understood. However,
it’s currently thought that the impact sepsis
has on blood pressure causes the decrease in
renal perfusion, thus causing the pre-renal
injury. It’s also thought that sepsis provokes
ATN by damaging the renal tubules as a result
of persistent hypoperfusion. Inflammatory
mediators released in huge quantities during
the sepsis disease process cause damage that,
in turn, worsens the ATN.
In the majority of cases of AKI, there’s little to no clinical manifestation of the AKI
itself, especially in the early phases. Patients
often seek medical attention for the underlying
causes of the AKI: sepsis, diabetic ketoacidosis, surgery, trauma, etc. However, regardless
of the cause, AKI represents a serious and
potentially life-threatening complication of
any critical illness.
In the initial, hyperacute phases of AKI,
the goal is treating the reversible causes, such
as hypovolemia/hypotension, hypervolemia
and urinary retention.
In most cases, the cause of AKI isn’t transient. For instance, sepsis and cardiorenal/
hepatorenal syndromes can take days or weeks
to overcome and return to a near-baseline status. In those cases, care teams will focus on
maximizing the patient’s hemodynamics and
overall clinical condition in order to preserve
as much renal function as possible.
In many critically ill patients, the AKI
will continue to progress despite renal-protective measures. In these patients, the AKI
can become very dangerous and its complications can become life-threatening. Once
the AKI has progressed to this point, surveillance for and treatment of the immediate life
threats become the focus. In persistent AKIs
that have progressed to a moderate or severe
course, there are four immediate life threats
Azotemia: An abnormal abundance of
nitrogenous waste products in the blood
that can be indicative of renal impairment.
Continuous renal replacement therapy
(CRR T): A variation of RR T used in critically ill
patients by which the efficiency of fluid and
waste product removal is greatly decreased
to preserve hemodynamic stability.
Creatinine: A byproduct of muscle metabolism that’s generally produced at a constant
rate and is unchanged by other organ systems. It’s excreted in the urine, unchanged
from its pre-renal state. It’s frequently measured via blood sample as an indirect indicator of kidney function.
Renal replacement therapy (RR T): Traditionally known as dialysis, RRT is the artificial means of clearing the blood of waste
products in the absence of adequate kidney function.
Uremia: The sequela of impaired renal function that consists of derangements in fluid/
electrolyte balance, metabolic functions, and