Acute Kidney Injury

Introduction

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.

Classification:

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:
Pre-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:

  • Nephrolithiasis
  • 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)
  • Cholera
  • Malaria
  • 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)

StageChange In Serum Creatinine
(scr)
% Increase in Serum Creatinine
(Scr)
Urine Volume
1Rise in Scr by > 0.3 mg/dLIncrease of >150 - 190 % (1.5 to 1.9 fold increase) from baselineUrine output less than 0.5ml/kg/hr for more than 6 Hours:
2Rise in serum creatinine by >200- 290 % (2 to 2.9- fold increase) from baselineUrine output less than 0.5ml/ kg/hr for more than 12 Hours.
3rise in serum creatinine to >300 % ( 3 fold) from baseline. OR eGFR <35ml/min/ 1.73 main those <18 yearsUrine output less than 0.3ml/ kg/hr for more than 12 Hours OR Anuria for ≥12 h

Clinical Features:

  • Asymptomatic
  • Reduction in urine output (oliguria),
  • features of uraemia,
  • fluid retention leading to oedema.
  • Uraemia present with different features in different systems:

Gastrointestinal system:

  • Nausea and vomiting,
  • Hiccups,
  • Diarrhoea,
  • Epigastric pain and rarely haematemesis.

Chest:

  • Central chest pain of pericarditis
  • breathlessness
  • Pulmonary oedema.

Central nervous system:

  • Uraemia manifest with tremors.
  • Derangement of sleep rhytmn
  • Drowsiness
  • Seizures
  • Stupor or coma

Skin:

  • dryness and pruritus

Haemopoietic system:

  • Anaemia (pallor)
  • Bleeding
  • Diathesis.

Diagnostic criteria: As in the definition and table above.

Differential Diagnoses:

  • Acute exacerbation of Chronic Kidney Disease.
  • End Stage Renal Failure

Complications

  • Pulmonary oedema
  • Infections
  • 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:

  • Encephalopathy,
  • Pulmonary oedema,
  • Persistent nausea and vomiting,
  • Pericarditis,
  • 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.

Dialysis:

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