Acute kidney injury for nursing students

1. Acute Kidney Injury
By Ms. Mahima Panhalkar (B.Sc. N)

2. Anatomy and
Physiology of
Kidney

3.  Renal cortex is the outer layer of the renal capsule,
which contains blood-filling mechanisms (glomeruli)
 Renal medulla is the inner region, which contains the
renal pyramids and renal tubules
 Together, renal cortex, pyramids, and medulla
constitute the parenchyma.

4. Nephron
• Located within
parenchyma
• Composed of
glomerulus and
tubules.
• Selectively secretes
and reabsorbs ions
and filtrates.

5. Functions of
kidneys
 Maintain acid-base balance
 Excrete end products of body metabolism
 Control fluid and electrolyte balance
 Excrete bacterial toxins, water-soluble medications,
and medication metabolites.
 Secrete renin to regulate the blood pressure and
erythropoietin to stimulate bone marrow to produce
RBC’S
 SynthesizeVitamin D for calcium absorption.

6. DEFINITION
 “Acute Kidney Injury is the term used to encompass the
entire range of the syndrome, ranging from slight
deterioration in kidney function to severe impairment.”
 AKI is characterized by loss of kidney function.
 Reversible but has a high mortality rate.

7. Normal Renal
Function
values
*Creatinine: is a waste product from muscle breakdown
and is solely filtered from the bloodstream via the
glomerulus and is NOT reabsorbed or secreted within
the nephron.Therefore, the rate of filtration of creatinine
by the glomerulus helps us to determine the efficiency of
the kidneys, which is why we collect blood levels to
measure creatinine levels.
Normal Creatinine level 0.6-1.20 mg/dL
Increasing Creatinine in the body = the kidneys are NOT
filtering properly

8. Creatinine clearance: the amount of blood the kidneys
can make per minute that is free of creatinine.
Normal creatinine clearance: 85-125 mL/min (female) &
95-140 mL/min (men)
A creatinine clearance value along with age, sex, weight,
race can help determine the GFR (glomerular filtration
rate).

9. Glomerular Filtration Rate: rate of blood flow through
the kidneys (ml/min).This shows how well the
glomerulus is filtering the blood. Normal GFR in
adults: 90 or higher ml/min
Normal GFR = normal urine output, normal BUN and
creatinine, normal electrolyte and water balance

10.  Decreased GFR = low urinary output along with an
increase in waste products in the blood (creatinine and
BUN), electrolyte/fluid imbalances, and buildup of fluid
• BUN (blood urea nitrogen): urea (measured as blood
urea nitrogen) is a waste product from protein
breakdown in the liver. It is secreted in the blood and
filtered out through the kidneys.
 Normal BUN: 6-20 mg/dL (in AKI this level becomes
greater than 20 mg/dL )

11. CAUSES-
1.PRERENAL
Hypovolemia Decreased CO Decreased PVR Decreased
blood flow
Dehydration Cardiac
dysrhythmia
Anaphylaxis Embolism
Hemorrhage Cardiogenic
Shock
Neurologic Injury Renal artery
syndrome
GI losses Heart failure Septic shock Hepatorenal
syndrome
Excessive
diuresis
MI Bilateral renal
vein thrombosis
Burns

12. INTERENAL
CAUSES
Nephrotoxic Injury Interstitial Nephritis Other Causes
Drugs: aminoglycosides
e.g. Amikacin
Allergies:
Antibiotics NSAIDs,
ACE inhibitor
Prolonged prerenal
ischemia
Contrast media Infection: fungal
(candidiasis)
Acute
glomerulonephritis
Hemolytic blood
transfusion reaction
Thrombotic disorder
Severe crush injury Toxemia of pregnancy

13. POST RENAL
CAUSES
 BPH
 Bladder cancer
 Calculi Formation
 Neuromuscular disorder
 Prostate cancer
 Stricture

14. Risk Factors
 Advanced age (60yrs >)
 Diabetes
 Hypertension
 Coronary artery disease
 Kidney disease
 Liver disease

15. Pathophysiology
Pre-renal causes
Impaired blood flow
Hypoperfusion of
the kidney
Decrease in GFR
Renal failure

16. Intrarenal
causes
Renal tissue
damage
Loss of nephron
function
Decrease in GFR
Renal failure

17. Postrenal causes
Obstruction in
postrenal part
Increased pressure in
renal tubule
Decreased GFR
Renal failure

18. CLINICAL
MANIFESTATIONS
Oliguric Phase
 Urinary changes- reduction in urine output- less than 400ml/day.
 Occurs within 1-7 days of the injury to the kidneys.
 Lasts about 10-14 days on average but can last for months.
 Longer the phase, the poorer the prognosis
 Increased Potassium (hyperkalemia) >5.1 mEq/L: due to the
nephrons decreased ability to excrete potassium. It builds up in
the blood and the patient is at risk for a significant cardiac event
 Increased fluid in the body: edema, at risk for fluid overload
(pulmonary, cardiac issues: hypertension)

