Acute Renal Failure (ARF)

OR
Acute Kidney Injury (AKI)

Dr P Mayurathan
Consultant Physician (Act)
 Acute Renal Failure (ARF)
• defined as an abrupt or rapid decline in renal parenchymal function over a
period of days or weeks

• This is usually reversible (but not invariably)

• Results will be failure to excrete nitrogenous waste products and electrolytes

imbalance

• Laboratory definition is;

– Increase serum creatinine level by more than 50% from the baseline

OR
– Decrease in calculated creatinine clearance by more than 50%
In 2004, an international expert group of renal and intensive care clinicians proposed to
change the term “ARF” to “acute kidney injury (AKI)” to better describe the spectrum of renal
disease.

In addition, they proposed a universal definition and staging system for AKI, termed RIFLE
which incorporates 3 stages of severity (Risk, Injury and Failure) and 2 outcome criteria (Loss of
renal function, End Stage Renal Failure).
Classification of AKI
 Pre-renal AKI
• Is defined as a reduction in GFR caused by impaired renal perfusion as a
result of hypotension or hypovolaemia

• The hypovolaemia may be due to blood loss, fluid loss, sepsis, impaired
cardiac pumping (heart diseases) or vascular disease limiting renal blood
flow or combination of these factors

• By definition, excretory function in pre-renal uraemia improves once the

renal perfusion has been restored
 Pathophysiology of Pre-renal AKI
• Is an appropriate physiological response to hypovolaemia

• This response results in intense renal conservation of Na and water at the

expense of decreased GFR

• ADH increases resulting reduced clearance of urea and creatinine

(reduction in clearance is more)

• In hypovolaemic patients systemic vasoconstriction may maintain mean

arterial pressure, but still AKI can occur due to intra-renal vasoconstriction
from
– Increased sympathetic tone
– Increased intra-renal production of angiotensin-II

• If hypovolaemia persists, it may lead to irreversible ischaemic renal injury

 Management of Pre-renal AKI
• Prompt replacement of hypovolaemia and hypotension with appropriate
fluid

• Most of the time pre-renal AKI is associated with intrinsic AKI, and fluid
challenge in the later situation may lead to volume overload

• Careful monitoring of features of fluid overload with pulmonary oedema

is vital - CVP monitoring is essential

• If the problem is due to cardiac pump insufficiency or occlusion of the

renal vasculature, appropriate measures need to be taken
 Post-Renal AKI
• Is due to obstruction of the urinary tract at any point from the calyces to
the external urethral orifice

• The obstruction may be;

– Within the lumen – stone, blood clot

– Within the wall – stricture

– Pressure from outside – retroperitoneal fibrosis, prostatic obstruction
 Pathophysiology of Post-Renal AKI
• Increased pressure within renal collecting system results in:
– Reduced GFR
– Reduced tubular reabsorption of Na and water

• Complete bilateral obstruction causes anuria, but is rare

• Partial chronic bilateral obstruction commonly leads to an increase in

urine flow rate (polyuria) as a result of impaired salt and water
reabsorption
 Management of Post-Renal AKI

• Relief the obstruction

 Intrinsic (Renal) AKI
• Most commonly due to acute renal tubular necrosis
• Other causes are;

– Vascular causes – Vasculitis, Accelerated HT, Cholesterol embolism,

Haemolytic uraemic syndrome (HUS), Thrombotic thrombocytopenic purpura
(TTP), Pre-eclampsia
– Glomerulonephritis

– Acute tubulointerstitial nephritis (Acute TIN)

– Tumor lysis syndrome (acute hyperuricaemic nephropathy)
– Acute pyelonephritis

– Haematological causes – Multiple myeloma, TTP, HUS

– Others – Contrast nephropathy, Rhabdomyolysis, Hepato-renal syndrome

 Acute Tubular Necrosis (ATN)
• Common cause for intrinsic AKI

• Mostly due to ischaemia of renal parenchyma

• But can also be caused by toxins (snake venon, myoglobin, haemoglobin,

etc) or drugs (NSAIDs, amynoglycosides, lithium, etc)
 Causes of Acute Tubular Necrosis (ATN)
• Haemorrhage
• Burns
• Diarrhoea and vomiting, fluid loss from fistulae
• Pancreatitis
• Diuretics
• Myocardial infarction
• CCF
• Endotoxic shock
• Snake bite
• Myoglobinuria/haemoglobinuria
• Hepatorenal syndrome
• Radiological contrast agents
• Drugs – Aminoglycosides, NSAIDs, ACEI, Platinum derivatives
• Abruptio placenta
• Pre-eclampsia and eclampsia
 Pathophysiology of ATN

Intrarenal microvascular vasoconstriction

Tubular cell injury

Tubular cellular recovery

Glomerular contraction leads to reduced surface area for filtration

‘Back-leak’ of filtrate in the PCT

Obstruction of the tubule by debris

 Clinical Course in ATN
• Variable and depending on the severity and duration of the renal insult
• Oliguria is common in early stages

• Non-oliguric AKI is usually a result of a less severe renal insult

• Recovery typically occurs after 7 – 21 days
• But recovery may be delayed by ongoing sepsis
• Clinical course is variable and ATN may last up to 6 weeks
• Eventually renal functions usually returned to normal or near normal,
although exceptions are there
• No known definitive treatment
• Only supportive treatment is available
 Clinical Features of ATN
• Symptoms of uraemia – Oliguria, Body swelling, LOA, Nausea, Vomiting,
Pruritus, Confusion, Drowsiness, Coma, Fits
• Pulmonary oedema
• Haemorrhages – Epistaxis and GI bleeding

• Rapidly increasing Blood urea and Creatinine

• Hyperkalaemia
• Metabolic acidosis
• Hyponatraemia
• Hypocalcaemia
• hyperphosphataemia
 Investigations - AKI
• How to differentiate pre-renal from intrinsic renal AKI?

Test Pre-renal AKI Intrinsic AKI

Urine Specific Gravity > 1.020 < 1.010

Urine Osmolality (mOsm/kg) > 500 < 350

Urine Sodium (mmol/l) < 20 > 40

Fractional Excretion of Sodium < 1% > 1%

 Investigations - AKI
• UFR
• RBC cast/WBC cast
• Urine culture and ABST
• Urine for Hb and Mb
• BU/SE/Cr
• Ca²⁺/PO4³ˉ/ALP
• FBC/Blood picture
• Blood culture and ABST
• ESR/CRP
• Coagulation studies
• USS KUB
• Drug screening
• Renal biopsy
 Management of AKI
• General – IP/OP chart, QHT chart, Daily weight chart, regular physiotherapy
and oral care

• Emergency management – Hyperkalaemia, Pulmonary oedema, Metabolic

acidosis, Sepsis, fluid and electrolyte imbalance

• Diet – Restriction of Na and K, normal protein diet, vitamin supplimentations

• Dialysis:
– Haemodialysis
– Haemofiltration
– Peritoneal dialysis