Acute renal failure is a sudden decline in kidney function that results in the buildup of waste products in the blood. It can be caused by decreased blood flow to the kidneys, obstruction of urine outflow, or direct damage to the kidneys. Symptoms include decreased urine output, fluid retention, electrolyte imbalances, and accumulation of waste products. Treatment focuses on restoring fluid and electrolyte balance, preventing complications, and addressing the underlying cause of kidney injury through medical management or renal replacement therapy if needed. Nursing care is aimed at monitoring fluid status, preventing infections, improving nutrition, and managing complications of acute renal failure.

1. A C U T E R E N A L
FA I L U R E
MS. K.UDAYASREE
TUTOR
APOLLO COLLEGE OF NURSING
CHIT TOOR

2. Abrupt decrease in renal function resulting in the
accumulation of nitrogenous compounds such as urea
and creatinine
ARF is a sudden decline in glomerular filtration rate (GFR)
often accompanied by a drop in urine output. Decreased
GFR results in accumulation of nitrogenous wastes and
alterations in fluid and electrolyte balance.
DEFINITION

3. INCIDENCE
• The incidence rises to approx. 20% in critically ill
patients. Renal replacement therapy (RRT) may be
necessary, depending on the severity of renal failure
and related clinical conditions
Type Incidence
Prerenal 35%
Intrarenal 55%
Postrenal 10%

4. CLASSIFICATION
• Prerenal failure: circumstances or conditions that
decrease blood flow to the kidneys
• Post renal failure: conditions that obstruct urine
outflow from the kidney
• Intrarenal failure: conditions affecting internal
structures of the kidney; most often, acute tubular
necrosis (ATN) , which develops when a toxin or
ischemia damages the renal tubules.

6. PRE-RENAL ACUTE RENAL FAILURE
 HYPOVOLEMIA
 Dehydration
 Hemorrhage
 GI losses (Diarrhea, Vomiting)
 Excessive diuresis
 Hypoalbuminemia
 Burns
 DECREASED CO
 Cardiac dysrhythmias
 Cariogenic shock
 Heart failure, MI
 DECREASED RENAL FLOW
 B/L renal vein thrombosis
 Embolism
 Hepatorenal syndrome
 Renal artery thrombosis
 CHANGE IN PVR
 Anaphylaxis
 Neurogenic injury
 Septic shock
 Antihypertensive drugs, drug
overdose

7. INTRA-RENAL ACUTE RENAL FAILURE
NEPHROTOXIC INJURY
 Drugs : Aminoglycosides, antineoplastics, NSAIDS
 Contrast media
 Hemolytic blood transfusion reaction
 Severe crush injury
 Chemical exposure :lead, arsenic
INTERSTITIAL NEPHRITIS
 Allergies : Antibiotics, NSAIDs
 Infections
OTHERS
 A/C Glomerulonephritis, toxemia, SLE

8. POST-RENAL ACUTE RENAL FAILURE
• BPH
• Bladder cancer
• Calculi formation
• Neuromuscular disorders
• Prostate cancer
• Spinal cord disease
• Strictures
• Trauma (Back, pelvis, perineum)
• Urinary tract infections

9. PATHOPHYSIOLOGY

10. PHASES
There are four phases of ARF
• INITIATION : The initiation period begins with the initial
and ends when oliguria develops
• OLIGURIA : The oliguria period is accompanied by an increase
increase in the serum concentration of substances usually
excreted by kidneys
• DIURESIS : The diuresis period is marked by a gradual increase
increase in urine output, which signals that glomerular
filtration has started to recover
• RECOVERY : The recovery period signals the improvement of
renal function and may take 3 to 12 months

11. CLINICAL FEATURES
•Oliguric phase
• Urinary changes :
– <400 ml/day
– Occurs within 7 days of injury(depending on cause and tissue injury)
– Lasts for about 10-14 days
– Longer it lasts, poor prognosis
• Fluid volume :
– Treat with fluid replacement
– If oliguria/ anuria fluid retention results which can lead to fluid excess
– Results in increased JVP
, bounding pulse, edema, hypertension
– It can lead to complications such as HF, pulmonary edema, pericardial
pleural effusion

12. • Metabolic acidosis:
– Impaired excretion of hydrogen ions and metabolic waste
products
– Decreased production of bicarbonate ions
– May develop Kussmaul respiration
• Sodium balance:
– Sodium may be below normal levels
• Potassium excess:
– Hyperkalemia
– Bleeding, blood transfusion & metabolic acidosis worsens
hyperkalemia

13.  Waste product accumulation :
o BUN, creatinine - elevated
Neurologic disorders :
oNeuro changes can occur as the nitrogenous waste products
accumulate in the brain & other nervous tissue
oManifestations : Fatigue, difficulty concentrating, seizures,
stupor & coma
Hematologic disorders :
oImpaired erythropoietin production
oPlatelet abnormalities
oDecreased WBC
oCalcium deficit and phosphate excess

