2. WHAT IS RENAL FAILURE
• A condition of reduced flow of urine
(<400ml/24hrs) coupled with increased blood
urea and other renal dysfunction symptoms
• Renal failure divided into acute and chronic
3. Definition of acute renal failure.
• This is the abrupt decline in renal
filtration function .
• Acute renal failure is a syndrome with
the following features:
• Rapidly rising plasma urea and creatinine
concentrations
• oliguria or anuria less than 400ml/24h
normal 1200-1500ml/24hrs
• There is marked decrease in the GFR
4. Aetiological classification of ARF
• Pre-renal renal failure
• Intrinsic renal failure
• Post renal renal failure
1.Pre-renal causes.
These include conditions that
reduce effective blood flow
to the kidneys.
However, there is normal
tubular and glomerular
function.
examples
• Heavy blood loss
• Dehydration
• Hypotension
• Heart failure
• Renal artery stenosis
• Burns
• Haemolytic uremic
syndrome
• Idiopathic
thrombocytopenia
thrombotic purpura
• Transfusion reactions
5. 2. Renal causes
These affect the kidneys
especially those damaging
the glomeruli and the
tubules.
Examples of renal causes:
– Drugs like gentamycin and
streptomycin aspirin,
ibuprofen, ACE inhibitor.
– Acute tubular necrosis
– Acute interstitial nephritis
– Autoimmune diseases like
acute nephritic syndrome
– acute tubular nephropathy,
for example ischaemic
acute tubular necrosis
– acute interstitial
nephropathy, for example
in ascending urinary tract
infection
– haemolytic uraemic
syndrome
– malignant hypertension
– following blood transfusion
– multiple myeloma
6. 3. Post renal causes
There is a sudden block that stops the urine
from flowing out of the kidneys.
Examples are;
• obstructive lesions like kidney stones, benign
prostatic hyperplasia, congenital obstructive
disorders, bladder stone, bladder urethral or
renal malignancy
7. PATHOPHYSIOLOGY
• All The Above Causes: Prerenal, Intrarenal And
Postrenal Whether Singly Or In Combination, Will
End In; Acute Tubular Necrosis→sloughing Of Cells
→Adherence To Other Cells→occlusion.
8. Mechanisms involved
• The precise molecular mechanisms
responsible for the development of acute
tubular necrosis remain unknown.
• Theories favoring either a tubular or vascular
basis have been proposed.
• It may be that both mechanisms act to
produce acute renal failure.
9. • According to the tubular theory, occlusion of
the tubular lumen with cellular debris forms a
cast that increases intratubular pressure
sufficiently to offset perfusion pressure and
decrease or abolish net filtration pressure.
10. A) VASCULAR THEORY
• Vasoconstriction of afferent arterioles and
vasodilation of efferent arterioles
Glomerula perfusion pressure and glomerular
filteration.
v
11. B) TUBULAR THEORY
• occlusion of the tubular lumen with cellular
debris forms a cast that increases intratubular
pressure sufficiently to offset perfusion
pressure and decrease or abolish net filtration
pressure.
12.
13. Stage Serum creatinine Urine output
1 1.5-1.9 times baseline
OR
0.3 mg/dl ( 26.5 µmol/l) increase
< 0.5ml/kg/h x 6 hr for
6-12 hours
2 2.0-2.9 times baseline < 0.5ml/kg/h for
12 hours
3 3.0 times baseline
OR
Increase in serum creatinine to
4.0 mg/dl (353.6 µmol/l)
OR
< 0.3ml/kg/h for
24 hours
OR
Anuria for 12 hours
Initiation of renal replacement therapy
OR, In patients < 18 years, decrease in
eGFR to < 35 ml/min per 1.73 m2
Staging of AKI
15. Clinical manifestations
• Incidental finding on blood tests
• Commonly oliguric on anuric, can be polyuric
or have normal urine volume
• Symptoms of metabolic acidosis
• Symptoms of salt and water overload
• Haematuria
• Drug overdose
16. Renal system.
• Hematuria
• Oliguria less than 400ml/24hr
• Proteinuria.
• Loin pain due to bladder expansion (in case of
post renal obstruction)
• Dysuria. (pain while passing urine incase of
infection).
• Reduced frequency of micturation.
17. Cardiovascular presentation
• Cardiac failure or angina associated with
anaemia , fluid overload, hypertension, anemia
and impaired ventricular contraction (uremic
cardiomyopathy)
• Tachycardia
• Raised blood pressure (HTN)
• Raised JVP
• Pedal pitting bilateral edema which can progress
to anasaca incase the obstruction is acute.
18. Hematological system
• Lethargy and breathlessness associated with
anemia owing to impaired production of
erythropoietin by the kidneys.
• Defective coagulation and excessive bruising
(advance renal failure).
• Hemorrhage from the GIT or the lungs.
19. • Electrolyte imbalances
– Breathlesness due to salt and water overload.
– Dyspnea (kussmaul respiration) due to acidosis.
– Lethargy and weakness due to hypokalemia.
20. Nervous system
• Hypertensive stroke and encephalopathy.
• Clouding of consciousness , fits and coma due
to accumulation of nitrogenous waste
products.
21. 1.Laboratory studies
• The tests done include;
– Blood urea nitrogen (BUN) and serum creatinine
– The most common indicators of acute renal failure
– Complete blood cell count and peripheral smear
– Urinalysis
– Urine electrolytes
22. Laboratory studies
1. Blood urea nitrogen and serum
creatinine
• Although increased levels of BUN and
creatinine are the hallmarks of renal
failure, the rates of BUN and
creatinine increases are also very
important.
