The document provides a comprehensive overview of renal failure, detailing its functions, classifications (acute and chronic), causes, pathophysiology, phases, management, and complications. It emphasizes the importance of understanding acute renal failure and its clinical implications for effective patient management. Treatment options and nursing care focus on addressing the underlying causes, restoring kidney function, and preventing complications.

1. RENAL FAILURE
BY MISS DIALO F

2. Introduction
• The kidneys perform a number of functions to sustain
life such as filtration of waste from blood, maintenance
of acid base balance and regulation of blood pressure.
Kidney failure affects the complex functions of the
kidney and is one of the most significant causes of
disability and death throughout the world.

3. General Objective
• At the end of the lecture/ discussion students
should be able to gain knowledge and manage
patients with renal failure.

4. Specific Objectives
At the end of the discussion/lecture, students should
be able to;
• Define acute renal failure.
• Mention the classification of renal failure.
• State the causes of renal failure

5. Conti…
• Describe the pathophysiology of acute renal failure.
• Explain the four phases of acute renal failure with
their signs and symptoms.
• Describe the Management of acute renal failure
• State the complications of acute renal failure

6. DEFINITION
• Renal failure or kidney failure is described as a
medical condition in which the kidneys fail to
adequately filter toxins & waste products from
blood.

7. Classification of Renal Failure
• Renal failure is classified into two forms, namely;
acute and chronic renal failure.

8. Acute Renal Failure
• Acute renal failure (ARF) “is a sudden and almost
complete loss of kidney function over a period of
hours to days with a fall in glomerular filtration rate
(GFR) accompanied by a rise in serum creatinine
and urea nitrogen.

9. Causes Of Acute Renal Failure
• The causes of ARF can be classified as
• Prerenal,
• Intrarenal and
• Post renal according to the predisposing factor

10. Pre-renal Causes
• This refers to causes outside the kidneys that
reduce renal blood flow and lead to hypo perfusion
of the kidney and a drop in glomerular filtration
rate.
• Common Prerenal clinical situations are:

11. Pre-renal cont
• Hypovolemia (volume-depletion) states such as in
hemorrhage, dehydration, vomiting, burns and
inappropriate use of diuretics.
• Hypotension due to shock and cardiac failure

12. Pre-Renal Cont..
• Impaired cardiac performance which leads to decreased
cardiac output such as in myocardial infarction, heart
failure or cardiogenic shock
• Systemic vasodilation or decreased peripheral resistance
due to sepsis, anaphylaxis, acidosis and neurologic injury.

13. Pre-Renal Cont…
• Renal vascular obstruction due to thrombosis of
renal arteries, bilateral renal vein thrombosis and
embolism.

14. Pre-renal cont..
• Drugs that may complicate pre renal are non-
steroidal anti-inflammatory drugs (NSAIDS) which
blocks synthesis of vasodilation prostaglandins and
angiotensin converting enzyme inhibition which
blocks synthesis of angiotensin.

15. Intra renal causes (intrinsic causes)
• Result of actual parenchymal damage to the glomeruli or
kidney tubules. They include:
• Conditions such as burns, crush injuries, and severe
trauma – In these conditions, myoglobin (a protein
released from muscle when injury occurs) and
hemoglobin are liberated, causing renal toxemia, ischemia
or both.

16. Intra-renal Cont…
• Severe blood transfusion reactions, hemoglobin is
released through hemolysis, filters through the
glomeruli, and becomes concentrated in the kidney
tubules to such a degree that precipitation of
hemoglobin occurs.

17. Intra-renal Cont..
• Nephrotoxicity agents such as aminoglycoside
antibiotics e.g. gentamycin; radio opaque contrast
agents; heavy metals e.g. lead and mercury; solvents
and chemicals e.g. Carbon Tetrachloride; NSAIDS
and angiotensin-converting inhibitors (ACE
inhibitors).

18. Intra-renal Cont..
• These interfere with the normal auto regulatory
mechanisms of the kidneys and may cause hypo
perfusion and eventual ischemia. Nephrotoxicity
may also result from herbal remedies and
conditions such as HIV infections.

19. Cont..
• Infectious processes such as acute pyelonephritis
and acute glomerulonephritis.

20. Post renal causes
• These are usually the result of an obstruction distal to
the kidney. This results in mechanical obstruction of
urinary outflow
• As the flow of urine is obstructed, urine refluxes into
the renal pelvis causing pressure to rise in the kidney
tubules.

