acute renal failure

1. VN. Karazin University.
Acute renal failure(ARF)
Made by: NANFUKA CATHERINE
GROUP; 501
Number; 4

2. TABLE OF CONTENT
1) Definition
2) Symptoms
3) Risk factors
4) Anatomy renal system, kidney and nephrons.
5) Physiology & function of kidney/nephrons
6) Diagnostic criteria of ARF
7) Stages of ARF
8) Phases of ARF
9) Classification of ARF
10) Causes of ARF & Pathophysiology of ARF
11) Prerenal ARF
12) Intrarenal ARF
13) Post-renal ARF
14) Diagnostic evaluation of ARF
15) Treatment of ARF
16) Prevention of ARF
17) Complications of ARF
18) Differential diagnosis of ARF
19) Prognosis of ARF

3. ACUTE RENAL FAILURE:
Definition Acute Renal failure;
Is a rapid decline (hours, days, weeks) in glomerular and tubular functions with loss of
the ability to maintain fluid and electrolyte homeostasis and to excrete organic solutes
including drugs and metabolites manifesting as:
• Rising BUN and creatinine
• Alteration in electrolyte concentrations: Na, K, Ca, PO4, CO2, H+
• Edema and intravascular volume excess
• Oliguria, polyuria, or normal urine output may be present

4. OTHER SYMPTOMS AF ARF
bloody stools
breath odor
slow, sluggish movements
generalized swelling or fluid retention
fatigue
pain between ribs and hips
hand tremor
bruising easily
changes in mental status or mood, especially if you’re older
decreased appetite
decreased sensation, especially in your hands or feet
prolonged bleeding
seizures
nausea
vomiting
high blood pressure
a metallic taste in your mouth

5. RISK FACTORS:
Advanced age, adults older than 75 years
Blockages in the blood vessels in your arms or legs
Diabetes
High blood pressure
Heart failure
Liver disease
persons with Kidney diseases e.g. preexisting chronic kidney disease
persons with sepsis.
those who are exposed to contrast agents or who are undergoing cardiac surgery.

6. ANATOMY OF THE URINARY SYSTEM:

7. PHYSIOLOGY OF THE KIDNEY;

8. Kidney nephron:

9. Renal physiology: Is the study of the physiology of the kidney. This includes all
functions of the kidney, including maintenance of acid-base balance; regulation
of fluid balance; regulation of sodium, potassium, and
other electrolytes; clearance of toxins; absorption of glucose, amino acids, and other
small molecules; regulation of blood pressure; production of various hormones, such
as erythropoietin; and activation of vitamin D.
The mnemonic A WET BED aids in memory of kidneys functions.
A – maintaining ACID-base balance
W – maintaining WATER balance
E – ELECTROLYTE balance
T – TOXIN removal
B – BLOOD Pressure control
E – making ERYTHROPOIETIN
D – Vitamin D metabolism.

10. Mechanisms
The kidney's ability to perform many of its functions depends on the three
fundamental functions of filtration, reabsorption, and secretion, whose sum is called
renal clearance or renal excretion.
Urinary excretion rate = Filtration rate – Reabsorption rate + Secretion rate

12. Functions of the kidney
This can be divided into three groups: secretion of hormones, gluconeogenesis and
extracellular homeostasis of pH and blood components. The nephron is the functional
unit of the kidney.
Secretion of hormones[edit]
Secretion of erythropoietin, which regulates red blood cell production in the bone
marrow.
Secretion of renin, which is a key part of the renin–angiotensin–aldosterone system.
Secretion of the active form of vitamin D (calcitriol) and prostaglandins.

13. Gluconeogenesis
The kidney in humans is capable of
producing glucose from lactate, glycerol and glutamine. The kidney is responsible for
about half of the total gluconeogenesis in fasting humans. The regulation of glucose
production in the kidney is achieved by action of insulin, catecholamines and other
hormones.[1] Renal gluconeogenesis takes place in the renal cortex. The renal
medulla is incapable of producing glucose due to absence of necessary enzymes.
Extracellular homeostasis
The kidney is responsible for maintaining a balance of the following substances:
glucose, urea, water, sodium, potassium, bicarbonate etc.