• BUN test findings showing an
increase that is disproportionately
larger than that of creatine suggest
prerenal ischemia. Typically, the
serum creatine increases 1-2
mg/dL/d; however, a rate of increase
greater than 5 mg/dL/d also can be
observed in patients with
rhabdomyolysis because muscle is a
major source of creatine, which is the
precursor of creatinine.
• The ratio of BUN to creatinine also is
an important finding because the
ratio can exceed 20:1 in conditions in
which enhanced reabsorption of urea
is favored (eg, in volume
contractions). In conditions such as
upper gastrointestinal bleeding and
in some cases of obstructive
uropathy, test findings may show a
further increase in the ratio. Other
conditions causing a BUN-to-
creatinine ratio of greater than 20:1
are increased enteral or parenteral
protein load, corticosteroid therapy,
and a hypercatabolic state.
23. 2. Complete blood cell count and
peripheral smear
• These tests may be useful, and the peripheral smear results
may show schistocytes in conditions such as hemolytic
uremic syndrome or thrombotic thrombocytopenic
purpura.
• A finding of increased rouleaux formation suggests multiple
myeloma, and the workup should be directed toward
protein electrophoresis of serum and urine.
• The presence of schistocytes, myoglobin or hemoglobin,
increased serum uric acid level, and other related findings
may help further define the etiology of ARF.
• Findings from serology tests for ANCA indicate intrinsic
renal disease due to vasculitis.
24. Urinalysis
• Urinalysis remains the most
important test in the initial
evaluation of ARF.
• Findings of granular muddy-brown
casts are suggestive of tubular
necrosis. The presence of tubular
cells or tubular cell casts also
supports the diagnosis of acute
tubular necrosis (ATN).
• When RBCs are present in the urine,
they can aid in establishing a
diagnosis. RBC casts are
pathognomonic for glomerular
disease. Dysmorphic RBCs also
support a glomerular cause such as
lupus nephritis. The presence of
WBCs or WBC casts may denote
pyelonephritis or acute interstitial
nephritis.
• Reddish brown or cola-colored urine
is present in patients with acute
glomerular nephritis or in the
presence of myoglobin or
hemoglobin. Dipstick assay findings
may show the presence of significant
proteinuria such as occurs in intrinsic
renal diseases, including
glomerulonephritis, acute interstitial
nephritis, tubular necrosis, and
vascular diseases.
25. Urine electrolytes
• Urine electrolyte findings also can
serve as valuable indicators of
functioning renal tubules.
• The fractional excretion of sodium
(FENa) is the commonly used
indicator. However, the interpretation
of results from patients in nonoliguric
states, those with
glomerulonephritis, and those
receiving or ingesting diuretics can
lead to an erroneous diagnosis. FENa
can be a valuable test for helping
detect an extreme renal avidity for
sodium in conditions such as
hepatorenal syndrome. The formula
for calculating the FENa is as follows:
• FENa = (UNa/PNa) / (UCr/PCr) X 100
• The FENa assay is useful in ARF only
in the presence of oliguria.
• In patients with prerenal azotemia,
the FENa is usually less than 1%. In
ATN, the FENa is greater than 1%.
Exceptions to this rule are ATN
caused by radiocontrast nephropathy
or severe burns.
• In the presence of liver disease, FENa
can be less than 1% in the presence
of ATN. On the other hand, because
administration of diuretics may cause
the FENa to be greater than 1%,
these findings cannot be used as the
sole indicators in ARF.
27. Ultrasound
• Renal ultrasonography is
useful for evaluating
obstruction of the urinary
collecting system.
• This technique is readily
available, and findings are
quite accurate for indicating
obstructive causes of renal
failure. This test is also useful
for detecting intrinsic renal
disease, which enhances renal
echogenicity; however, this
finding is nonspecific.
– Ultrasonography also aids in
performing a renal biopsy,
which may be necessary in the
diagnosis of cases of ARF due
to vasculitis or interstitial renal
diseases. Obtaining images of
the kidneys can be technically
difficult in patients who are
obese or in those with
abdominal distension due to
ascites, gas, or retroperitoneal
fluid collection.
– Ultrasound scans or other
imaging studies showing small
kidneys suggest chronic renal
failure. The presence of the
radiological and clinical
features of
hyperparathyroidism also
supports the presence of
chronic renal failure.
28. • Doppler scans
– Doppler scans are useful for detecting the
presence and nature of renal blood flow.
– Because renal blood flow is reduced in prerenal or
intrarenal ARF, test findings are of little use in the
diagnosis of ARF.
• Doppler scans can be quite useful in the
diagnosis of thromboembolic or renovascular
disease
29. Procedures:
• Renal biopsy
– A renal biopsy can be very useful in the diagnosis of
intrarenal causes of ARF. Performing a renal biopsy is
comparatively easy, and the findings establish the
diagnosis in most cases.
– In as many as 40% of cases, renal biopsy results reveal
an unexpected diagnosis.
– A renal biopsy is especially useful in rapidly
progressive glomerulonephritis due to crescentic
glomerulonephritis when clinical differentiation
between acute glomerulonephritis and interstitial
nephritis becomes difficult. Acute cellular rejection in
a renal transplant can be definitively diagnosed only
by performing a renal biopsy.
30. Complications of ARF
• Electrolyte imbalances
– Hyperkalemia leading to changes in ECG.
– Hypocalcaemia
– Hyponatraemia
• Pulmonary edema
• Bleeding (due to reduced erythropoeitin
production)
• Metabolic acidosis
32. • N.B: ARF can often be prevented
• Avoid dehydration in high risk patients e.g.
:diabetics, myeloma, CRF
NBM
Surgery
IV contrast
• Caution with NSAIDs and aminoglycosides
