2. Diagnosis of acute kidney injury

Question 1

What is the definition of acute kidney injury?

Answer 1

AKA acute renal failure (ARF)

It is a rapid decline in renal unfction with increased serum creatinin. The creatinin may be normal despite a markedly reduced GFR in the early stages of AKI as it takes time for creatinin to accumulate in the body.

It is NOT a diagnosis or a disease, but rather a clinical syndrome that is caused by a wide range of disorders!

Question 2

What are the KDIGO (Kidney Disease: Improved global outcome) for diagnosing AKI?

Answer 2

• Increased SCr by ≥ 0.3mg/dl (≥26.5 µM) within 48h
• Increased SCr by ≥ 1.5 x baseline
• Urine volume is <0.5ml/Kg/h for 6h

Question 3

What are the KDIGO (Kidney Disease: Improved global outcome) for staging AKI?

Answer 3

Question 4

What are the different urine outputs and water-related symptoms to AKI?

Answer 4

• AKI may be oliguric, anuric, or nonoliguric.
• Severe AKI may occur without a reduction in urine output (nonoliguric AKI).
• Weight gain and edema are the most common clinical findings in pts with AKI. This is due to a positive water and sodium balance.

Question 5

What is azotemia and its possible causes?

Answer 5

AKI is characterized by azotemia

• Elevated BUN and Cr
  
  • Elevated BUN is also seen with the catabolism of certain drugs (e.g. steroid), GI or soft tissue bleeding and dietary protein intake
  • Elevated Cr is also seen with increased muscle breakdown and various drugs. Baseline Cr is proportional to muscle mass

Question 6

What is the prognosis of AKI?

Answer 6

• >80% patients recover completely
• Prognosis depends on severity of renal failure and presence of comorbid conditions
  
  • The older the patient and the more severe the insult, the lower the likelyhood of complete recovery
• The most common cause of death is infection (75% of deaths) followed by cardiorespiratory complications

Question 7

What is the frequency of prerenal failure?

Answer 7

Most common cause of AKI.

Potentially reversible.

Question 8

What are the possible causes of prerenal failure?

Answer 8

We have a decreased systemic arterial blood volume or renal perfusion:

• Hypovolemia (dehydration, excessive diuretics, vomiting, diarrhera, burns, hemorrhage)
• CHF (decreased CO)
• Hypotension (sepsis, excessive hypertensive medication, bleeding, dehydration)
• Renal artery obstruction
• Cirrhosis, hepatorenal syndrome
• Patients using NSAIDs, ACE inhibtiors (afferent arteriol vasodilation) and cyclosporine can precipitate prerenal failure

Question 9

What is the pathophysiology of prerenal failure?

Answer 9

• Decreased RBF –> decreases GFR ==> decreased clearance of metabolites (BUN, Cr, uremic toxins)
• Undamage parenchyma, thus preserved tubular function (thus concentrating ability)
  
  • Therefore, proper kidney response by conserving as much Na⁺ and water as possible.
• Reversible by restoring RBF, but if hypoperfusion persists ==> ischemia ==> ATN

Question 10

What are the clinical features and lab findings of prerenal failure?

Answer 10

Clinical features:

• Signs of volume depletion (dry mucous membrane, hypotension, reflex tachycardia, decreased tissue turgor, oligo-/anuria)

Lab findings:

• Oliguria (always in prerenal failure in order to preserve volume)
• Increased BUN/SCr ratio (> 20:1 is the classic ratio)
• Increased urine osmolality (>500mosm/Kg of H₂O) because the kidney reabsorbs water
• Decreased urine Na⁺ and normal FE_Na
• Increased urine/plasma Cr ratio (> 40:1) as most of the filtrate is reabsorbed, except Cr
• Bland urine sediment

Question 11

What is intrinsic renal failure?

Answer 11

Kidney parenchyma is damaged leading to glomerular filtration and tubular function impairement. The kidney are unable to concentrate urine effectively.