14. DIURETIC PHASE :
• Begins with gradual increase in output and it reach to 5L /day
• High urine volume caused by osmotic diuresis from the high
urea concentration in the glomerular filtrate & inability to
concentrate urine
• Hypovolemia, hypokalemia, hypotension & dehydration can
occur from massive fluid losses
• May last 1-3 weeks
• Near the end, acid-base, electrolyte, BUN, creatinine values
stabilize

15. RECOVERY PHASE :
• Begins when the GFR increases
• BUN & creatinine comes to decrease
• 1-2wks but may last for 12 months
• Some individuals do not recover & progress to ESRD

16. DIAGNOSIS
• History
• Physical examination
 Urine output
• Urine analysis
 Urine specific gravity : <1.020
 Osmolality: Less than 350 mosm/kg
 Twenty–four–hour urine tests
 Presence of dirty brown casts, crystals
• Blood tests
 BUN, S.creatinine, S. electrolytes, Hb, RBC
• Arterial blood gases (ABGs)
 Metabolic acidosis

17. DIAGNOSIS
 Kidney, ureter, bladder (KUB) X-ray :
 Demonstrates size of kidneys/ureters/bladder,
presence of cysts, tumors, stones
 Retrograde pyelogram:
 Outlines abnormalities of renal pelvis and ureters
 Renal arteriogram:
 Voiding cystoureterogram:
Shows bladder size, reflux into ureters,
retention
 Renal ultrasound

18. DIAGNOSIS
 Nonnuclear computed tomography (CT) scan: Cross-
sectional view of kidney and urinary tract detects
presence/extent of disease
 Magnetic resonance imaging (MRI): Provides information
about soft tissue damage
 Excretory urography (intravenous urogram
or pyelogram): Radiopaque contrast
concentrates in urine and facilitates
visualization of KUB.

19. DIAGNOSIS
• Endourology: Direct visualization may be done of urethra,
bladder, ureters, and kidney to diagnose problems, biopsy,
and remove small lesions and/or calculi
• Electrocardiogram (ECG): May be abnormal, reflecting
electrolyte and acid-base imbalances
• Renal biopsy : A sample of the kidney tissue (biopsy) is
sometimes required in cases in which the cause of the kidney
disease is unclear

20. MEDICAL MANAGEMENT
• Treat the underlying disease
• Strictly monitor I/O, weight
• Monitor serum electrolytes
• Adjust medication dosages according to GFR
• Avoid highly nephrotoxic drugs
• Determine adequate CO to ensure kidney perfusion

21. MEDICAL MANAGEMENT
• Maximize perfusion
Intravenous fluids
Plasma expanders (i.e., albumin)
Blood transfusion
Pressor agents (i.e., dopamine / dobutamine)
Unloading agents (i.e., nipride/ nitroglycerine) in
cases of congestive heart failure

22. • Stop fluid loss
Assess and control bleeding sites
Replace GI fluid losses and treat bacterial infections with appropriate
antibiotics
Broad-spectrum antibiotics for sepsis
Excisison of eschar and grafting in burn injuries
• Eliminate renal toxins
Diuresis with saline plus IV loop diuretic may prevent ARF due to
contrast.
Alkalinization of the urine with acetazolimide or sodium bicarbonate
may help prevent intratubular precipitation of uric acid (acetazolamide
150 – 500 mg IV)
Withdraw nephrotoxic drugs (i.e., ACE inhibitors, NSAIDS,

23. • Relieve obstruction
Foley catheter
Ureteral stents
Ureteroscopic stone removal
Lithotripsy
• Percutaneous nephrostomy
• Renal replacement therapy
Hemodialysis
Continuous arteriovenous hemoinfiltration (CAHF)
Peritoneal dialysis

24. • Therapies for elevated potassium levels
 Regular insulin IV : K+ moves into cells, given with glucose
to prevent hypoglycemia
 Sodium bicarbonate : correct acidosis & cause a shift of K+
into cells
 Calcium gluconate IV : Used in hyperkalemia ECG changes
 Hemodialysis
 Sodium polystyrene sulfonate: cation-exchange resin
(mouth or enema), it removes 1mEq/drug, it is mixed with
sorbitol to produce osmotic diarrhea, allowing for
evacuation of potassium-rich stool from body

25. NUTRITIONAL THERAPY
• Potassium intake is limited to 40mEq/day
• Low-protein, high-calorie diet : Caloric intake – 30-35kcal/kg &
0.8 – 1g of protein/kg of body weight to prevent breakdown of
body protein
• Sodium is restricted (To prevent edema, hypertension, HF)
• Dietary fat intake is increased (To prevent ketosis & endogenous
fat breakdown)
• Fat emulsion IV infusion
• TPN
• Potassium or phosphorus diet are restricted