14. ARF DIAGNOSTIC CRITERIA
Acute Renal Failure is defined when one of the following criteria is met;
serum creatinine rises by >= 26 µmol/L within 48 hours or
serum creatinine rises >= 1.5 fold from the reference value, which is known or
presumed to have occurred within one week or
oliguria (urine output is < 0.5ml/kg/hr for >6 consecutive hours) or
a 25% or greater fall in GFR in children and young people within the past 7 days (3)

15. The reference serum creatinine should be the lowest creatinine value recorded within
3 months of the event
If a reference serum creatinine value is not available within 3 months and AKI is
suspected
repeat serum creatinine within 24 hours
a reference serum creatinine value can be estimated from the nadir serum creatinine
value if patient recovers from AKI

16. STAGING OF ARF
Stage
of ARF
Serum creatinine (SCr) criteria Urine output criteria
1
increase >=26 µmol/L within 48hrs or
increase >= 1.5 to 1.9 X reference SCr
<0.5 mL/kg/hr for > 6 consecutive hrs
2 increase >= 2 to 2.9 X reference SCr <0.5 mL/kg/ hr for > 12 hrs
3
increase >=3 X reference SCr or
increase >=354 µmol/L or
commenced on renal replacement therapy (RRT)
irrespective of stage
<0.3 mL/kg/ hr for > 24 hrs or anuria for 12 hrs

17. Phases of arf;
Initial stage: it begins hours after an insult or injury.
Oliguric phase: begins 1- 7 days after insult but lasts 10 – 14 days.
Urine volume less than 400 ml per 24 hours; increased in serum creatinine, urea, uric
acid, organic acids, potassium, and magnesium; lasts 3 to 5 days in infants and children,
10 to 14 days in adolescents and adults.
Diuretic phase:
Begins when urine output exceeds 500 ml per 24 hours, end when BUN and creatinine
levels stop rising; length is available.
Recovery phase:
Asymptomatic; last several months to 1 year; some scar tissue may remain.

18. CLASSIFICATION OF ARF:
1. Prerenal failure – results from conditions that interrupt the renal blood supply;
thereby reducing renal perfusion (hypovolemia, shock, hemorrhage, burns
impaired cardiac output, diuretic therapy and NSAIDs).
2. Postrenal failure – results from obstruction of urine flow.
3. Intrarenal failure – results from injury to the kidneys themselves (ischemia, toxins,
immunologic processes, systemic and vascular disorders).

19. CAURSES OF ARF

20. CONTINUATION OF CAUSES
Pre-renal causes:
hypovolaemia, for example acute haemorrhage, burns
circulatory failure - heart failure or shock
Renal causes:
acute tubular nephropathy, for example ischaemic acute tubular necrosis
acute interstitial nephropathy, for example in ascending urinary tract infection
acute glomerulonephritis - Goodpasture's syndrome
haemolytic uraemic syndrome
drugs - cytotoxics such as cisplatin or streptozotocin, aminoglycosides such as gentamicin, tetracyclines, NSAIDs, ACE-
inhibitors
malignant hypertension
following blood transfusion
multiple myeloma
hepatorenal syndrome
Post renal causes:
obstructive lesions like stones, prostatic hypertrophy, congenital obstructive disorders

21. Prerenal arf:
Pre means before so this means anything that happens before the kidney that affects
the kidney function.
Anything that causes problem with blood flow to the kidney.
There are mainly 3 major causes:
1. decreased cardiac output: these may include;
a) Hypotension
b) Decreased blood volume due to haemorriage.
c) Chronic heart failure and
d) Decreased perfusion

22. 2. Vascular constriction:
This can be due to use of NSAIDs and other drugs that cause vasospasm eg cocain.
NSAIDs blocks prostaglandins (which is a vasodilator) causing vasoconstriction
especially to the afferent aterials thus decreasing blood flow to the nephrons.
3.Vesoocclusion; this may include;
a) Emboli
b) Artherosclerosis

23. Due to decreased blood flow to the kidney during prerenal ARF, there is usually;
1. increased reabsorption of sodium and water.
2. Oliguria
3. Increased osmolarity of urine.

24. Intrarenal arf:
This occurs when the cause of ARF is with in the kidney. Due to damage of the kidney
nephrons.
There are 2 parts that can be damage:
1. Glomerular (anything that causes glomerulonephritis) these include;
a) Infections especially strep infection.
b) Autoimmune
2. The kidney tubules (anything causing acute tubular necrosis) these include;
a) Ischemia
b) Drugs/ toxins
c) Hemolysis

25. During intrarenal ARF, there is damage of kidney nephron cells and due to this there is
usually decreased reabsorption leading;
1) Increased sodium in the urine + water
2) Polyuria
3) Decreased osmolarity (dilute urine)

26. Postrenal ARF:
This is due to obstruction after the kidney.
Its usually cased by;
1. Kidney stones which can clog up the ureter, bladder or urethra.
2. Tumors of the ureter, bladder or urethra.
3. Prostatic hyperplasia / prostatic caner.
4. Neurologic bladder (over distended bladder caused by inability to empty)
5. Renal injury eg in automobile accidents or while playing sports.
6. Retroperitoneal fibrosis.

