Acute kidney injury (AKI) is defined as a sudden clinical and/or laboratory manifestation of abnormal kidney function occurring within 48 hours or 7 days of kidney injury.
There is a reduction in urine output documented as less than 0.5 ml/kg/hour for more than 6 hours.
There is also an absolute increase in serum creatinine of more than or equal to 0.3 mg/dl (26.5 umol/L) occurring within 48 hours of an insult to the kidneys.
In AKI, there is a percentage increase in serum creatinine of more than or equal to 50% (1.5 fold from baseline) which is known or presumed to have occurred within 7 days.
AKI is seen in about 5% of patients admitted to medical wards.
Up to 30% of intensive care admissions may manifest and develop AKI.
AKI could be classified variably depending on the defining criteria.
Hospital acquired AKI typically develops as a complication of another clinical condition.
Community acquired AKI typically evolve in these patients while in their homes.
AKI is classified according to the:
Medical specialty in which it evolves i.e.
- Surgical AKI if it complicates surgery,
- Obstetric or Gynaecologic AKI
Volume of urine being excreted at the
time the AKI is developing:
- non-oliguric AKI when urine volume is more than 400mls/day
- oliguric AKI when urine volume is less than 400mls/day and anuric
- AKI when urine volume is less than 150mls/day.
Site of physiologic or anatomic
derangements or toxic insult into pre renal, intrinsic renal and post renal AKI:
- This is a systemic derangement leading to hypoperfusion of the kidneys leading to AKI e.g. diarrhoea and vomiting, haemorrhage, cardiac failure etc.
Intrinsic renal AKI:
- Direct nephrotoxic injury to renal tubules or there could be inflammation of interstitial, glomerular or vascular structures.
Post renal AKI:
- Obstruction to the outflow of urine, which could be at different levels e.g. renal pelvis, ureter, urinary bladder or urethra.
Examples of causes of post-renal AKI include:
- Netroperitoneal fibrosis and tumours
- Bladder cancer
- Benign prostatic hypertrophy
- Prostate cancer or even urethritis
Peculiar causes of AKI among Nigerians include:
- Nephrotoxins (native herbs, CuSO4 (green water), drugs
- Ethylene glycol poisoning etc)
- Septicaemia (particularly typhoid)
- Obstetric causes (ante partum haemorrhage, post partum haemorrhage, septic abortion, eclampsia).
Staging of Acute Kidney Injury
AKI could now be staged according to severity (See table below)[table “6” not found /]
- Reduction in urine output (oliguria),
- features of uraemia,
- fluid retention leading to oedema.
- Uraemia present with different features in different systems:
- Nausea and vomiting,
- Epigastric pain and rarely haematemesis.
- Central chest pain of pericarditis
- Pulmonary oedema.
Central nervous system:
- Uraemia manifest with tremors.
- Derangement of sleep rhytmn
- Stupor or coma
- dryness and pruritus
- Anaemia (pallor)
Diagnostic criteria: As in the definition and table above.
- Acute exacerbation of Chronic Kidney Disease.
- End Stage Renal Failure
- Pulmonary oedema
- Electrolyte abnormalities:
- Hyperkalemia in acute cases and hypokalaemia and hyponatreamia in polyuric phases.
Relevant investigations & management
Urine Examination (Volume/ microscopy /Urinalysis/ Electrolytes).
- Allow quantification of total daily urine output, which could be used in staging. Microscopy would reveal the types of cells, casts, crystals or other substances in the urine.
- Urinal athy.
Renal biopsy: Mandatory in the following:
- Any evidence of glomerular disease:
- nephrotic range proteinuria
- sub-nephrotic range proteinuria with haematuria
- RBC cast
- AKI not resolving in 6 weeks
- AKI in connective tissue disease
- AKI in renal allograft
- Determine the prognosis and chance of recovery of renal function in dialysis dependent AKI.
Principles of management in patients with AKI include:
- Maintenance of fluid homeostasis
Control of biochemical abnormalities
- Maintenance of nutrition
- Treat the underlying cause
- Dialysis where indicated
- Maintenance of fluid homeostasis:
Entails strict regulation of fluid intake to insensible loss (500-1200mls/day)
Replacement of fluids totalling volume of
urine and other documented losses in previous 24 hours.
Avoid potassium containing fluids
- Control of biochemical abnormalities:
Hyperkalaemia in these patients should be treated in one of 3 ways:
- Forcing the potassium (K) into cells using Glucose-Insulin Infusion or Glucose Infusion
- Antagonising the effects of K on the heart using 10% Calcium gluconate
- Dialysis or use of ion exchange resin like kayexelate
Maintenance of nutrition:
AKI patients are usually hypercatabolic
hence the following
- High calorie low protein diet is
recommended in acute or oliguric phase while
- High calorie, normal protein is recommended in recovery phase.
- Parenteral hyperalimentation is seldom necessary in prolonged cases.
- Dialysis where indicated:
Manifestation of clinical and biochemical features of uraemia or development of electrolyte and acid-base complications of AKI:
Clinical features include:
- Pulmonary oedema,
- Persistent nausea and vomiting,
- Refractory oedema,
- Uncontrolled HT
- Bleeding diathesis
Biochemical indications include:
- Hyperkalemia > 6.5mmol/l,
- Serum bicarbonate <12mmol/l,
- Urea > 25 mmol/l,
- Creatinine >600micromol/1
Manifestations of features of hypercatabolism:
- K+ rate of rise > 1mmol/day,
- urea rate of rise > 10 mmol/day
- a creatinine rate of rise >100micromol/day.
The patients could benefit from
- Daily Haemodialysis,
- Extended Daily Dialysis,
- Slow low efficient Dialysis,
- Acute Peritoneal Dialysis,
- intermittent Peritoneal Dialysis,
- Haemofiltration or Haemodiafiltration.
Prevention of AKI:
- Avoidance of nephrotoxins in all forms.
- Provision of pipe borne water.
- Prompt treatment of accident victims.
- Prompt treatment of infections.
- Good maternal, child and reproductive health care.
- Adequate hydration during contrast investigations.