21. Examples of what can cause obstruction in
the kidneys
• Myeloma
• Bilateral urinary tract blockage
• Calculi
• Schistosoma haematobium
• Prostatic Hypertrophy.

23. Pathophysiology
• The glomerulus requires sufficient blood flow in
order to carry out filtration.
• A reduction in renal blood flow results in a reduction
in Glomerular Filtration Pressure (GFP) and
thereafter lowering the Glomerular Filtration Rate
(GFR)

24. Pathophysiology Cont…
• Lowered GFP and GFR impairs secretion of water
soluble waste products resulting in their increased
levels in blood.

25. Cont..
• A reduced blood volume results in reduced renal
perfusion. This stimulates the juxtaglomerular
apparatus to secrete renin which converts
angiotensinogen into angiotensin I. Angiotensin I
is converted to angiotensin II by the angiotensin-
converting enzyme from the lungs.

26. Cont…
• Angiotensin II acts on the blood vessels to cause
vasoconstriction which increases the peripheral
resistance as a way of restoring blood volume by
increasing blood pressure.

27. Cont..
• Angiotensin II also directly acts on adrenal cortex
to cause secretion of aldosterone which increases
the sodium and water reabsorption in proximal
tubules.

28. Conti…
• The overall effect is to expand the blood levels; so
as to maintain the extracellular fluid volume.
• Ischemia alters glomerular epithelial cells and
decreases glomerular capillary permeability. This
reduces blood flow and leads to tubular dysfunction.

29. Cont..
• When tubules are damaged, interstitial edema
occurs, and necrotic epithelial cells accumulate in
the tubules.

30. Conti…
• The debris lowers the GFR by obstructing the tubules
and intra-tubular fluid flow. The sodium levels though
will continue to be low in blood because of the water
retention and the water produced from excessive
metabolic processes in the body.
• Blood urea nitrogen (BUN) accumulate with oliguria

32. Clinical phases of Renal Failure
There are four clinical phases of renal failure;
1. Initiating phase
This begins at the time of the insult and continues
until the signs and symptoms become apparent or
significant. It can last hours to days.

33. 2. Oliguric phase
• This follows within one day of the onset and the
duration is dependent upon the type of the toxic injury
and duration of ischemia.
The major problems in this phase are-;
• The inability to excrete fluid loads, regulate electrolytes
and excrete metabolic waste products.

34. Cont...
• Uremic symptoms first appear when the urine output
is less than 400 mls/24 hours as a result of increased
serum urea nitrogen and creatinine.
• BUN may increase to 20mg/dl/day whereas serum
creatinine rises by at least 0.5 mg/dl/day.
• Nausea

35. Cont..
• Vomiting
• Drowsiness
• Confusion
• Coma
• Gastrointestinal bleeding

36. Cont…
• Pericarditis.
• Later, life threatening conditions such as hyperkalaemia
occurs when urine output is less than 30 mls/24 hours
because of the inability to regulate fluid
• overload also occurs

37. Conti…
The symptoms at this stage include-;
• Dysarthymias
• Kussmaul’s respirations (rapid, deep breathing)
• CCF
• Pulmonary edema.

38. Cont…
• Neck vein distension with bounding pulse
• Hypertension
• Fatigue and bleeding.

39. Diuretic phase
• The diuretic phase begins with the gradual increase
in daily urine output of 1 to 3 liters’ per day, but
may reach 3 to 5 liters’ or more per day.

40. Conti…
• Urine production is increased because of high urea
concentration in the glomerular filtrate that causes
osmotic diuresis and inability of the tubules to
concentrate the urine.
• This last for 2-6 weeks after onset of oliguria, but the
duration varies accordingly.

41. Recovery phase
• This begins when the glomerular filtration rate
increases, allowing the BUN and serum creatinine to
stabilize and then decrease.
• Major improvements occur in the first 1 to 2 weeks
of this phase but renal function may take up to 12
months to stabilize.

42. Cont..
• The major symptom is decreased energy levels
which last for 3-12 months.

44. Management
Aims
• To remove the precipitating factors
• Maintain homeostatic balance
• Prevent complications until the kidneys are able to
resume function.

