Acute kidney injury is common among hospitalized patients. It affects some 3–7% of patients admitted to the hospital and approximately 25–30% of patients in the intensive care unit.

1. Acute kidney injury
(AKI)
By:Mr.Jagdish sambad
M.Sc. Nursing
IKDRC COLLEGE OF NURSING

2. Learning outcome
 To understand the different types and causes of
acute kidney injury (AKI).
 To help and support the patient and family
during an episode of AKI.
 To describe the signs and symptoms of AKI.
 To analyse the management of those with AKI.
 To evaluate the various treatment options for
AKI.

3. INTRODUCTION
 The kidney has multiple functions and the
management of the patient with AKI has been
likened to ‘juggling’ as the nurse has to be
aware of many different aspects of care at one
time (Davies 2009).
 Approximately one in five people who are
admitted to hospital as an emergency will
suffer some degree of acute kidney injury(AKI)

4. Introduction
 Acute kidney injury is viewed as a spectrum of injury, which
may result in organ failure and the need for renal replacement
therapy (RRT).
 Clinically AKI is characterized by a rapid reduction in kidney
function resulting in a failure to maintain fluid, electrolyte and
acid-base homoeostasis Depending on its severity and
duration, AKI is often transient in nature and, with careful
nursing care, the patient can regain normal renal function.
However, without appropriate specialized treatment, the
patient may be denied the opportunity to make a full recovery
and a precipitation of further impairment may lead to chronic
kidney disease (CKD) and established renal failure (ERF).

5. Mortality
 There are a number of patient groups for which AKI has a
particularly high mortality rate. For example, AKI occurs in
up to 65% of patients with septic shock and is
independently associated with an increased risk of death
in patients with sepsis (Bagshawet al. 2009).
 The need for rapid identification of the cause of AKI and
those patients at highest risk is essential so that the
correct course of treatment can be adopted (DuBose et al.
1997). Therefore it is vital for the nurse to play a major
role in assisting physicians in the treatment options
available for this fragile group of patients.
 The development of new biochemical markers may enable
a diagnosis to be made before changes are seen in either
serum creatinine or the urine output.

6. Prerenal Aetiology
Stage Major causes Aetiology
Prerenal Cardiovascular
Vasodilation
Hypovolemia
Congestive cardiac failure
Myocardial infarction
Cardiogenic shock
Cardiac tamponade
Pulmonary embolism
Sepsis
Anaphylaxis
Haemorrhage, including blood loss due
to surgery
Burns
Gastrointestinal loss
Renal loss

7. Intrarenal Aetiology
Stage Major causes Aetiology
intrarenal Glomerulonephritis
Vascular
Intratubular Pigment
Protein
Crystal
Poststreptococcal infection
Systemic lupus erythematosus
Haemolytic-uraemic syndrome
Wegener’s granulomatosis
Goodpasture’s syndrome
Vasculitis
Hypertension
Eclampsia of pregnancy
Renal artery stenosis
Renal vein thrombosis
Myoglobin (rhabdomyolysis)
Myeloma
Nephrotoxin

8. Postrenal Aetiology
Stage Major causes Aetiology
Postrenal Obstruction of lower
urinary tract
Obstruction of upper
urinary tract
Prostatic hypertrophy
Ureteric obstruction (clots,
extrinsic compression,
calculi)

9. Classification
1. Prerenal – relates to the ineffective
perfusion of the kidneys, which are
structurally normal
2. Renal (intrinsic) – damage to the
renal parenchyma, sometimes
secondary to Prerenal problems
3. Postrenal – disordered urinary
drainage of both kidneys or of a
single functioning kidney.

10. 1.Prerenal failure
 Prerenal causes of AKI are directly related to hypoperfusion
states or a decline in the blood supply to the kidneys. The
structure of the kidneys is normal. However, when the renal
blood supply is restricted, glomerular filtration is reduced,
causing decreased perfusion of the kidneys. The net effect is a
decreased blood flow to the glomeruli, which therefore leads to
ineffective filtration because of inadequate blood flow. Without
an effective renal plasma flow rate the glomeruli are unable to
filter waste from the blood but the structure of the renal
tubules remains intact .
 In this prerenal state, urine osmolarity is high and sodium low,
which is consistent with renal hypoperfusion and well-preserved
renal function. If, at this stage, renal blood flow can be
restored, then normal renal function will return.

