Acute Kidney Injury / Acute Renal Failure

Acute Kidney Injury / Acute Renal Failure

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Introduction

Acute kidney injury (AKI), also referred to as acute renal failure, describes the situation where there is a sudden and often reversible loss of renal function, which develops over days or weeks and is usually accompanied by a reduction in urine volume.

Epidemiology

Approximately 7% of all hospitalised patients and 20% of acutely ill patients develop signs of AKI.

Pathophysiology
  • Histologically, the kidney shows inflammatory changes
  • focal breaks in the tubular basement membrane and interstitial oedema
  • Dead tubular cells may also be shed into the tubular lumen
  • Leading to tubular lumen
  • Tubular cell damage is the dominant feature under the microscope
  • There may also be profound alterations in the renal microcirculation
Etiology
  1. PRE-RENAL
    • Impaired perfusion:
      1. Cardiac failure
      2. Sepsis
      3. Blood loss
      4. Dehydration
      5. Vascular occlusion
  2. RENAL
  1.  Glomerulonephritis 
  2.  Small-vessel vasculitis 
  3. Acute tubular necrosis

      1. Drugs- (Aminoglycosides, amphotericin , Paracetamol overdose)
      2. Toxins- Radiographic contrast media
      3. Prolonged hypotension
     4.  Interstitial nephritis
      1. Drugs- NSAIDs, penicillins, proton pump inhibitors, Lithium
      2. Toxins- mushroom
      3. Inflammatory disease
      4. Infection
  1. POST-RENAL
0.                  Urinary calculi
1.                  Retroperitoneal fibrosis
2.                  Benign prostatic enlargement(BEP)
3.                  Prostate cancer
4.                  Cervical cancer
5.                  Urethral stricture
6.                  Meatal stenosis/phimosis

RIFLE classification for acute kidney injury
Various criteria have been proposed to classify AKI
  • to identify high risk patients
  • to guide treatment and
  • to provide information regarding prognosis
The most commonly used are the KDIGO and RIFLE criteria.
RIFLE classification for acute kidney injury
Grade
GFR criteria
urinary output criteria
Risk
SCr × 1.5 within 48 hr
UO <0.5 mL/kg per h × 6 h
Injury
SCr × 2−3
UO <0.5 mL/kg per h × 12 h
Failure
SCr × 3 or SCr
>350 μm with an acute rise >40 μmol/L
UO <0.3 mL/kg per h × 24 h
Loss
Persistent AKI >4 weeks