45. History/Physical Examination
• History of the signs and symptoms
• Determine whether the patient has been taking
nephrotoxic agents or has been exposed to
environmental toxins i.e. Gentamycin, mercury etc.

46. Cont…
• Skin (rash which could be due allergic interstitial
nephritis or systemic lupus erythromatous.
• Gastrointestinal tract (diarrhea, vomiting or poor
intake which could lead to hypovolemia).

47. Cont..
• Genitourinary (prostate enlargement leading to
obstruction).
• Vital signs – increased temperature due to possible
infection, hypertension or hypotension due to
depletion of fluid volume or sepsis.

48. Cont….
• Mouth – signs of dehydration.
• Neck – distended jugular veins with visible
bounding pulse due to fluid overload

49. Cont…
• Pulmonary system – signs of congestive heart failure;
and crackles in the lungs due to edema
• Heart – heart murmurs or signs of congestive heart
failure.
• Abdomen – bladder distension suggesting urethral
obstruction.

50. Investigations
• Urinalysis – urine amount is reduced initially. If the
cause is pre renal, the specific gravity is high
whereas for intrinsic causes, the specific gravity
may be normal.
• There are urine sediments containing abundant
cells, casts or proteins suggesting intrinsic causes.

51. Cont…
• Renal ultrasound provides information about the
anatomy and physiology of the kidneys.
• Blood for urea, nitrogen and creatinine levels.
• Serum for electrolyte levels e.g. there may be
hyperkalaemia, high phosphate concentrations and low
calcium levels.

52. Conti…
• Full blood count may reveal anemia due to reduced
erythropoietin production, uremic gastric intestinal
lesions and reduced red blood cell life span.
• Computed Tomography (CT) scan and magnetic
resonance imaging (MRI) can identify masses and
vascular anomalies.

53. Treatment
Since acute renal failure is potentially reversible, the
primary goals of treatment are;
• To eliminate the cause,
• To manage the signs and symptoms and
• To prevent complications while the kidneys recover

54. Treatment Cont…
• Treat the cause
• Restrict fluids: Replace losses plus 400ml/24hrs.
• Medications that are handled primarily by the
kidney will require modification of dosage or
frequency to prevent medication toxicity.

55. Cont…
• Diuretics: In oliguric ARF for fluid removal, e.g.
Furosemide or Mannitol.
• Antihypertensive: to control blood pressure.
Aldoment or atinolol
• Aluminium hydroxide antiacids to control
hyperphosphatemia

56. 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

57. Cont..
• Packed cells for active bleeding or if anaemia is
poorly tolerated.
• Diet: Increase carbohydrates, reduce proteins, reduce
Potassium and reduce sodium in-take, however,
because of loss of K during the diuretic phase, K
⁺ ⁺
may need to be increased during that time.

58. Dialysis
This is required when conservative management is not
effective.
• It is a process by which waste products in the blood
are filtered through a semi-permeable membrane.
• There are two (2) methods that are used i.e.,
peritoneal and hemodialysis.

59. Peritoneal dialysis
• It is when fluid containing special mixture of
glucose and salt is infused in the abdominal cavity
where it draws toxic substances from the tissue.
The fluid is then drained out.
• Quantity of glucose is adjusted to remove more or
less toxic substances.

61. Hemodialysis-
• Blood moves from the body and is pumped into the
machine that filters the toxic substances using an
artificial membrane, then returns purified back to the
patient.
• Hemodialysis involves removing “unfiltered” blood
from the patient Filtering out electrolytes, urea,
creatinine, etc through the dialysis process.

62. Complications of hemodialysis
• Infection
• Embolization
• Clotting & hemorrhage

64. Nursing care
Aims:
• Eliminate the cause.
• To restore kidney functions.
• To prevent complications

65. Environment
• Nurse the patient in a clean, quiet and well
ventilated environment to prevent infections
• Prevent injury; assess orientation and reorient
confused patient.

66. Observations
• When patient is ambulant, assess motor skills and
monitor ambulation, assist patient if necessary.
• Assess patient for signs of bleeding

67. Obs cont..
• Assess for signs and symptoms of infection.
• Assess the level of consciousness (LOC) of the
patient.
• Assess pressure areas for any sore or swelling.

