The document outlines the definition, causes, pathophysiology, clinical manifestations, and management of acute renal failure (ARF). ARF is characterized by the sudden loss of kidney function, with specific phases including initiation, oliguria, diuretic, and recovery; it can result from pre-renal, intra-renal, or post-renal causes. Effective treatment and nursing care focus on addressing underlying causes, maintaining homeostasis, and preventing complications related to the condition.

1. COPPERBELT NURSING
POLYTECHNIC
ACUTE RENAL FAILURE
By
CAROL MWIMBA

2. INTRODUCTION
A health adult eating a normal diet needs a
minimum daily urine output of approximately
400mls to excrete the body’s waste products
through the kidney.
An amount lower than this indicates a decreased
GFR. Oliguria refers to daily output of urine
between 100 and 400mls.
Anuria refers to output less than 100mls per day.

3. CONT.
 Thus, acute renal failure is the sudden interruption
of renal function resulting from obstruction,
reduced circulation, or renal parenchyma disease.
 The disease is classified as pre-renal, intra-renal or
post –renal and normally passes through 4 distinct
phases-Initiation, oliguric, diuretic and recovery.
 However, it is usually reversible with medical
treatment.

4. GENERAL OBJECTIVE
✓ At the end of this lecture/discussion, students
should be able to acquire the basic knowledge
and understanding of acute renal failure.

5. SPECIFIC OBJECTIVES
❖ At the end of the lesson, nursing students
should be able to:
1. Define acute renal failure
2. State the causes of acute renal failure.
3. Explain the pathophysiology of acute renal failure.
4. Outline the clinical manifestation of acute renal
failure.
5. Discuss the management of acute renal failure.
6. List the complications of acute renal failure.

6. DEFINITION OF ACUTE RENAL FAILURE
Acute renal failure (ARF) refers to the abrupt
loss of kidney function over a period of hours to
a few days, with a fall in glomerular filtration
rate (GFR) accompanied by a rise in serum
creatinine and urea nitrogen (Lewis 2011).
Acute renal failure is the sudden interruption of
renal function resulting from obstruction,
reduced circulation, or renal parenchyma
disease characterized by azotemia (Martin,
2020).

8. THE CAUSES OF ACUTE RENAL FAILURE
1. Pre-renal causes:
➢ These interfere with renal perfusion as a result
cardiac output and vascular volume is decreased.
➢ The kidney depends on an adequate delivery of
blood to be filtered by the glomeruli.
➢ Therefore, a reduced renal blood flow obviously
decreases the GFR.
➢ Some of the causes are:

9. CONT…
• Hypovolemia (due to bleeding, or diarrhoea),
• Systemic vasodilation (due to infection),
• Renal vasoconstriction (due to NSAIDS,
cirrhosis).
• Shock, and cardiac failure,
• Severe dehydration in burns,
• Occlusion of renal artery by a thrombus,
embolism, dissection or abdominal mass.

10. CONT…
2. Intra Renal/Renal causes:
➢ Refers to parenchymal changes from disease or
nephrotoxic substances.
➢ It occurs in conditions like;
• Glomerulonephritis,
• acute tubular necrosis,
• acute pyelonephritis,

11. CONT.
• Chemical biological products and infections,
• Trauma,
• Toxins: drugs (aminoglycosides).
3. Post-renal causes:
➢ These arises from obstruction in the urinary
tract anywhere from the tubules to the urethral
meatus and to the exterior;

12. CONT.
• Prostatic hypertrophy.
• Renal Calculi (Renal stones).
• Urethral strictures.
• Schistosomiasis
• Pregnancy

13. CONT.

14. THE PATHOPHYSIOLOGY OF RENAL FAILURE
➢ In renal failure there is either glomerular or
tubular dysfunction.
❑Glomerular dysfunction; as the main function
of glomeruli is filtration, glomerular dysfunction
leads to fall in GFR with retention of substances
that are cleared by filtration including water.