12. 2.Renal failure
 This cause is sometimes referred to as intrinsic or
intrarenal failure and is associated with structural
damage to the glomeruli and renal tubules. The
difference between pre- and post renal failure and
intrinsic failure is that in intrinsic failure the correction
of the aetiology will not guarantee the complete
recovery of renal function because of damage to the
nephron itself. Here the episode of AKI may have a
lengthy duration and can often lead to CKD.
 The clinical course of intrinsic renal failure is often
complex and, depending upon underlying disorders,
the recovery may be prolonged for up to six weeks.

13. 3.Postrenal failure
 Postrenal conditions obstruct the flow of urine,
so the obstruction has to be bilateral in order
to cause failure. The rapidity of recovery will
depend on the duration and completeness of
the obstruction. The urinary tract may be
obstructed by three mechanisms:
 obstruction from within (e.g. ureteric stones)
 disease of the wall
 obstruction from outside (e.g. prostatic hypertrophy).

14. AKIN-Classification
Category Serum creatinine Urine output
Stage-1 Serum creatinine ≥ 150–200% from baseline <0.5 ml/kg/h for > 6 h
Stage-2 Serum creatinine ≥ 200–300% from baseline <0.5 ml/kg/h for > 12 h
Stage-3 Serum creatinine ≥ 300% from baseline
OR serum creatinine ≥ 54 μmol/l with an acute
rise of at least 44 μmol/l
< 0.3 ml/kg/h for > 24 h
or
anuria for >12 h

16. Diagnostic test
 History and physical examination
 Identification of precipitating cause
 Serum creatinine and BUN level
 Serum electrolyte
 Renal ultrasound
 Renal scan as indicated
 CT scan and MRI as indicated
 Retrograde pylogram as indicated

17. Management of Acute
Kidney Injury
 Since normal kidney function is essential to
homeostasis of the body, particularly with
regard to volume, electrolyte balance, acid-
base balance and excretion of nitrogenous
waste products, loss of these functions can
lead to hyperkalaemia, volume overload,
acidosis and uraemia.

18. Continue…
 Prevention is better than a cure, so early detection
and treatment of AKI will prevent rapid deterioration.
Some people are at a greater risk of AKI – these
include patients who have chronic kidney disease,
cardiac failure and liver disease, diabetes and those
who are over 60 years of age.
 The clinical management goals for patients with AKI
can be divided into three main categories:
 restoration of renal perfusion
 minimizing toxic effects
 correction of metabolic derangements.

19. Hyperkalemia
 Hyperkalaemia is often a fatal complication
in AKI. The failing kidney is unable to
excrete potassium effectively when the
patient is oliguric (<400 ml urine day) or,
worse, anuric (no urine). It is further
complicated by the very complex treatment
of an individual who is often septic, hypoxic
and requiring blood transfusions and
potassium containing drugs.

20. Fluid overload
 Successful volume homeostasis permits maintenance
of a constant internal circulatory and extracellular
volume despite consumption of varying quantities of
water and salt intake and variable invisible losses of
water.
 The presence of oedema may be seen in the feet,
legs and sacral area. This is often pitting in nature.
The skin is particularly at risk at this stage and extra
care must be taken.

21. Fluid overload continue…
 Each patient in AKI should have an individual
prescription for fluid and sodium intake. As a
generalization, the fluid intake volume should
equal the daily urine output plus 300–500 ml.
 Patients with a large insensible loss, such as
happens with burns, obviously need a larger fluid
intake and special care should be taken. It is
important that the patient and family are involved
in accurate fluid balance.