ESKD
Persistent renal failure>3 months

SCr=serum creatinine; ESKD, end-stage kidney disease;
RIFLE=Risk, Injury, Failure, Loss, End-stage renal disease.
Clinical Assessment
  1. Symptoms of uraemia:
    • Anorexia, nausea, vomiting
    • Pruritus
    • Altered mental status- drowsiness,fits, coma
    • Haemorrhagic episodes (Epistaxis and gastrointestinal haemorrhage are relatively common).
  2. To establish whether this is an acute/acute on chronic phenomenon/CKD
    • Previous measurements of renal function can be of great value in differentiating these possibilities
    • Patients with AKI need to be assessed quickly to determine the likely underlying cause
  3. Looking at coexisting diseases such as diabetes, vascular disease and liver disease
  4. Pre-renal, renal or post-renal uraemia?
Prerenal AKI 
  • Typically hypotensive and tachycardic
  • Signs of poor peripheral perfusion, such as delayed capillary return
  • Tachycardia and postural hypotension
    • (a fall in blood pressure of > 20/10 mmHg from lying to standing) are valuable signs of early hypovolaemia
    • It is important to note that prerenal AKI may also occur without systemic hypotension, particularly in patients taking  NSAIDs or ACE inhibitors.
  • To look for concealed blood loss specially into
    -the gastrointestinal tract
    -the pelvis or femur (particularly in fractures following trauma) and
    -into the pregnant uterus
  • To look for intravascular fluid loss
    -after crush injuries or burns, and
    -in severe inflammatory skin diseases or
    -sepsis.
Renal AKI
  • Patients with glomerulonephritis usually demonstrate significant haematuria and proteinuria.
  • clinical manifestations of an underlying disease (SLE or systemic vasculitis)
  • New Drug history : Commonly include-
    • Gentamicin
    • cisplatin
    • amphotericin B.
    • Paracetamol,
    • herbal medicines
    • tenofovir
    • NSAIDs
    • ACE inhibitors
Post Renal
  • Patients should be examined clinically to look for evidence of bladder enlargement
Investigations
  1. Urine microscopy:
    • Marked haematuria- suggests glomerulonephritis, tumour of renal tract or bleeding disorder
    • Heavy proteinuria -suggests glomerular disease.
    • Casts or dysmorphic red cells- suggest glomerulonephritis
    • Leucocytes- suggest infection/interstitial nephritis
    • Crystals- may be observed in drug-induced or uric acid nephropathy
  1. Urea and creatinine
  2. Electrolytes: If potassium > 6 mmol/L, treat urgently
  3. CBC: Anaemia may indicate CKD
  4. Calcium and phosphate: Low calcium and high phosphate may indicate CKD
  5. Albumin: ↓ in nephrotic syndrome & in sepsis
  6. Clotting screen- Low platelets and abnormal coagulation in DIC, including sepsis.
  7. C-reactive protein-
ESR is misleading in renal failure
High CRP may indicate sepsis or inflammatory disease
  1. Renal ultrasound-
Hydronephrosis ± enlarged bladder in urinary tract obstruction.
  1. Culture- For Infection surveillance.
  2. Chest X-ray-Pulmonary oedema in fluid overload.
  3. Serology-HIV and hepatitis serology (if dialysis is needed)
  4. ECG-If patient is > 40 yrs or has electrolyte abnormalities or risk of cardiac disease 
Management
  1. Hypovolaemia:
if present should be corrected by intravenous fluid or blood
Caution:
    • excessive administration of fluid should be avoided
(may worsen outcome in AKI due to the development of pulmonary oedema). 
    • Monitoring of the central venous pressure may be of value in determining the rate of administration.
    • Balanced salt solutions, such as Hartmann’s/Ringer’s lactate may be preferable to isotonic (0.9%) saline when large volumes of fluid resuscitation are required, 
± inotropic drugs to restore an effective blood pressure
Caution:  Clinical trials do not support a specific role for low-dose dopamine 
  1. Hyperkalaemia:
Administer glucose and insulin to correct if K+ > 6.5 mmol/L
(See details in hyperkalaemia section)
  1. Acidosis
Consider administering sodium bicarbonate (50 mL of 8.4%) to correct if pH < 7.0 
  1. Nephrotoxic drugs:
Discontinue/ reduce potential nephrotoxic drug (according to level of renal function) 
  1. Fluid and electrolyte balance:
    • Match fluid intake to urine output plus an additional 500 mL
    • Measure body weight on a regular basis as a guide to fluid requirements.
    • Febrile patients will require an additional allowance.
    • Sodium and potassium intake should be minimized. 
  1. Diet :
    • Ensure adequate nutritional support
      (Though dietary protein restriction is controversialP )
    • High protein intake should be avoided D
  1. Screen for intercurrent infections : Treat promptly if present.
  2. PPI: Administer proton pump inhibitor to reduce the risk of upper gastrointestinal bleeding 
In post-renal AKI :
  1. The obstruction should be relieved as soon as possible
    • catheterisation in urethral obstruction
    • correction of ureteric obstruction with a ureteric stent or percutaneous nephrostomy.
  1. Renal replacement therapy (RRT)
required in patients who are not showing signs of recovery with these measures.
Typically, the decision to start RRT is driven by-
    1. Hyperkalaemia
    2. fluid overload
    3. acidosis
    4. Severe uraemia
    5. pericarditis
    6. uraemic encephalopathy
  • No specific cut-off values for serum urea or creatinine.
  • RRT should be made on an individual basis, taking account of the potential risks and benefits, comorbidity and other aspects of the patient’s care, including an assessment of whether earlyor delayed recovery is likely. 
Recovery Phase:
  • AKI usually heralded by a gradual return of urine output and a steady improvement in plasma biochemistry.
  • During recovery, there is often a diuretic phase in which urine output increases rapidly and remains excessive for several days before returning to normal.
  • During the recovery phase of AKI, it may be necessary to provide supplements of sodium chloride, sodium bicarbonate, potassium chloride and sometimes phosphate temporarily, to compensate for increased urinary losses.
Prognosis
  • Uncomplicated AKI, such as that due to haemorrhage or drugs, mortality is low, even when renal replacement therapy is  
  • In AKI associated with serious infection and multiple organ failure, mortality is 50–70%
Further reading
  1. Davidson’s Principles & Practice of Medicine 22nd edition.
  2. Kumar & Clark’s Clinical Medicine 8th edition.

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