Acute renal failure
Dr. H. N. Sarker
MBBS, FCPS, MACP(USA)
Associate professor
medicine
Introduction

Acute renal failure (ARF) refers to a sudden and
usually reversible loss of renal function, which
develops over a period of days or weeks and is
usually accompanied by a reduction in urine
volume.
Introduction

Acute renal failure (ARF) is a rapid loss of
renal function due to damage to the kidneys,
resulting in retention of nitrogenous (urea and
creatinine) and non-nitrogenous waste products
that are normally excreted by the kidney.
Introduction

Depending on the severity and duration of the
renal dysfunction, this accumulation is
accompanied by metabolic disturbances, such as
metabolic acidosis (acidification of the blood)
and hyperkalaemia (elevated potassium levels),
changes in body fluid balance, and effects on
many other organ systems.
Introduction

It can be characterised by oliguria or anuria
(decrease or cessation of urine production),
although non-oliguric ARF may occur. It is a lifethreatening medical emergency
Causes


Acute renal failure is usually categorised (as in
the flowchart below) according to pre-renal,
intrinsic and post-renal causes.
Pre-renal
Intrinsic
Post-renal
Pre-renal (causes in the blood
supply):
hypovolemia (decreased blood volume), usually from
shock or dehydration and fluid loss or excessive
diuretics use.
 Heart failure.
 hepatorenal syndrome in which renal perfusion is
compromised in liver failure
 vascular problems, such as atheroembolic disease
and renal vein thrombosis (which can occur as a
complication of the nephrotic syndrome)

Pre-renal
infection usually sepsis, systemic inflammation due
to infection
 severe burns
 sequestration due to pericarditis and pancreatitis
 hypotension due to antihypertensives and
vasodilators

Intrinsic (damage to the kidney
itself)




Toxins or medication (e.g. some NSAIDs,
aminoglycoside antibiotics)
Sepsis
Rhabdomyolysis (breakdown of muscle tissue)
Haemolysis (breakdown of red blood cells)
Post-renal (obstructive causes in the
urinary tract )
benign prostatic hypertrophy or prostate cancer.
 kidney stones.
 due to abdominal malignancy (e.g. ovarian cancer,
colorectal cancer

REVERSIBLE PRE-RENAL
ACUTE RENAL FAILURE

Haemodynamic disturbances can initially
produce acute renal dysfunction that has the
potential to be rapidly reversed, prompt
recognition and treatment are important.

These topics are considered separately from
established acute renal failure.
Pathogenesis



The kidney can regulate its own blood flow and
GFR over a wide range of perfusion pressures.
When the perfusion pressure falls-as in
hypovolaemia, shock, heart failure or narrowing
of the renal arteries-the resistance vessels in the
kidney dilate to facilitate flow.
Vasodilator prostaglandins are important, and
this mechanism is markedly impaired by
NSAIDs .
Pathogenesis



If autoregulation of blood flow fails, the GFR
can still be maintained by selective constriction
of the post-glomerular (efferent) arteriole.
This is mediated through the release of renin
and generation of angiotensin II, which
preferentially constricts this vessel.
ACE inhibitors interfere with this response .
Pathogenesis

More severe or prolonged under-perfusion of
the kidneys may lead to failure of these
compensatory mechanisms and hence an acute
decline in GFR.

The renal tubules are intact and become
hyperfunctional; that is, tubular reabsorption of
sodium and water is increased.
Pathogenesis

This leads to the formation of a low volume of
urine which is concentrated (osmolality > 600
mOsm/kg) but low in sodium (< 20 mmol/l).
Clinical assessment


The clinical picture is often dominated by the
underlying condition (e.g. septic shock,
trauma,diarrhoea)
There may be marked hypotension and signs of poor
peripheral perfusion, such as delayed capillary return.
Clinical assessment


Postural hypotension (a fall in blood pressure >
20/10 mmHg from lying to standing) is a
valuable sign of early hypovolaemia.
Metabolic acidosis and hyperkalaemia are often
present.
Management


Establish and correct the underlying cause of the ARF.
If hypovolaemia is present, restore blood volume as
rapidly as possible (with blood, plasma or isotonic
saline (0.9%), depending on what has been lost).
Management

Optimise systemic haemodynamics. Monitoring
of the central venous pressure or pulmonary
wedge pressure as an adjunct to clinical
examination may aid in determining the rate of
administration of fluid.
Management