15. CONT.
❑Tubular dysfunction; the main function of
tubules is reabsorption, tubular failure results
in voiding large volume of dilute urine
(polyuria) of low specific gravity along with
electrolytes and nutrients.
➢ The damaged tubule cannot conserve sodium
normally, which leads to renin-angiotensin
aldosterone system activation.

16. CONT.
➢ Regardless of severity most forms of Acute
Renal Failure (ARF) are reversible.
➢ The resulting ischemia may cause an increase in
vasopressin, cellular swelling and inhibition of
prostaglandin synthesis.
➢ The reduced blood flow decreases glomerular
pressure, GFR and tubular flow, thus oliguria
occurs.
➢ Decreased renal blood flow leads to decreased
O₂ delivery to the proximal tubules.

17. CONT.
➢ This will result in increase in metabolic end
products such as urea, creatinine etc.
➢ The effects of ARF are widespread.
➢ The major consequences are: Acidosis; Fluid
and electrolyte imbalances (fluid overload or
depletion, hyponatremia, hypocalcaemia and
hyperkalemia); Increased susceptibility to
infections; Anemia; Platelet dysfunction;
Gastrointestinal complications (anorexia,
nausea, vomiting, diarrhea, constipation); and
Uremic encephalopathy.

18. CONT.

19. THE CLINICAL MANIFESTATION OF ACUTE
RENAL FAILURE
❖Clinical Manifestations according To Phases
➢ The most common overall sign of ARF is
alteration in the expected urine output:
a) Initiation phase: patient may excrete as much
as 2L/day and this need to be recognized as a
possible sign of ARF.

20. CONT.
• The urine is dilute and nearly isomolar
• Hypertension and tachypnea as signs of fluid
overload are frequently found.
• There are also signs of dehydration such as dry
mucous membranes, poor skin turgor.
• There is less degree and shorter duration of
Azotemia (Elevated nitrogenous products in blood)

21. CONT.
b) Oliguria phase: Urine production falls below
400ml/day. Clinical manifestations are increased
BUN and Creatinine.
C) Diuretic phase: During the diuretic phase,
large amount of fluids (4 to 5 L/day) and
electrolytes are lost.

22. CONT.
d). Recovery phase: This may last up to 12
months, with most patients left with some
residual renal dysfunction.
➢ Kidney may return to normal functioning state
or there may be some residual renal
insufficiency.

23. CONT.
❖GENERAL SIGNS AND SYMPTOMS
o Muscle weakness due to electrolyte imbalance.
o Pruritus due to uremic frost.
o Oliguria due to impaired kidney function.
o Pitting edema due to fluid retention.
o Hypertension due to sodium retention.
o Pulmonary edema due to fluid retention

24. CONT.
o Metabolic acidosis with Kussmaul's respirations
(hyperventilation).
o Altered mental state due to accumulation of waste
products in the brain.
o Anorexia and Nausea due azotemia.
o Uremic frost (yellow white urea crystals deposits on
the skin) due to azotemia.

25. THE MANAGEMENT OF ACUTE RENAL FAILURE
A. Medical Management
❑Investigations
o History and physical examination for oedema
and other related features
o Blood for levels of BUN, and serum electrolytes
o Urinalysis, check for proteins, cats, sodium.
Urinary output should be determine.

26. CONT.
o Renal ultrasound to detect damage to the
glomerulus
o Renal scan may be indicated.
o ECG will reveal tall T waves, widening QRS
Complex, and disappearing P waves if
hyperkalaemia is present.

27. CONT.
❑Treatment
Aims
1. To remove the precipitating factors
2. To maintain homeostatic balance
3. To prevent complications until the kidneys are
able to resume function.