19.  Metabolic acidosis: blood pH less than 7.35 due to the decrease in
the excretion of hydrogen ions by the nephrons. Patient may be
confused and have Kussmaul breathing.This is deep and rapid
breathing.The respiratory system is trying to compensate by
blowing off carbon dioxide (which is an acid) to help increase the
blood’s pH.
 High phosphorus and low calcium: nephron can’t regulate
phosphate and calcium levels

20. Diuretic Phase
 Urine output slowly rises, followed by diuresis (1 to 3 L may reach
to 5L )
 Excessive urine output indicates that damaged nephrons are
recovering their ability to excrete wastes.
 Dehydration, hypovolemia, hypotension, and tachycardia can
occur.
 Levels of consciousness improve.

21. Recovery Phase
 Begins when GFR increases, allowing BUN levels to plateau and
then decrease.
 Recovery is a slow process
 Major improvements occur in the first 1 to 2 weeks, normal kidney
function may take up to 12 months.
 Urine volume returns to normal

22. DIAGNOSTIC
STUDY
 History and physical examination
 Serum creatinine and BUN levels
 Serum electrolytes
 Urinalysis- an examination of the urine to determine
kidney function, usually including measurement of pH,
tests for protein, glucose, ketones, and blood, and
microscopic evaluation of sediment obtained by
centrifugation.

23.  Renal ultrasound-Although the rate of abnormal
ultrasound findings in the setting of AKI is not high
(about 10%), these findings can have a significant
impact on patient management
 Renal scan/Renogram-A renal scan involves the use of
nuclear radioactive material to examine your kidneys
and assess their function.
 CT scan
RENOGRAMOF
DILATED R. KIDNEY

24. Complications
 High levels of potassium in the blood – in severe cases,
this can lead to muscle weakness, paralysis, and heart
rhythm problems
 Too much fluid in the body, which can cause a build-up
of fluid in the arms and legs (edema) or in the lungs
(pulmonary edema)
 Acidic blood (metabolic acidosis) – which can cause
nausea, vomiting, drowsiness, and breathlessness
 Chronic kidney disease

25. Collaborative
Care
 Diuretic therapy is often administered but not recommended in
high doses.
 Usually loop diuretics (furosemide, Bumetanide) or osmotic
diuretic ( eg., mannitol ) is administered.
 Hyperkalemia is one of the most serious complications because it
can cause life-threatening cardiac dysrhythmias
 Both insulin and sodium bicarbonate can serve as a temporary
measure for treatment of hyperkalemia by promoting a shift of
potassium will eventually be released.

26.  Nutritional therapy – Primary goal is to maintain adequate caloric
intake (30-35kcal/kg and 0.8 to 1.0 g of protein per kg)to prevent
breakdown of body protein for energy purposes.
oPotassium and phosphate restriction
o Sodium intake is restricted- to prevent edema, hypertension, and
HF.
oDietary fat is increased so that patient receives at least 30% to 40
% of total calories.
 Initiation of dialysis or CRRT (if necessary)

27. Therapies for Elevated Potassium Levels
Regular Insulin IV
 Potassium moves into cells when insulin is given
 Iv glucose is given concurrently to prevent hypoglycemia.
 When the effects of insulin diminish, potassium shifts back out of
cells.
Sodium bicarbonate
 Therapy can correct the acidosis and cause a shift of potassium into
cells.
Calcium Gluconate IV
 Generally used in advanced cardiac toxicity ( with evidence of
hyperkalemic ECG changes)

28. Nursing
Diagnosis
 Excessive fluid volume related to kidney failure
 Risk for infection related to invasive lines
 Fatigue related to anemia, metabolic acidosis
 Anxiety related to disease processes, therapeutic interventions

29. Nursing
Management
 Monitor vital signs, especially for signs of hypertension,
tachycardia, tachypnea, and an irregular heart rate.
 Monitor urine and intake and output hourly and urine colour and
characteristics
 Monitor daily weights (same scale, same clothes, same time of
day) notice an increase of 0.25-0.5kg/day indicates fluid retention.
 Monitor changes in BUN , Sr. creatinine, and serum electrolyte
levels.
 Monitor for acidosis
 Administer prescribed diet, which is usually a low to moderate –
protein (to decrease the workload of kidneys) and high
carbohydrate diet; ill clients may require nutritional support with
supplements, enteral feedings, or parentral nutrition.

30.  Administer medications as prescribed.
 Prepare patients for CRRT may be used in AKI
to treat fluid volume overload or rapidly
developing azotemia and metabolic acidosis.