Acute Kidney Injury

Dr B Parag
Department of Nephrology
Definition
 Functional or structural abnormalities , or
markers of kidney damage ( including
abnormalities in blood, urine, tissue tests or
imaging studies), present for less than 3 months

 Diagnostic criteria: an abrupt ( within 48hours)

reduction in kidney function

 Assumes adequate fluid resuscitation and that

obstruction has been excluded
KDIGO staging classification
Incidence
 7% of general admissions

 20-25% of patients with sepsis , 50

% with septic shock

 65% of ICU admissions- ( mortality 43-88%)

Prognosis
 Overall mortality in dialysis requiring ARF
remains > 50%

 Mortality is higher in the elderly and those

with multi organ failure
Causes
 Pre renal ARF

 Intrinsic renal ARF

 Postrenal ARF
Prerenal ARF
 Decreased effective circulating volume
◦ Haemorrhage
◦ Volume depletion
◦ Low cardiac output
◦ Sepsis
◦ CCF
◦ Cirrhosis
 Renal Arterial stenosis/occlusion

 Vasomotor- NSAIDS, ACEI/ARBs

Intrinsic renal ARF
 ATN- acute tubular necrosis

 Acute Tubular Interstitial Nephritis

 Acute GN

 Vascular – Vasculitis, Thrombotic

microangiopathies, Hypertensive emergencies
ATN
 Ischaemic i.e. poor blood supply

 Nephrotoxic
 Endogenous – Haemaglobinuria, myoglobinuria,
myeloma casts, intratubular crystals

 Exogenous- nephrotoxic drugs, radiocontrast

Postrenal ARF
 Obstruction

◦ Bladder outlet obstruction

◦ Bilateral ureteral obstruction

Prevention
 Older patients- require careful monitoring
 Pre-existing renal disease
 Inc Cr, dec eGFR or proteinuria
 Surgery
 DM
 Volume depletion- vomiting, diarrhoea, burns
 LV dysfunction
 Cirrhosis-decreased effective arterial volume
 Drugs-ACEI, ARB,NSAIDS
 Jaundice
 Multiple myeloma
Nephrotoxins
 NSAIDs, COX-2 inhibitors
 Diuretics, ACEI, ARB esp in volume depleted

patients
 Antibiotics- Aminoglycosides, vancomycin
 Amphotericin B
 Immunosuppressants – Ciclosporin,

Tacrolimus
 Chemotherapeutic agents ( cisplatin)
 IV contrast
Presenting Features of ARF
 Increase urea and creatnine

 Decrease urine output ( < 400ml/d)

 Volume depletion OR

 Volume overload – pulmonary oedema

 Hyperkalaemia ( arrythmias or cardiac arrest)

 Uraemic symptoms

 Hypertension or hypotension

 Metabolic acidosis
Acute vs Chronic
 Documented previous measurements of renal
function

 Ultrasound – long standing renal disease

leads to loss of renal parenchyma and a
decrease in kidney size ( < 9-10cm)

 Normal size kidneys – ARF. Except in Diabetic

nephropathy kidneys larger than normal
Acute vs Chronic
 Laboratory findings
◦ Rarely helpful

◦ Anaemia – decrease in erthyropoietin production in

CRF( can also occur in ARF – blood loss)

◦ Low calcium and high phosphate – suggests

chronic dx due to impaired Vit D synthesis and
hyperparathyroidism.
Assessing ARF
 Urine dipstick and urine MCS