26. NURSING MANAGEMENT
The goals for a patient with ARF are:
–Restore fluid & electrolyte balance
–Promote pulmonary function
–Prevent infection
–Promote skin care
–Improve nutritional intake

27. NURSING MANAGEMENT
• MAINTAIN FLUID & ELECTROLYTE BALANCE
 Fluid restriction- 24hrs fluid loss + 600ml
 Monitor daily weight (0.2-0.5kg/day)
 Diuretic therapy (Eg: Lasix)
 Monitor electrolytes & ABG
 Electrolyte replacement
 Acidosis is treated with bicarbonate
 ECG monitoring
 Dark green veg’s, unrefined grains, seeds, nuts, antacids & osmotic
laxatives containing magnesium should be avoided

28. NURSING MANAGEMENT
• PROMOTE PULMONARY FUNCTION
 Assisted to turn, cough, and take deep breaths
frequently to prevent atelectasis and respiratory tract
infection
 Teach deep breathing exercises
• PREVENT INFECTION
 Asepsis is essential with invasive lines and catheters to
minimize the risk of infection
 Maintain personal hygiene
 Urinary catheters are avoided

29. NURSING MANAGEMENT
PROVIDE SKIN CARE
 Bathing the patient with cool water
 Frequent turning
 keep the skin clean and well moisturized
 keep the fingernails trimmed to avoid excoriation and prevent
skin breakdown
IMPROVE NUTRITIONAL INTAKE
 Low-protein, high-calorie diet
 Sodium, potassium & phosphorus restricted diet

30. EXCESS FLUID VOLUME RELATED TO COMPROMISED
REGULATORY MECHANISM
INTERVENTIONS RATIONALE
• Accurately record intake and
output (I&O)
• Weigh daily at same time of day,
with same equipment
• Auscultate lung and heart sounds
• Monitor serum electrolytes,
• Monitor BUN, creatinine
• Restrict fluid intake
• Administer diuretics
• Decrease in output may indicate
acute failure
• Daily body weight is best monitor
of fluid status
• Fluid overload may lead to
pulmonary edema and HF
• Fluid overload leads to electrolyte
imbalances
• Lack of renal excretion leads to
accumulation of waste products
• To prevent further fluid
accumulation
• To promote diuresis

31. DEFICIENT KNOWLEDGE RELATED TO INFORMATION
MISINTERPRETATION
INTERVENTIONS RATIONALE
• Review disease process,
prognosis, and precipitating
factors if known
• Discuss renal dialysis or
transplantation if these are likely
options for the future
• Review dietary plan and
restrictions. Include fact sheet
listing food restrictions
• Encourage patient to observe
urine output, weight
• Encourage for fluid restriction &
use ice for thirst
• Provides knowledge base from
which patient can make informed
choices
• Possible treatment
• Adequate nutrition is necessary to
promote tissue healing; adherence
to restrictions may prevent
complications
• To identify any alterations
• To prevent excess fluid
accumulation

32. RISK FOR INFECTION RELATED TO DEPRESSION OF
IMMUNOLOGIC DEFENSES
INTERVENTIONS RATIONALE
• Avoid invasive procedures and
manipulation of indwelling
catheters whenever possible
• Assess skin integrity
• Encourage deep breathing,
coughing, frequent position
changes
• Follow aseptic technique
• Limits introduction of bacteria
into body
• Excoriations from scratching
may become secondarily
infected
• Prevents atelectasis and
mobilizes secretions to reduce
risk of pulmonary infections
• To prevent infection

33. COMPLICATIONS
• Metabolic acidosis
• Fluid and electrolyte imbalances : Hyperkalemia, Hyperphosphatemia,
Hypocalcemia
• Anemia
• Bleeding
• Cardiopulmonary : Arrhythmia, pericarditis, pericardial effusion,
pulmonary edema
• Hyperuricemia
• Infection : Pneumonia, sepsis
• GI : Nausea, vomiting, malnutrition, GI bleeding
• CNS : Asterixis, mental changes, seizures
• Uremic syndrome

34. REFERENCES
• Brunner and suddarth’s, “Textbook of medical surgical nursing”, volume
2, 13th edition, wolter Kluwer publications.
• Lewis ‘s, “Medical surgical nursing assessment and management of
clinical problems”,7th edition, Elsevier publications.
• BT.Basavanthappa, “Medical surgical nursing”, 1st edition, Jaypee
brother medical publishers.
• Joyce M. Black, Jane Hokanson Hawks, “Medical surgical nursing clinical
management for positive outcomes”, volume-1, 7th edition, Elsevier
publications.
• Cambell - Walsh, “Text book of urology”, volume-2, 10th edition, Elsevier publications.
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