College of Nursing

1. ACUTE RENAL FAILURE
By
Soudamini Rath (Tutor),
College of Nursing, Berhampur

2. Structure of the kidney
•
•
• Specific components are nephrons,
collecting ducts and a unique
microvasculature
Multipapillary kidney of humans – 1 million
nephrons
This number already established
prenatally
– Lost nephrons cannot be replaced

3. Nephrons
• A renal corpuscle (glomerulus)
– A knot of capillaries
– Connected to a complicated and twisted tubule
– Finally drains into a collecting duct

4. Urine formation:

5. Renal physiology
• Prime function – to maintain a stable
milieu interieur
– By selective retention and elimination of
• Water
• Electrolytes
• And other solutes

6. RENAL FAILURE
• Results when the kidneys cannot remove
the body’s metabolic wastes or perform
their regulatory functions.
•
• The substances normally eliminated in the
urine accumulate in the body fluids as a
result of impaired renal excretion.
• Leading to a disruption in endocrine and
metabolic functions as well as fluid,
electrolyte, and acid-base disturbances.
• I

7. ACUTE RENAL FAILURE
 A rapid deteriorating condition ofrenal functions,
resulting in accumulation of nitrogenous waste in
the body.
 It is a reversible clinical syndrome where there is a
sudden and almost complete loss of kidney
function (decreased GFR) over a period of hours to
days with failure to excrete nitrogenous waste
products and to maintain fluid and electrolyte
homeostasis.
 ARF manifests as an increase in serum
Creatinine (M=53-132umol/L; F=44-97umol/L) and
BUN (7-20mg/dl). Urine volume may be normal, or
changes may occur. Possible changes include
oliguria (<400ml/day), nonoliguria (>400ml/ day), or
anuria (<50 ml/day)

8. Acute renal failure can further devided into
1. Prerenal
2. Intrarenal
3. Postrena
according to the etiology

9. Categories of Acute Renal Failure
1. Prerenal- occurs in 60%-70% of
cases, is the result of impaired blood
flow to that leads to hypoperfusion of
the kidney and a decrease in the
GFR. Common clinical conditions are
volume-depletion states (hemorrhage
or GI losses), impaired cardiac
performance (MI, HF, or cardiogenic
shock), and vasodilation (sepsis or
anaphylaxis)

10. 2. Intrarenal- is the result of actual
parenchymal damage to glomeruli or
kidney tubules. Nephrotoxic agents such as
aminoglycosides and radiocontrast agents
account for 30% of cases of acute tubular
necrosis (ATN), and ischemia due to
decreased renal perfusion accounts for
more than 50% of cases
• Characteristics of ATN are intratubular back
leak (abnormal absorption of filtrate and
decreased urine flow through the tubule),
vasoconstriction, and changes in glomerular
permeability. These processes result in a
decrease of GFR, progressive azotemia, and
impaired fluid and electrolyte balance.


11. 3. Postrenal – is usually the result
of an obstruction somewhere
distal to the kidneys. Pressure
rises in the kidney tubules and
eventually, the GFR decreases

12. Comparing Categories of Acute Renal Failure
Characteristics Categories
Prerenal Intrarenal Postrenal
Etiology Hypoperfusion Parenchymal
damage
Obstruction
BUN value Increased Increased increased
Creatinine Increased Increased Increased
Urine output Decreased Varies, often
decreased
Varies, may be
decreased, or
sudden anuria
Urine sodium Decreased to < 20
mEq/L
Increased to
>40mEq/L
Varies, often
decreased to
20mEq/L or less
Urinary sediment Normal, few hyaline
casts
Abnormal casts
and debris
Usually normal
Urine osmolality Increased to
500mOsm
About 350 mOsm
similar to serum
Varies, increased
or equal to serum
Urine specific
gravity
Increased Low normal Varies

13. Caus es of Acute Re nal Failure
A. Prerenal
1. Volume depletion resulting from:
a. hemorrhage
b. renal losses (diuretics)
c. GI losses (vomiting, diarrhea, NG suctioning)
2. Impaired cardiac efficiency resulting from:
a. MI
b. Heart failure
c. Dysrhythmias
d. Cardiogenic shock
3. Vasodilation resulting from:
a. sepsis
b. anaphylaxis
c. antihypertensive medications or
other medications that cause
vasodilation