28. CONT.
✓ Treat specific causes e.g. urinary structure
surgical intervention may be sought (Antibiotics
/Diuretics)
✓ Fluids intake should be restricted to about 600
ml per day.
✓ Sodium, potassium and phosphate should be
restricted

29. CONT.
Medications that are handled primarily by the
kidney will require modification of dosage or
frequency to prevent medication toxicity.
✓ Diuretics: In oliguric phase ARF for fluid
removal, e.g. Furosemide or Mannitol.
✓ Antihypertensive: to control blood pressure.
Aldoment or atenolol.

30. CONT.
✓ Sodium bicarbonate to control acidosis.
✓ Intravenous calcium to reverse the cardiac
effects of life-threatening hyperkalemia.
✓ Vitamins B and C to replace losses if patient is
on dialysis.
✓ Packed cells for active bleeding or if anemia is
poorly tolerated.

31. CONT.
✓ Peritoneal dialysis or hemodialysis may be done
✓ Aluminum hydroxide antacids to control
hyperphosphataemia.
✓ Diet: Increase carbohydrates, reduce proteins,
reduce Potassium and reduce sodium in-takes,
however, because of loss of K⁺ during the
diuretic phase, K⁺ may need to be increased
during that time.

32. CONT.
B. Nursing Care Plan
AIMS
1. To remove the precipitating factors
2. To maintain homeostatic balance
3. To prevent complications

33. CONT.
NURSING DIAGNOSIS:
1. Fluid volume increase related to fluid
retention as evidenced by edema.
Goal: To maintain adequate hydration and
prevent over hydration.
Nursing interventions/rationale:
• Limit fluid and salt intake diet to prevent
increased sodium and fluid retention;

34. CONT.
• the patient will be on strict fluid intake to
prevent further increase in fluid volume;
• the client should be given prescribed diuretics
such as furosemide to block the absorption of
sodium chloride thereby promoting elimination
of excess fluids.
• And digoxin to improve cardiac output;

35. CONT.
• Since the patient will be on strict bed rest in the
acute phase, do passive exercises to promote
blood circulation and prevent deep vein
thrombosis;
• Do regular weight checks in order to monitor
improvement or worsening of oedema.

36. CONT.
2. Altered nutritional status less than body
requirement related to Gastrointestinal
complications (such as anorexia, nausea, vomiting,
diarrhea, constipation) evidenced by azotaemia.
Goal: To preserve protein stores until normal
function is gained.

37. CONT.
Nursing interventions/Rationale:
• Give the patient 100g of carbohydrates daily to
prevent metabolism of tissue protein.
• small frequent meals to prevent nausea
• give 50% dextrose IV, with vitamin supplements
for energy and strong immune system

38. CONT.
• Restrict sodium (Na), potassium (K) and
Phosphate intake to reduce Na, and K serum
levels.
• Proteins should also be reduced to prevent
excessive accumulation of urea in the blood

39. CONT.
3. Altered urinary output related to impaired
kidney function evidenced by edema and
oliguria.
Goal: to restore homeostasis within 48 hours of
admission
Nursing interventions: Assist in removing the
cause, gastric lavage may be done. and collect
biomedical disorders.

40. CONT.
• Observe hourly urine output.
• Give specific prescribed drugs for the diseases.
• Prepare for dialysis if need arise
Rationale: To prevent metabolic deterioration

41. CONT.
4. Potential/risk for impairment of the oral
mucosa and skin integraterelated to Uremic
frost (yellow white urea crystals deposits on the
skin) due to azotemia.
Goal: Maintain oral mucus and prevent skin
destruction throughout hospitalization

42. CONT.
Nursing interventions:
• Frequent oral care with prescribed antiseptic
e.g. Diluted H2 O2.
• Apply lemon juice or linsing the mouth before
and after a meal.
Rationale: Stimulate salivation and moisten
mucus membrane; to prevent skin breakage and
maintain it intact.