 Exclude bladder outflow obstruction

 +/- Urine electrolytes

Urinanalysis
 Normal
◦ Prerenal ARF, ATN
◦ Post renal ARF
Urinanalysis
 Red cell casts, dysmorphic red cells,
proteinuria
◦ Active GN, Vasculitis, Thrombotic microangiopathy
 White cell casts
◦ Obstruction, AIN, pyelonephritis
 Eosinophils
◦ AIN
◦ Artheroembolic disease
 Haematuria
◦ Post renal ARF, vasculitis, Acute GN, Trauma
Urinanalysis
 Pigment casts
◦ Myoglobinuria
◦ Haemoglobinuria
 Granular and epithelial cell casts
◦ ATN
◦ Acute GN , vasculitis
 Crystalluria
◦ Urate nephropathy ( Tumour lysis syndrome), drugs,
ethylene glycol
 Low grade proteinuria
◦ Myeloma, tubulointerstitial disease
Urine electrolytes
 Typical pre-renal ARF
◦ Low urine Na+,(<20mmol/l) High urea and creat in
urine, urine osmolality high i.e. Urine is
concentrated

 Typical ATN
◦ High urine Na(>40mmol/l), low urea and creat,
urine osmolality relatively low

 Diuretics will confound the analysis- diluting

the urine with an inc Na content
Blood work
 FBC, ESR
 Clotting profile
 U/E
 LFT
 CPM
 CRP
 Creatine kinase
 Urate
 PSA
 Urine and blood culture

 Hepatitis serology

 Arterial Blood Gas

Nephritic and myeloma screen
 ANA
 ANCA
 Anti-GBM ( not routinely available)
 ASOT
 Protein electrophoresis (serum and urine)
 Immunoglobulins
 Rheumatoid factor
 Viral serology
 Cryoglobulins
 Antiphospholipid antibodies
 Complement- c3,c4
Imaging and Histology
 CXR

 Ultrasound Renal Tract

 Renal biopsy
Treatment
 Prerenal ARF
◦ CVP ( 8-12cm)

◦ Fluids-
 crystalloids vs colloids
 Resuscitation, replacement, maintenance

◦ Sodium bicarbonate (pH<7.15, inc K) caution: can

dec calcium

◦ Albumin – ARF due to cirrhosis, nephrotic syndrome

Intrinsic ARF
 ATN
◦ Low GFR
◦ Oliguric or non oliguric
◦ Structural injury to renal parenchyma
◦ Bland urine on dipstix
◦ 60% full recovery
◦ 30% recovery short of baseline
◦ 5-10% will require long term renal replacement
therapy

 Treat the cause

Post renal ARF
 Obstruction needs to be addressed

 Domain of urology
Treatment
 Hyperkalemia
◦ Cardiac arrythmias- ECG
◦ Treat urgently when the K> 6.5mmol/L
◦ Potassium shift- calcium, insulin / glucose
◦ Sodium bicarbonate
◦ B2 – agonists
◦ Diuretics
◦ Gut K+ wasting- cation exchange resins
◦ Dialysis
◦ Diet
◦ Stop precipitating drugs –ACEI,ARB,spironolactone,
NSAIDS
Pulmonary oedema
 Sit up
 Stop all ivi fluids
 Oxygen
 Diuretics i.e. Ivi Furosemide
 Opiates-morphine (use with caution as it

accumulates in ARF)
 Dialysis
 Ventilation
Electrolytes
 Hyperphosphataemia
 Marked inc in rhabdomyolyis, TLS, haemolysis
 Diet restriction
 Oral phosphate binders
 Dialysis
 Hypocalcaemia
 Prolonged and severe ARF
 Dec vit D3 synthesis
 Oral replacement
 Hypokalaemia- non oliguric ATN ( amphotericin,
aminoglycosides)
 Hypomagnasaemia - non oliguric ATN
Metabolic acidosis
 High anion gap metabolic acidosis

 Sodium bicarbonate

 Dialysis
Other strategies
 Anaemia – bleeding( GIT)/ haemolyiss

 Infection

 Nutrition
Renal replacement therapy
 Hemodialysis
 Peritoneal dialysis

 Indications
 Persistent hyperkalaemia
 Pulmonary oedema
 Intractable acidosis
 Olig/ anuria
 Uraemic pericarditis
 Uraemic encephalopathy