14. Caus es of Acute Re nalFailure
B. Intrarenal
1. Prolonged renal ischemia resulting from:
a. pigment nephropathy (associated with the breakdown of
blood cells containing pigments that in turn occlude
kidney structures)
b. Myoglobinuria (trauma, crush injury, burns)
c. Hemoglobinuria (transfusion reaction, hemolytic anemia)
2. Nephrotoxic agents such as:
a. Aminoglycosides antibiotics (gentamicin, tobramycin)
b. Radiopaque contrast media
c. Heavy metals (lead, mercury)
d. Solvents and chemicals (carbon tetrachloride, arsenic)
e. NSAIDs, ACE inhibitors
3. Infectious processes such as:
a. acute pyelonephritis
b. acute GN

15. Causes of Acute Renal Failure
C. Postrenal
1. Urinary tract obstruction, including:
a. calculi (stones)
b. BPH
c. Strictures
d. Trauma or Blood clots
e. Spinal cord diseases
f. Blader or prostate cancer

16. Stages in ARF
I. Renal impairment is the first stage of damage:The GFR is 40
to 50% of normal.
II. Renal insufficiency: the 20 to 40% of normal and fuctional
loss also as azotaemia, high BUN and anaemia also occur.
III. Renal failure there is only 10% GFR remaining. Fluid and
electrolyte imbalances occurs and function of kidney
diminished
IV. Uraemia :represent stage of kidney failure I,e .ESRD, High
nitrogenous waste product, multiple clinical manifestation with
blood accumulalated. It is very fatal stage

17. PATHOPHYSIOLOGY
Related to underlying causes
Damage to the nephron and loss of filtering action, diminished
reabsorption
Loss of ability to produce rennin, erythropoietin and other
substances
As the nephrons destroyed and tubular reabsorption
Increasedsodium concentration and distal tubule stimulates
production of rennin causing vasoconstriction and reducing
renal blood flow,

18. Cellular edema
Decreased glomerular capillary permeability
Intratubular obstruction
Leakage of glomerular filtrate, which reduce the intra tubular
fluid flow

19. Preventing ARF
1. Provide adequate hydration to patients at risk of
dehydration:
a. surgical patients before, during and after surgery.
b. Patients undergoing intensive diagnostic studies
requiring fluid restrictions and contrast agents
c. Patients with neoplastic disorders of metabolism
and those receiving chemotherapy
2. Prevent and treat shock promptly with blood and
fluid replacement.
3. Monitor CV and arterial pressures and hourly urine
output of critically ill patients to detect the onset of
renal failure as early as possible.
4. Treat hypotension promptly.
5. Continually assess renal function when appropriate.

20. Preventing ARF
6. Take precautions to ensure that the
appropriate blood is administered to the
correct patient in order to avoid severe
transfusion reactions, which can precipitate
renal failure.
7. Prevent and treat infections promptly.
Infections can produce progressive renal
damage.
8. Pay special attention to wounds, burns and
other precursors of sepsis
9. To prevent infections from ascending in the
urinary tract, give meticulous care to patients
with indwelling catheters. Remove catheter
ASAP.
10. To prevent toxic drug effects, closely monitor
dosage, duration of use, and blood levels of
all medications metabolized or excreted by
the kidneys.

21. Medical Management:
1. Pharmacologic therapy
a. hyperkalemia is the most life-threatening of the F/E
changes that occur in RF, the elevated K levels
may be reduced by administering cation-exchange
resins (sodium polystyrene sulfonate [Kayexalate]
orally or by retention enema. It works by
exchanging sodium ions for potassium ions in the
intestinal tract.
b. Sorbitol may be administered in combination with
Kayexalate to induce diarrhea type effect (induce
water loss in the GIT)
c. If hemodynamically unstable, IV dextrose
50%,insulin and calcium replacement may be
administered to shift potassium back into the cells.
d. Diuretics are often administered to control fluid
volume, but they have not been shown to hasten
the recovery form ARF.

22. Medical Management
2. Nutritional Therapy
a. Dietary proteins are individualized to provide
the maximum benefit. Caloric requirements
are met with high-carbohydrate meals,
because carbohydrates have a protein-
sparing effect.
b. Foods and fluids containing potassium or
phosphorous such as banana, citrus fruits
and juices, coffee are restricted

23. Nursing Management
•
•
•
•
•
•
Monitoring fluid and electrolyte balance
Maintaining nutrition
Promoting comfort and safety
Preventing infection
Prevent injury
Providing skin care
• facilitate coping

24. CHRONIC RENAL FAILURE/END S TAGE
RENAL DISEASE (ESRD)
 Is a progressive, irreversible
deterioration in renal function
in which the body’s ability to
maintain metabolic and fluid
and electrolyte balance fails,
resulting in uremia and
azotemia.