43. CONT.
Other problems:
Knowledge deficit
Self-Care Deficit

44. COMPLICATIONS OF ACUTE RENAL FAILURE
➢ Acute renal failure is a serious condition that can
lead to multiple, potentially life-threatening
complications if not managed promptly and
effectively.
➢ The complications arise from the kidneys' inability
to perform their normal functions, which leads to
systemic imbalances affecting almost every organ
system.

45. CONT.
1.Fluid Overload: The kidneys regulate fluid balance
in the body. In ARF, reduced urine output can lead to
fluid retention.
➢ This can cause edema (swelling), pulmonary edema
(fluid accumulation in the lungs), and hypertension
(high blood pressure).
➢ Pulmonary edema can be life-threatening as it
impairs gas exchange, leading to respiratory
distress.

46. CONT.
2.Electrolyte Imbalances: The kidneys excrete
potassium, and in ARF, potassium levels can rise
dangerously.
➢ Hyperkalemia can cause life-threatening cardiac
arrhythmias or sudden cardiac arrest.

47. CONT.
3.Metabolic Acidosis: The kidneys play a role in
maintaining acid-base balance.
➢ In ARF, the kidneys are unable to excrete hydrogen
ions and produce bicarbonate, leading to metabolic
acidosis.
➢ Severe acidosis can cause arrhythmias, decreased
cardiac contractility, and can depress the central
nervous system, leading to confusion, lethargy, or
coma.

48. CONT.
4. Uremia: Accumulation of waste products (such as
urea and creatinine) in the blood due to impaired
kidney function.
• Uremia can lead to pericarditis (inflammation of the
pericardium), encephalopathy (brain dysfunction),
bleeding tendencies due to platelet dysfunction,
and uremic frost (white powdery deposits on the
skin).

49. CONT.
5. Anemia: The kidneys produce erythropoietin,
which stimulates red blood cell production.
➢ In ARF, this production is impaired.
➢ This can lead to anemia, contributing to fatigue,
weakness, and decreased oxygen-carrying capacity
of the blood.

50. CONT.
6. Multi-Organ Failure: ARF can lead to or
exacerbate the failure of other organs due to the
systemic effects of fluid overload, electrolyte
imbalances, acidosis, and uremia.
➢ This may include respiratory failure, liver
dysfunction, or worsening of pre-existing conditions,
potentially leading to multi-organ dysfunction
syndrome (MODS)

51. THE END
THANK
YOU!

52. EVALUATION
1. What is acute renal failure?
2. What is the aetiology for acute renal failure?
3. What is the pathophysiology of renal failure?
4. What are the clinical manifestation of acute renal
failure?
5. What is the management of a patient with acute renal
failure?
6. What are the complications of acute renal failure?

53. SUMMARY
 Well, we have come to the end of the topic. In this topic
you were looking at malaria. We therefore defined
acute renal failure; stated the causes of acute renal
failure; explained the pathophysiology of acute renal
failure; outlined the clinical manifestation of acute
renal failure; discussed the management of acute renal
failure; and listed the complications of acute renal
failure.

54. ASSIGNMENT
Discuss the nursing management of Mr. John who
has been diagnosed with acute renal failure
Due date: 28/08/24

55. References
 Lewis S.M, Heitkemper M.M, and Dirksen. S. R, (2011) Medical-
Surgical Nursing Assessment and Management of Clinical Problems,
6th edition, Philadelphia Mosby Corporation.
 Lubin, Michael F., and Robert B.S. (2018) Medical Management of the
Surgical Patient, 4th ed., Cambridge, UK: Cambridge University
Press.
 Martin E.A., (2020) Oxford Concise Medical Dictionary, 6th Ed, New
Delhi: Oxford Press.
 Smeltzer C. S. and Bare G. B. (2019) Brunner and Suddarth’s
Textbook of Medical Surgical Nursing, 7th edition, New York: J. B.
Lippincott Company.
 Skidmore-Roth .L. (2017) Mosby’s Drug Guide for Nurses 7th Ed, St
Louis Missouri, Mosby Elsevier.