Acute Renal Failure

DR. SAMI ABDO RADMAN

 Acute Renal Failure
Definition
Acute renal failure (ARF) is a syndrome
defined as an abrupt decrease in
glomerular filtration rate sufficient to
result in retention of nitrogenous waste
products (blood urea nitrogen [BUN] and
creatinine) and perturbation of
extracellular fluid volume and electrolyte
and acid-base homeostasis
Usually, but not invariably, reversible over a
period of days or weeks.
sufficiently severe to result in uraemia
Oliguria is usually, but not invariably, a
feature.
Cause sudden, life-threatening biochemical
Deterioration in renal function is
disturbances
 Is a medical emergency..
Causes
ARF can result from
(1) diseases that cause a decrease of renal blood
flow (prerenal azotemia (
 (2diseases that directly involve renal parenchyma
(renal azotemia)
(3) diseases associated with urinary tract
obstruction (postrenal azotemia)
Prerenal uraemia

Is the most common form of ARF

There is impaired perfusion of the kidneys with
blood.
Hypovolaemia,
Hypotension,
Impaired cardiac pump efficiency or
Vascular disease limiting renal blood flow,
 Or combinations of these factors
Excretory function in prerenal uraemia improves
once normal renal perfusion has been restored.
CLINICAL MANIFESTATIONS
Thirst, dizziness
Hypotension and tachycardia,
Reduced jugular venous pressure,
Decreased skin turgor,
Dry mucous membranes,
Reduced axillary sweating.
History of intake of hypotensive drugs
Management

Correction of hypovolaemia and

hypotension,
Treatment of the undelying cause
 recovery typically takes 1 to 2
weeks after normalization of renal
perfusion
 Postrenal uraemia
Obstruction of the urinary tract at any point from the
calyces to the external urethral orifice.
Clinical exam:
Tenderness on the suprabubic region or renal angle
History of stones
 History of Prostatic disease
Treatment
Removal of the obstruction
Renal Azotemia
Acute uraemia due to renal
parenchymal disease (Acute tubular
necrosis, ATN)
This is most commonly due to acute
renal tubular necrosis (Due to acute
ischemic or nephrotoxic insult)
Causes
Haemorrhage
Burns
Diarrhoea and vomiting
Diuretics
Myocardial infarction
Congestive cardiac failure
Snake bite
Myoglobinaemia
Haemoglobinaemia
(due to haemolysis, e.g. in falciparum
malaria, 'blackwater fever)
Hepatorenal syndrome
Drugs, e.g. aminoglycosides, NSAIDs,
ACE inhibitors
N.B:
In liver failure, acute renal result from rapidly reversible
vasomotor abnormalities within the kidney.
 A kidney removed from a patient with hepatic cirrhosis
and liver failure dying with oliguric renal failure may
function normally immediately after transplantation into a
normal individual
Pathogenesis
Intrarenal microvascular
vasoconstriction:
Tubular cell injury
Ischaemic injury results in rapid depletion
of intracellular ATP stores resulting in cell
death
Glomerular contraction reducing the
surface area available for filtration
Obstruction of the tubule by debris
shed from ischaemic tubular cells
Clinical Course
Depending on the severity and duration of the
renal insult.
Oliguria is common in the early stages: non-
oliguric renal failure is usually a result of a less
severe renal insult.
Recovery of renal function typically occurs after
7-21 days,
ATN may last for up to 6 weeks, even after a
relatively short-lived initial insult
Clinical and biochemical features
The features of the causal condition
together with features of rapidly
progressive uraemia
serum urea and creatinine
concentrations depend upon the rate of
tissue breakdown(trauma, sepsis and
surgery)
Pulmonary oedema
Symptoms of uraemia such as
anorexia,
nausea, vomiting
 pruritus develop,
drowsiness, fits, coma and haemorrhagic
episodes.
Epistaxes and gastrointestinal haemorrhage
Severe infection may have initiated the acute
renal failure or have complicated it owing to the
( impaired immune defences)
 URINALYSIS in ARF
Anuria suggests complete urinary tract
obstruction OR severe cases of prerenal or
intrinsic renal ARF
Wide fluctuations in urine output raise the
possibility of intermittent obstruction,
Polyuria in partial urinary tract obstruction
Transparent hyaline casts In prerenal ARF,
(secreted by epithelial cells of the loop of Henle)
Hematuria and pyuria are common in patients with
intraluminal obstruction or prostatic disease.
Epithelial casts present in ATN (ischemic or
nephrotoxic ARF)
Red blood cell casts indicate glomerular injury
Eosinophiluria is common in
antibiotic-induced allergic interstitial
nephritis
Bilirubinuria may provide a clue to
the presence of hepatorenal syndrome.
Urine should be tested for free
haemoglobin and myoglobin,
Laboratory findings in ARF
Blood tests include measurement of serum
urea, electrolytes, creatinine, calcium,
phosphate, albumin,
Increase serum Creatinine
Hyperkalemia, hyperphosphatemia,
hypocalcemia
Severe anemia in the absence of hemorrhage
indicates hemolysis
Systemic eosinophilia suggests allergic
interstitial nephritis
RADIOLOGICAL
INVESTIGATIONS
A plain film of the abdomen
 Ultrasonography
Pelvicalyceal dilatation is usual
with urinary tract obstruction
Retrograde or anterograde
pyelography
Management
General measures
Consistent documentation of fluid intake and output,
Measurement of daily bodyweight
Emergency measures
Correction of acidosis with intravenous sodium
bicarbonate
Pulmonary oedema Duiretics
Treatment of sepsis
Fluid and electrolyte balance
Diet
Protien restriction (40 gm daily)
sodium and potassium restriction
Management …cont
Dialysis is indicated in
Symptoms of uraemia
Complications of uraemia, such as pericarditis
Hyperkalaemia not controlled by conservative measures
Pulmonary oedema
Severe acidosis
For removal of drugs causing the acute renal failure, e.g.
Gentamicin, lithium, severe aspirin overdose.