25. ESRD
Causes:
1. DM, HPN, chronic glomerulonephritis,
pyelonephritis, obstruction of the urinary
tract, hereditary lesions as in polycystic
kidney disease, vascular disorders,
infections, medications, or toxic agents.
2. Environmental and occupational agents
that have been implicated in CRF
include lead, mercury and chromium.
Dialysis or kidney transplantation
eventually becomes necessary for
patient’s survival.

26. Pathophysiology
As renal function declines, the end products of CHON
metabolism (which are normally excreted in urine)
accumulate in the blood. Uremia develops and
adversely affects every system in the body.
Stages of CRF: are based on the GFR. The normal
GFR is 125cc/min/1.73m2
1. Stage 1 = GFR > 90 ml/min/1.73m2. Kidney
damage with normal or increased GFR.
2. Stage 2 = GFR = 60-89 mL/min/1.73m2. Mild
decrease in GFR.
3. Stage 3 = GFR = 30-59 mL/min/1.73m2. Moderate
decrease in GFR.
4. Stage 4 = GFR = 15-29 mL/min/1.73m2. Severe
decrease in GFR.
5. Stage 5 = GFR <15 mL/min/1.73 m2. Kidney failure

27. Clinical Manifestations
1. CV manifestations:
a. HPN – due to Na and H20 retention or from R-
A-A activation,
b. heart failure and edema - due to fluid overload
c. pericarditis - due to irritation of pericardial lining
by uremic toxins
2. Dermatologic manifestations
a. severe pruritus is common
b. uremic frost, the deposit of urea crystals on the
skin.
3. GI manifestations:
a. anorexia, nausea and vomiting, and hiccups
b. The patient’s breath may have the odor of urine
(uremic fetor); this may be associated with
inadequate dialysis
4. Neurologic manifestations
a. altered LOC, inability to concentrate, muscle
twitching, agitation, confusion and seizures.
b. Peripheral neuropathy, a disorder of the
peripheral NS, is present in some patients

28. As s es s ment and Diagnos tic
Findings
1. GFR
2. Sodium and water retention
3. acidosis – due to inability of the kidneys to
excrete increased load of acid
4. Anemia
5. calcium and phosphorous imbalance –
hypocalcemia and increase in
phosphorous

29. Complications
1. Hyperkalemia due to decreased excretion,
metabolic acidosis, catabolism and excessive
intake (diet, meds and fluids)
2. Pericarditis, pericardial effusion and pericardial
tamponade due to retention of uremic waste
products and inadequate dialysis.
and water
the R-A-A
3. Hypertension due to sodium
retention and malfunction of
system
4. Anemia due to decreased erythropoietin
production, decreased RBC life span,
bleeding in the GIT from irritating toxins and
ulcer formation, and blood loss during
hemodialysis
5. Bone disease and metastatic and vascular
calcifications due to retention of phosphorous,
low serum calcium levels, abnormal vitamin D
metabolism and elevated aluminum levels.

30. Medical Management
1. Pharmacologic Therapy
a. calcium carbonate (Os-cal) or calcium
acetate (Phoslo) are prescribed to treat
hyperphosphatemia and hypocalcemia
b. Antiseizure agents – diazepam (Valium)
or phenytoin (Dilantin)
c. Antihypertensive and CV drugs -
digoxin (Lanoxin) and dobutamine
(Dobutrex)
d. Erythropoietin (Epogen) to treat anemia. It
is initiated to reach a hematocrit of 33%
- 385 and a target hemoglobin of 12g/dl.
2. Nutritional Therapy
a. low sodium, low CHON and low K diet
3. Dialysis

31. Nursing Management
Nursing Management:
1. Assessing fluid status and
identifying potential sources of
imbalance.
2. implementing a dietary program to
ensure proper nutritional intake
3. promoting positive feelings by
encouraging increased self-care and
greater independence.
4. Provide explanations and information to
the patient and family concerning ESRD,
treatment options and potential
complications.
5. Provide emotional support to the
patient and family.

32. DIALYSIS
 Is used to substitute some kidney functions
during renal failure.
 It is used to remove fluid and uremic waste
products from the body when the kidneys are unable
to do so.
 It may be indicated to treat patients with edema
that do not respond to treatment.
 Acute dialysis is indicated when there is a high
and increasing level of serum
potassium, fluid overload, or
pulmonary edema, iincreasing
impending
acidosis,
pericarditis and severe confusion. It may also be
used to certain medications or other toxins in the
blood.