22. Metabolic acidosis
 The presence of AKI must not lead the nurse to think that
it is the only cause of acidosis until other causes have
been eliminated, for example ketoacidosis, lactic acidosis.
 Acidosis in kidney injury occurs when the renal tubules fail
to regenerate bicarbonate and secrete hydrogen ions into
the urine, which in turn causes an acid-base imbalance.
 As most acid comes from the breakdown of dietary
protein, it is possible to reduce the level of acidosis by
limiting the level of intake of protein. Another alternative
is to infuse sodium bicarbonate but one has to be aware
of fluid overload and hypernatremia. The most efficient
way of treating acute acidosis via RRT.

23. Uremia
 The accumulation of nitrogenous waste
products will produce acute uremia and
symptoms of uremia often include nausea,
vomiting, hiccups, increasing bleeding,
infection risks, neurological problems,
irritability, confusion and twitching. As
previously mentioned, it is necessary to
begin appropriate dialysis.

24. Nutrition
 The aims of nutritional support are to:
 Prevent protein energy wasting
 Preserve lean body mass/prevent or minimize
malnutrition
 Avoid further metabolic arrangements
 Stimulate immunocompetence
 Repair tissue damage
 Preserve organ function
 Maintain biochemistry/fluid balance
 Enhance recovery.

25. Nutrition continue..
 Adequate protein intake (0.6-2 mg/kg/day)
depending on the degree of catabolism
 Potassium restriction
 Phosphate restriction
 Sodium restriction

26. RRT In Acute Kidney Injury
 The purpose of RRT is to prevent morbidity and to
support the kidney during its recovery phase. The
amount, type and frequency of RRT are dictated by the
severity of the patient’s condition.
 Indications for RRT are:
 Uraemic symptoms, such as pericarditis
 Volume overload
 Hyperkalemia
 Metabolic acidosis
 space-making’ – for example, nutrition, transfusions;

27. RRT
 There are a variety of treatment options available for AKI
and the choice will depend on physician preference, nurse
expertise and availability of the appropriate equipment.
 The options fall broadly into two categories:
 Intermittent treatments (acute haemodialysis and
haemodiafi ltration) and continuous renal replacement
therapies, of which there are three basic types: continuous
haemofiltration, and continuous haemodialysis and
continuous haemodiafiltration.
 Treatments performed continuously over long periods of
time allow optimal values to be obtained for urea and fluid
exchange control,and electrolyte and acid-base balance.

28. Clinical course of AKI
1. Initiating stage
 This occurs when the kidneys are
injured and when diagnosis is made
and treatment established. It can last
anything from hours to days.

29. Clinical course of AKI
2. Oliguric stage
 This can last from 5 days to over 15 days. When
AKI persists for weeks, endocrine problems, such
as reduced erythropoietin production, are noticed.
Functional renal changes occur, such as decreased
tubular transport, reduced urine formation and
lowered glomerular filtration. Renal healing will
begin to occur, with the basement membrane
being replaced with fibrous scar tissue and the
nephron clogged with inflammatory products.
 The patient is particularly susceptible to bleeding
and infection during this stage.

30. Clinical course of AKI
3. Diuretic stage
 With continued healing the kidney begins
to regain most of its lost function, but this
depends on the severity of the initial
injury. The signs and symptoms of the
original condition begin to disappear. Urine
output can begin to increase back to
normal levels of up to 3 L day.

31. Clinical course of AKI
4. Recovery stage:
 The recovery stage can last from several
months to over a year. The basement
membrane is restored to its previous
structure; scar tissue will remain but is not
clinically significant. The kidneys respond
in a regulatory excretory function to the
body’s needs.

32. Nursing assessment
 Obtain subjective data and
 Subjective data
 History and physical examination
 Intake output chart monitoring
 Hemodynamic monitoring
 Prevention of infection

33. Nursing diagnosis
1. Excess fluid volume related to renal failure
and fluid retention.
2. Risk for infection related to invasive line,
uremic toxins and altered immune repose
secondary to kidney failure.
3. Imbalanced nutrition less than body
requirement related to altered metabolic
star and dietary restriction.

34. Thank you…