68. Conti…
• Take vital signs every after 6 hours.
• Follow a strict input and output programme and record
accurately.
• Monitor weight daily.
• Observe for indicators of fluid volume excess, including
oedema, rayles, tachycardia.

69. Cont…
• Observe for muscular twitching, disorientation,
increased drowsiness and report immediately if is going
into uremic state, cerebral edema may proceed coma.

70. Fluid and Nutrition
• Correct hypovolemia by oral or IV route to maintain
cardiac output for adequate perfusion of kidneys.
• Fluids limited to 500mls per day and amount equal to
urinary output in 24hours. 500mls fluid loss will be
through skin and lungs. The type of fluid given will
depend on laboratory results.

71. Cont..
• Maintain an accurate fluid balance record of intake
and output
• Watch for signs of dehydration in diuretic phase,
Monitor urinary output and specific gravity

72. Cont…
• Explain to the patient why you are restricting fluids and
diet.
• Restrict potassium intake
• Restrict protein intake to avoid further rise in urea to
reduce accumulation of urea and creatinine about 125g
of protein per day.

73. Cont…
• Adequate nutrition with 2000 Kcal per day and
vitamins. Give adequate carbohydrates Limit
dietary protein intake during oliguric phase to 60g
per day to prevent rises in blood urea. A normal
diet is resumed as recovery begins.

74. Electrolyte balance
• Monitor fluid status by paying particular attention to
fluid intake and fluid output.
• Monitor for increase in blood pressure, periorbital,
sacral and peripheral edema and dyspnea which are
indicators of fluid excess

75. Cont..
• All parenteral fluids, oral feeds and medications
should be screened carefully to ensure that hidden
sources of electrolytes especially potassium.
• Provide low sodium diet and fluid restrictions until
diuresis is achieved.

76. Cont…
• Daily weighing to monitor response to diuretic
therapy, as it is a more sensitive indicator of fluid
balance than intake and output.
• Elevate the feet to promote venous return
• Give prescribed medication especially diuretics.

77. Rest
• Patient’s activities are minimized to avoid
increasing metabolic production of wastes. This is
done to conserve energy.
• Resume activities slowly to resume renal function.

78. Hygiene
• Mouth care is done frequently to stimulate salivation
and promote appetite.
• Bath patient daily to promote comfort and blood
circulation
• Do pressure area care

79. Psychological Care
• Reassure patient and family that mental capacities
will return with recovery of kidney function.
Structuring the environment and activities may
help with coping in the initial phase.
• Assist patient to explore feelings concerning the
nature of the illness.

80. IEC
• Teach the patient about the cause of renal failure
and problems with recurrent failure.
• Identification of preventable environmental or
health factors contributing to the illness, such as
hypertension and nephrotoxic drugs is taught.

81. IEC Cont..
• Teach patient about medication regimen, including
name of medication, dosage reason for taking and side
effects.
• Teach patient about prescribed dietary regimen.
• Explain the risk of hypokalemia and to report
symptoms (muscle weakness, anorexia, nausea and vomiting, lethargy).

82. Cont
• Teach about signs and symptoms of returning
renal failure (decreased urine output)
• Teach about signs and symptoms of infection;
methods to avoid infection.
• Emphasize the need for ongoing follow-up care.

83. Cont
• Give information about options for future;
explanation of transplantation of kidney and
dialysis if these are a possibility.
• If patient requires dialysis after discharge, co-
ordinate discharge planning with dialysis unit staff.
Arrange visit to dialysis unit if possible.

84. Complications of renal failure
• Hyperkalaemia
• Convulsions
• Comma – due to uremia
• Confusion, disorientation- due to uremia
• Cardiac arrest.
• Chronic renal failure

85. SUMMARY
• We have come to the end of our lecture , we have defined renal failure which
we said it is described as a medical condition in which the kidneys fail to
adequately filter toxins & waste products from blood. We feather discussed
the classifications ,the pathophysiology and the phases of renal failure. We
also looked at the management and lastly the complications.

86. EVALUATION
1. What is acute renal failure?
2. What are the classifications of acute renal failure?
3. Briefly explain the pathophysiology of acute renal failure
4. Briefly explain the phases of acute renal failure
5. Briefly explain the management of acute renal failure
6. List the complications of acute renal failure

87. THANK YOU