Critically ill patients may require invasive
haemodynamic monitoring to assess cardiac output and
systemic vascular resistance, and the use of inotropic
drugs to restore an effective blood pressure .
Management



Correct metabolic acidosis.
Restoration of blood volume will correct
acidosis by restoring kidney function.
Isotonic sodium bicarbonate (e.g. 500 ml of
1.26%) may be used.
ESTABLISHED ACUTE RENAL
FAILURE


Established ARF may develop following severe
or prolonged under-perfusion of the kidney
(pre-renal ARF). In such cases, the histological
pattern of acute tubular necrosis is usually seen.
'renal' and 'post-renal' causes produce
established ARF
Features of established ARF

These reflect the causal condition, such as
trauma, septicaemia or systemic disease, together
with features of renal failure.

'Uraemic' features -anorexia, nausea and
vomiting followed by drowsiness, apathy,
confusion, muscle-twitching, hiccoughs, fits and
coma.
Features of established of ARF

Alterations in urine volume
Patients are usually oliguric (urine volume <
500 ml daily).
Anuria (complete absence of urine) is rare and
usually indicates acute urinary tract obstruction
or vascular occlusion
Features established of ARF


In about 20% of cases, the urine volume is
normal or increased (non-oliguric ARF).
Disturbances of water, electrolyte and acid-base
balance
Hyperkalaemia is common
Metabolic acidosis .
Features established of ARF



Hypocalcaemia, due to reduced renal production
of 1,25-dihydroxycholecalciferol, is common.
Respiratory rate -increased due to acidosis,
pulmonary oedema or respiratory infection.
Anaemia is common, due to excessive blood
loss, haemolysis or decreased erythropoiesis .
DiagnosisConsensus criteria for the diagnosis of ARF are:


Risk: serum creatinine increased 1.5 times OR
urine production of <0.5 ml/kg/h body weight
for 6 hours
Injury: creatinine 2.0 times OR urine production
<0.5 ml/kg/h for 12 h
Diagnosis
Failure: creatinine 3.0 times OR creatinine >355
μmol/l (with a rise of >44) OR urine output
below 0.3 ml/kg/h for 24 h

Loss: persistent ARF or complete loss of kidney
function for more than four weeks

End-stage Renal Disease: complete loss of
kidney function for more than three months
DiagnosisRoutine investigationurine for R/E
Blood urea & electrolytes
S. creatinine
ABG
Diagnosis

Imaging. Renal ultrasound: usually required urgently to
confirm/refute two equal-sized, unobstructed
kidneys
Chest X-ray, X-ray KUB
ECG: if > 40 years or there are risk factors for
cardiac disease
Diagnosis





Microbiology
Blood cultures
C-reactive protein (ESR is misleading in ARF)
Mid-stream urine
Other cultures, e.g. wound, sputum, catheters
Hepatitis and HIV serology: urgent if dialysis is needed
(isolation of dialysis machine if positive)
Management



Emergency resuscitation –
Hyperkalaemia (a plasma K+ concentration > 6
mmol/l) must be treated immediately to prevent
the development of life-threatening cardiac
arrhythmias.
Circulating blood volume should be optimised
to ensure adequate renal perfusion.
Management



Hypovolaemia must be treated as for reversible
pre-renal ARF monitoring of central venous or
pulmonary wedge pressure as required.
Patients with pulmonary oedema usually require
dialysis to remove sodium and water.
Severe acidosis can be ameliorated with isotonic
sodium bicarbonate (e.g. 500 ml of 1.26%) if
volume status allows.
Management




In an anuric or volume-overloaded patient, renal
replacement therapy may be required.
Treatment of the underlying cause of the ARF .
Fluid and electrolyte balance
After initial resuscitation, daily fluid intake
should equal urine output, plus an additional 500
ml to cover insensible losses
Management

Protein and energy intake
In patients in whom dialysis is likely to be
avoided, accumulation of urea is slowed by
dietary protein restriction (to about 40 g/day)

Infection control.

Renal replacement therapy
Prognosis

In uncomplicated ARF, such as that due to
simple haemorrhage or drugs, mortality is low
even when renal replacement therapy is
required.

In ARF associated with serious infection and
multiple organ failure, mortality is 50-70%.
Prognosis

Outcome is usually determined by the severity
of the underlying disorder and other
complications, rather than by renal failure itself.