27. Pathophysiology of postrenal arf
Normally filtration of urine is brought about by difference in pressure ie,
High pressure in the glomerulous and low pressure in the bowmanns capsule.
When the ureter, bladder or urethra get blocked eg by kidney stone or tumors, the urine is
pushed back in to the kidney to the bowmanns capsule causing increasing pressure in the
bowmanns capsule thus disabling filtration.
In this case we see;
1. Oliguria or anuria in sever cases
2. Dificult urination
3. Normal urine osmolarity.
4. Severe hematuria (blood in the urine)
5. Edema due to fluid retention and swelling.
6. Distended bladder if obstraction is in the urethra
7. Hypertension (high BP)

28. Note: the 4 major/ commonest causes of ARF include:
1) Decreased blood volume
2) Use of NSAIDs
3) Acute tubular necrosis due to ischemia
4) Drugs and toxins.
Pre and intra renal failure are the commonest causes of ARF.
Post-renal ARF if the most rare and its easily reversible as compared to the others.

29. PATHOPHYSIOLOGY OF ARF;

30. Diagnostic Evaluation:
:
History collection.
Physical examination.
1 Asterixis and myoclonus
2 Peripheral edema (if volume overload is present)
3 Pulmonary rales (if volume overload is present)
4 Elevated right atrial pressure (if volume overload is present)
Blood studies  elevated BUN, serum creatinine, and potassium levels; decreased
bicarbonate level, hematocrit, and hemoglobin; and acid ph
Urine studies  casts, cellular debris, and decreased specific gravity; in glomerular
diseases, proteinuria and urine osmolality close to serum osmolality; sodium level less
than 20 meq/L if oliguria results from decreased perfusion, and more than 40 meq/L if
cause is intrarenal

31. Creatinine clearance test measuring GFR and reflecting the number of remaining
functioning nephrons
Electrocardiogram (ECG) showing tall, peaked T waves; widening QRS complex; and
disappearing P waves if hyperkalemia is present.
RENAL BIOPSY: is reserved for patients in whom prerenal and postrenal causes of
acute kidney injury have been excluded and the cause of intrinsic renal injury is
unclear.
Ultrasonography, plain films of the abdomen, kidney-ureter-bladder radiography,
excretory urography, renal scan, retrograde pyelography, computed tomographic
scans, and nephrotomography
abdominal X-ray, abdominal CT scan and abdominal MRI can also help to determine if
there’s a blockage in your urinary tract.

32. TREATMENT OF ARF;
1.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.
C. restrict your diet and the amount of liquids you eat and drink
d. Patient may require parenteral nutrition.

33. 2. Pharmacologic therapy:
a. hyperkalemia is the most life-threatening of the 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.
Calcium and insulin can help avoid dangerous increases in your blood potassium levels.
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. Diuretic therapy to treat oliguric phase, Diuretics are often administered to control fluid volume.

34. Doctor may prescribe antibiotics to treat or prevent any infections
May need dialysis, but it’s not always necessary. Dialysis involves diverting blood out of
your body into a machine that filters out waste.
Can do surgery in case of post renal failure e.g. obstruction by stone in the ureter,
urethra or bladder. Even in case of prostatic hyperplasia.
kidney transplatation

35. 3. Nursing Management:
Monitoring fluid and electrolyte balance
Reducing metabolic rate
Promoting pulmonary function
Preventing infection
Providing skin care
Providing support

36. Prevention OF ARF:
A careful history taking (nephrotoxic antibiotic agent aminoglycosides, gentamicin, tobramicine, etc.)
It is important for primary care physicians to identify patients who are at high risk of developing this
type of injury and to implement preventive strategies. Those at highest risk include adults older than
75 years;
blood tests and urinalysis
Drink enough fluids
Difficulties urinating or blood in the urine should prompt a visit
Treat hypotension promptly.
Prevent and treat infections promptly.
Pay special attention to wound, burns and other precursors of sepsis.

37. COMPLICATION OF ARF
chronic kidney failure
heart damage, Pericarditis
nervous system damage
end-stage renal failure
high blood pressure
Infection
Hyperkalaemia, Hyperphosphataemia, hyponatraemia
water overload
Pulmonary edema.

38. Differential DIAGNOSIS OF ARF:
Abdominal aneurysm
Alcohol toxicity
Alcoholic ketoacidosis
Chronic renal failure
Dehydration
Diabetic ketoacidosis
Gastrointestinal (GI) bleeding
Heart failure
Metabolic acidosis
Obstructive uropathy
Protein overloading
Renal calculi
Sickle cell anemia
Steroid use
Urinary obstruction
Urinary tract infection

39. Prognosis:
Patients with acute kidney injury are more likely to develop chronic kidney disease in
the future. They are also at higher risk of end-stage renal disease and premature
death.
25-27 Patients who have an episode of acute kidney injury should be monitored for
the development or worsening of chronic kidney disease.
Prognosis is good ARF if there is early treatment the kidney gains back its normal
function.

40. THANK YOU
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