Acute Kidney Injury Flashcards
What is Acute kidney injury ?
- a problem resulting in an acute decrease in kidney function (rapid decreased GFR) within hours/days
- frequently accompanied by a decreased in the urine output -> oliguria, rarely anuria
Diagnostic criteria of acute kidney injury:
- increased se creatinine > 0.3 mg/dL within 48 hours, or
- increased se creatinine > 1.5 times the baseline (0.6 to 1.2 mg/dL) in 7 days
and - urine volume < 0.5 ml/kg/h for 6 hours
AKI mortality:
- 20-50%
AKI risk factors:
- older age
- previous cardiac or renal insufficiency
- medications
- DM
etc. ..
Symptoms of acute renal failure:
- edema,
- periorbital edema
- fatigue
- dyspnea: due to pulmonary edema from hypervolemia
- anuria/oliguria
- nausea if uremia
- if metabolic acidosis is present, the patient may have Kussmaul breathing (a deep and difficulty breathing), hyperventilation
Immediate complications of AKI:
- accumulation of uremic toxins
- electrolyte and fluid disturbance
- acid-base disturbance -> metabolic acidosis (although more related to chronic renal failure)
- complications: GI, endocrine, etc..
Clinical consequences of AKI:
- increased risk of mortality
- increased risk for developing Chronic kidney disease
Classification of AKI:
Based on the origin of the problem
- prerenal
- renal
- postrenal
Prerenal AKI: different etiologies
Anything causing hemodynamic changes leading to a decrease in GFR.
- excessive fluid loss -> bleeding, diarrhea
- cardiogenic or septic shock -> leading to a decreased effective circulating volume and vasodilation
- vasoconstriction of afferent arteriole
- vasodilation of efferent arteriole -> ex: with ACEi use
Prerenal AKI: clinical features
- oliguria
- low BP
- reflex tachycardia
Renal: different etiologies
- Glomerular disease: GN
- tubular injury: Acute tubular necrosis (the most common cause of AKI)
- acute tubular interstitial nephritis: due to drugs or infections
- vascular disease: vasculitis, cholesterol, emboli, thrombosis, etc…
Post-renal: different etiologies
Mainly due to obstruction
- tumor (inside the ureter or outside, compressing it)
- kidney stone
- blood clot
- BPH
- tumor causing obstruction of bladder
Acute tubular necrosis: def
- most common cause of AKI
- characterized by damaged to the tubular epithelial cells, which are sensitive to hypoxia and toxins
- PCT and TAL -> most sensitive parts
Acute tubular necrosis: different types
- ischemic ATN: cariogenic shock, or anything causing a decreased blood flow to the kidneys
- nephrotoxic ATN: poisons -> heavy metals, drugs
- pigment ATN: crush syndrome
- others: sepsis, iodinated contrast material, uric acid, tumor lysis syndrome
Acute tubular necrosis: lab shows
- sediment in urine: brown granules
- ANT casts
Phases of Acute kidney injury
- Introductory phase: signs and symptoms of the underlying disease
- Oliguric-anuric, uremic phase: 1-2 weeks
- volume and electrolyte disturbances
- uremia, and encephalopathy
- complications: anemia, infections, vomiting, pericarditis, HF - Polyuric phase: 2-6 weeks
- may lead to 4-6L/day of urine output with electrolyte disturbances
Diagnostical approach: 1. Identify the underlying cause
- medical history: previous kidney disease, systemic diseases etc…
- physical examination: BP, HR, Skin, Lungs, signs of systemic illness like hepatosplenomegaly, percussion of bladder
Diagnostical approach: 2. labs
- BUN (blood urea nitrogen), creatinine ratio:
.Normal: between 10:1 and 20:1
.Increased ratio: condition that causes a decrease in the flow of blood to the kidneys -> congestive heart failure or dehydration
.decreased ratio: liver disease (due to decrease in the formation of urea) and malnutrition. - CBC, electrolytes (Na, K, P, Ca), pH, HCO3, Uric acid
- immunulogy
- Urine output, protein, blood, Na in urine, osmolarity, specific gravity
- Urinary sediment: .dysmorphic RBC -> glomerular origin .Hyaline cast -> prerenal .ANT cast -> renal .WBC casts -> interstitial nephritis .RBC casts -> glomerulonephritis .Crystals -> uric acid
Diagnostical approach: 3. radiology
- US
- CXR
Diagnostical approach: 4. renal biopsy
Performed only if signs and symptoms of intrinsic renal cause, not in case of acute tubular necrosis.
Perform in case of acute tubular necrosis, if it doesn’t resolve after 2 weeks
Treatment: prerenal and post renal AKI
Prerenal:
- treat volume depletion by replacing volume, stop ACEi/ARB, or diuretic use
- if HF: optimize cardiac function
Postrenal:
- treat the underlying cause
Treatment: renal AKI
Supportive therapy:
- acidosis: Na-HCO3
- hyperkalemia: insulin + glucose
- hypervolemia: diuretic + dialysis
- hyperphosphatemia: give Ca-carbonate orally
Indications of renal replacement therapy (dialysis):
- resistant hypervolemia, resistant hyperkalemia, resistant acidosis
- uremic encephalopathy, pericarditis
- very high BUN,creatinine
Methods of dialysis can be continuous (24h in ICU) or intermittent
