3- AKI

• Types of Renal Failure


  • Acute renal failure (Acute kidney injury)
  • Rapidly progressive renal failure
  • Chronic renal failure (Chronic kidney disease)
• Acute kidney injury (AKI)


  Rapid reduction in kidney function over hours to days, as measured by serum urea and creatinine and leading to a failure to maintain fluid, electrolyte and acid-base homeostasis. Reversible in most cases. Normal sized kidneys (unless obstructed)
• Diagnostic criteria for AKI (one or more of three criteria)


  • Rise in creatinine >26 µmol/L in 48hrs
  • Rise in creatinine 1.5 x baseline over 7 days
  • Urine output <0.5 mL/kg/h for >6 consecutive hours
• KDIGO staging system for AKI


  • Stage 1: Increase >26 µmol/L in 48h OR increase> 1.5 x baseline, Urine output <0.5mL/kg/h for >6 consecutive hours
  • Stage 2: Increase 2-2.9 x baseline, Urine output <0.5mL/kg/h for>12h
  • Stage 3: Increase >3 x baseline OR >354 µmol/L OR commenced on renal replacement therapy irrespective of stage, Urine output <0.3mL/kg/h for >24h or anuria for 12h
• Risk factors for AKI


  • Age >75
  • Diabetes
  • Chronic kidney disease
  • Drugs (esp. newly started)
  • Cardiac failure
  • Sepsis
  • Peripheral vascular disease
  • Poor fluid intake/increased losses
  • Chronic liver disease
  • History of urinary symptoms
• Causes of AKI


  • Pre-renal (40-70%): due to renal hypoperfusion
  • Intrinsic renal (10-50 %): may require a renal biopsy for diagnosis
  • Post-renal (10-25%): caused by urinary tract obstruction
• Pre-renal causes


  • Hypotension (sepsis, anaphylaxis, bleeding, dehydration)
  • Hypovolemia (diuretics, burns, pancreatitis, ↓ pump function (HF), low albumin, cirrhosis)
  • Renovascular disease (renal artery stenosis, fibromuscular dysplasia)
• Intrinsic renal causes


  • Tubular-acute tubular necrosis (ATN)
  • Glomerular-autoimmune such as SLE, HSP, drugs, infections, primary glomerulonephritis
  • Interstitial (acute interstitial nephritis): drugs, infiltration (ex: lymphoma, infection), tumor lysis syndrome following chemotherapy
  • Vascular-vasculitis, malignant ­BP, thrombus or cholesterol emboli from angiography, HUS/TTP, large vessel occlusion (ex: dissection or thrombus)
• Post-renal causes


  • BPH
  • Ureteral stone
  • Cervical cancer
  • Urethral stone
  • Neurogenic bladder
  • Retroperitoneal fibrosis (chemotherapy or external- beam therapy)
  • Mural-malignancy (ex: ureteric, bladder, prostate)
  • Strictures
  • Sloughed papillae
• Distinguishing features of AKI types


  • Prerenal: Urine Na low, FENA low (<1%), Urine Osm high, BUN:Cr high (>20:1)
  • Postrenal: Urine Na low, FENA low (<1%), Urine Osm high, BUN:Cr high (>20:1)
  • ATN: Urine Na high (>40), FENA high (>1%), Urine Osm low (<350), BUN:Cr ~ 10:1
• NSAIDs and ACEI constrict the afferent arteriole, therefore they may also have an aspect of prerenal AKI due to lower glomerular filtration
• Contrast-induced AKI is a form of ATN; however, the urinary lab values are an exception from ATN and are the same as the values of prerenal & postrenal AKI
• Specific gravity correlates with urine osmolality, & FENA correlates with Urine Na
• Assessment of AKI


  1. Assess volume status: BP, JVP, skin turgor, capillary refill (<2s), urine output

  2. Check an urgent K level and an ECG to check for life-threatening hyperkalemia

  3. Check for risk factors, comorbidities, previous renal disease, recent fluid intake and losses, new drugs, systemic features such as rash, joint pain, fevers. Other systems-productive cough, hemoptysis, GU or GI symptoms, etc.

  4. Look for include a palpable bladder, palpable kidneys (polycystic disease), abdominal/pelvic masses renal bruits (signs of renovascular disease), rashes

  5. Urine dipstick can suggest infection (leucocytes + nitrites), glomerular disease (blood + protein). Microscopy for casts, crystals and cells. Culture for infection.

  6. Renal US can help to distinguish obstruction (ex: prostatic) and hydronephrosis.

  7. Is the injury acute or the damage chronic?
• General measures for AKI


  • Assess volume status: look for ¯urine volume, non-visible JVP, poor tissue turgor, ¯BP, ­pulse. Signs of fluid overload: ­BP, ­JVP, lung crepitations, peripheral edema, gallop rhythm on cardiac auscultation.
  • Aim for euvolemia
  • Stop nephrotoxic drugs: ex: NSAIDS, ACE inhibitor, gentamicin, amphotericin.
  • Monitoring
  • Nutrition is vital in the critically unwell patient: aim for normal calorie intake (more if catabolism­­, ex: burns, sepsis) and protein 0.5g/kg/d. If oral intake is poor, consider nasogastric nutrition early.
• Treat underlying cause of AKI

  1. Pre-renal: Correct volume depletion with appropriate fluids, treat sepsis with antibiotics, consider referral to ICU for inotropic support if signs of shock

  2. Post-renal: Catheterize and consider CT of renal tract (CTKUB) and urology referral if obstruction likely cause.

  3. Intrinsic renal: Refer early to nephrology if concern over tubulointerstitial or glomerular pathology, any signs of systemic disease, multi-organ involvement (ex: pulmonary-renal, hepatorenal syndromes) or indications for dialysis
• Manage complications of AKI

  • Hyperkalemia
  • Pulmonary edema
  • Uremia-may require dialysis if severe or complications, ex: encephalopathy, pericarditis. Otherwise symptomatic management
  • Acidemia-may require dialysis, consider sodium bicarbonate orally or IV if in HDU/ICU setting
• Hemodialysis


  Renal replacement therapy that requires large-bore venous access, usually done intermittently, allows good clearance of solutes in short periods but requires the patient to be hemodynamically stable
• Hemofiltration


  Renal replacement therapy that requires large-bore venous access, much slower at clearing solutes, usually performed continuously while the patient is in established renal failure
• Indications for dialysis


  • Refractory pulmonary edema
  • Persistent hyperkalemia (K >7mmol/L)
  • Severe metabolic acidosis (pH<7.2 or base excess <10)
  • Uremic complications such as encephalopathy or Uremic pericarditis
  • Drug overdose-BLAST: Barbiturates, Lithium, Alcohol (and ethylene glycol), Salicylates, Theophylline