Question 12

What are the possible causes of intrinsic renal failure?

Answer 12

• Tubular disease: E.g. ATN (due to ischemia, most commonly, or nephrotoxins)
• Glomerular disease: E.g. Acute GN (Goodpasture’s, Wegener, post-strep GN, SLE)
• Vascular disease: vasculites, HUS, TTP, DIC
• Interstitial disease: E.g. allergic interstitial nephritis due to hypersensitivity reactions to drugs

Question 13

What are the clinical features and lab findings of intrinsic renal failure?

Answer 13

Clinical features:

• Edema
• Recovery is possible, but takes longer than prerenal

Lab findings:

• Decreased BUN/SCr ratio (<20:1) compared to prerenal. Both BUN and SCr are still elevated, but less urea is reabsorbed than in prerenal failure.
• Increased urine Na⁺ and FE_Na>2-3% (due to tubular dysfunction)
• Decerased urine/plasma Cr ratio (<40:1

Question 14

What are the phases of ATN?

Answer 14

1. Oliguric phase: azotemia and uremia with urine output < 400-500ml/day
2. Diuretic phase: Fluid overload and osmotic diuresis due to retained fluid and solutes with urine output >500 ml/day
3. Recovery

Question 15

What is post-renal failure?

Answer 15

• Least common cause of AKI
• Obstruction of any segment of the urinary tract with intact kidneys ==> increased tubular pressure (ø excretion of urine) ==> decreased GFR
  
  • Both kidneys need to be obstructed for creatinin to rise
• Blood supply and renal parenchyma are intact
• Renal function is restored if resolution of obstruction before kidney damage. If untreated, can lead to ATN

Question 16

What are the causes of post-renal failure?

Answer 16

• Urethral obstruction secondary to benign prostate hyperplasia (most common)
• Obstruction of solitary kidney
• Nephrolithiasis
• Obstructing neoplasm
• Retroperitoneal fibrosis
• Ureteral obstruction (uncommon as obstruction needs to be bilateral to cause renal failure)

Question 17

What are the diagnostic tests of AKI?

Answer 17

1. Blood test:
   
   1. ​​​Elevated BUN and SCr
   2. Elevated K⁺, Ca²⁺, Pi
   3. Elevated albumin and complete blood count
2. ​Urinalysis:
   
   1. Hyaline casts (prerenal)
   2. ​Dipstick test positive for proteins (intrinsic)
   3. RBC casts (Glomerular disease - intrinsic)
   4. WBC casts (renal parenchymal inflammation - intrinsic)
   5. Fatty casts (nephrotic syndrome - intrinsic)
3. Urine chemistry:
   
   1. FE_Na < 1% (prerenal)
   2. FE_Na > 2-3% (ATN - Intrinsic)
4. Urine culture and sensitivities
5. Renal US
   
   1. ​Evaluation of kidney size, urinary tract obstructions, masses, …
6. CT scan
7. Renal biopsy
8. MRI arteriography

Question 18

What are the complications of AKI?

Answer 18

• ECF volume expansion and resulting pulmonary edema. (Treat with diuretic (flurosemide))
• Metabolic:
  
  • Hyperkalemia: due to ↓ excretion of K⁺ and the movement of K⁺ from IC to EC due to tissue distribution and acidosis.
  • Anion gap metabolic acidos: due to ↓ excretion of hydrogen ions. If severe, correct with Na-bicarbonate.
  • Hypocalcemia: loss of ability to form active vitamin D and rapid development of PTH resistance
  • Hyponatremia: dilutional due to water retention or due to excessive loss
  • Hyperphosphatemia
  • Hyperuricemia
• Uremia: toxic end products of metabolism (especially from protein metabolism)
• Infection: a common and serious complication of AKI. The cause is probably multifactorial. Examples include pneumonia, UTI, wound infection and sepsis.