Acute Kidney Injury

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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)

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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.

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