33. PERITONEAL DIALYSIS
TYPES:
2.Intermittent peritoneal dialysis =
acute or chronic renal failure
3.Continuous ambulatory
peritoneal dialysis = chronic
renal failure
4.Continuous cycling peritoneal
dialysis = prolonged dwelling
time

34. PERITONEAL DIALYSIS
• Indwelling catheter is implanted into the
peritoneum.
• The technique for peritoneal dialysis involves
preparing the patient and setting up the
equipment, inserting the catheter, instilling the
dialysate.
• The catheter insertion may be done in operating
room or at the bedside under local or general
anesthesia.
• The preferred site for insertion is about 3 to 5cm
below the umbilicus, an area which is relatively
avascular and has less fascial resistance.
• The tip of the catheter is usually positioned so that
it lied deeply with the pelvic gutter, the correct
position will often give the patient the urge to
defecate.
• The catheter is generally sutured in place to avoid
accidental dislodgment.

35. • A connecting tube is attached to the external
end of peritoneal catheter T –tube.
• Plastic bag of dialysate solution is inserted
to the end of T-tube; the other end is recap.
• Dialysate bag is raised to shoulder
level and infused by gravity in the
peritoneal cavity
• Infusion time = 10 minutes/2
liters; dwelling time is 4-6 hours
depending on doctor’s order.
• At the end of dwelling time,
dialysis fluid is drained from the
peritoneal cavity by gravity
• Draining time is 10-20 minutes/2 liters
• Then repeat the procedure when necessary

36. Peritoneal Dialysis
• Usually for patients with absolutely no
other options of dialysis
• Or as a temporary measure until options
of dialysis sorted out

37. PERITONEAL DIALYSIS

38. PERITONEAL DIALYSIS

39. NURSING RESPONSIBILITIES IN PERITONIAL DIALYSIS:
Before Dialysis
• Prepare the patient emotionally and physically
• See that the consent form is signed
• Weigh the patient
• Check vital signs
• Empty bladder
• Assist with insertion of CVP catheter ECG
monitoring is also employed
• Make the patient comfortable in supine
position and set up the instruments

40. During Dialysis
• Assist the physician in inserting the peritoneal catheter
• After the procedure, if the fluid is not draining properly, move
the patient from side to side.
• Then the outflow ceases, clamp off the drainage tube and
infuse next exchange.
• Take B.P. and pulse every 15min during the first exchange
and every hour thereafter.
• Maintain a record of patient’s fluid balance.
• Promote patient comfort during dialysis frequent back care
and changing position.
• Observe breathing difficulty, abdominal pain
and leakage arround the catheter.
After Dialysis
• Take the patient’s temperature
• Look for complication

41. Complications
• Perforation of the bowel
• Puncture of abdominal aorta
• Oedema of the anterior abdominal wall
• Pain
• Plural effusion
• Peritonites
• Hypernatraemia
• Hypokalamia
• Hyperglycaemia
• Disequilbrium
• Pulmonary etc.

42. HEMODIALYSIS
 it is the process of cleansing the blood of
accumulated waste products.
Patient’s access is prepared and cannulated
surgically
 One needle is inserted to the artery (brachial)
then blood flow is directed to dialyzer (dialysis
machine)
 The machine is equipped with semi-permeable
membrane surrounded with dialysis solution
 Waste products in the blood move to the
dialysis solution passing through the membrane
by means of diffusion
 Excess water is also removed from the blood
by way of ultrafiltration
 The blood is then returned to the vein after it
has been cleansed.

43. HEMODIALYSIS

44. HEMODIALYSIS
Patient Access
Vascular catheter
A-V fistula
Synthetic vascular
graft

45. HEMODIALYSIS

46. HEMODIALYSIS
NURSING CONSIDERATIONS:
1. The dialyser to be prepared by proper setting, can
be heparinized unless it is contraindicated to
prevent blood clot.
2. Dialysis solution has some electrolytes and
acetate and HCO3 added to achieve proper pH
balance.
3. Methods of circulatory access: AV fistula; AV graft or
U-tube
4. Assess the access site for bruit, signs of infections
and ischemia of the hand.
5. Aseptic technique must be follow.
6. No BP taking on the access site.

47. 7. Cover the access site with adhesive bandage
8. Dietary adjustments of Carbohydrate, Na and fluid intake.
9. Monitor VS regularly
10. Check blood chemistry
11. Constant monitoring of hemodynamic status, electrolytes
and acid-base balance.

48. 13) Observation of patient s pulse and B.P every half an hour and
respiration every hour.
14) Observe for hypothermia, cardiac irregularities, and twitching.
15) Observe the machine a sudden break in the circuit, high
venous pressure due to kinking which leads low
arterial pressure and failure of blood pump.
16) Dietary adjustment of protein, sodium, and
potassium and fluid intake.
17) Psychological and emotional support to the
patient as in stress.

49. Complication:
• Acute circulatory overload
• Haemorrhage
• Cardiac arrest
• Dialysis disequilibrium syndrome etc

50. •
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