This is a mechanism of disease map for acute tubular necrosis (ATN), which covers the etiologies of ATN as well as the progression of the disease through the four stages of acute kidney injury.
ADDITIONAL TAGS:
Acute tubular necrosis
Etiology
Pathophysiologic phases and manifestations
Progressive deterioration of kidney function
Core concepts
Electrolyte disruption
Inflammation / cell damage
Genetic / hereditary
Microbial pathogenesis
Cardiovascular pathology
Biochemistry
Autoregulatory mechanism
Pharmacology / toxicity
Immune system dysfunction
Flow gradients physiology
Nervous system pathology
Respiratory gas regulation
Signs / symptoms
Labs / tests / imaging results
Reduced urine production (oliguria), 50 ml/24 hrs = anuria
Intravascular fluid expansion
Hypertension
Edema (peripheral, pulmonary)
Decreased renal blood flow
Hypotension
Shock:
-Hypovolemic (hemorrhage, severe dehydration)
-Septic / infectious
-Cardiogenic (heart failure)
-Neurogenic shock
Thromboemboli
/ cholesterol embolism
Thrombotic microangiopathy
Atrial fibrillation, myocardial infarction, valvular heart disease, atherosclerosis, arteritis, aortic aneurysm/ dissection
HUS
TTP
ADAMTS13 deficiency / inhibition
E. coli O157:H7 (EHEC) infection → Shiga-like toxin
Direct injury due to nephrotoxic substances
Medication: aminoglycosides, cisplatin, amphotericin
Lead poisoning
Ethylene glycol
IV administration of iodinated contrast medium
Pigment nephropathy
Rhabdomyolysis (crush syndrome)
Hemolysis
Myoglobinuria
Hemoglobinuria
Urate crystal deposition in kidney (uric acid nephropathy)
Tumor lysis syndrome
Complicated gout
toxic
ischemic
AKI phase I: initiation
(lasting hours to days)
Debris obstructs tubules
Necrotic proximal tubular cells fall into the tubular lumen
Decreased GFR
Activation of renin-angiotensin system
Increased aldosterone release
Increased reabsorp.
of Na+, H2O
Increased urine osmolality
Secretion of antidiuretic hormone
Increased reabsorp.
of H2O and urea
AKI phase II: oligo-anuria (lasting 1-3 weeks)
Azotemia
Asterixis
Pericarditis
Encephalopathy
Heart failure
Dyspnea
Tubular system remains damaged after glomerular recovery (GFR normalizes)
AKI phase III: polyuria
(lasting ~2 weeks)
Increased urine production (polyuria)
Excess loss of electrolytes and water
Dehydration
Hypo- kalemia
Hypo- natremia
AKI phase IV: recovery
(months to years)
Kidney function and urine production normalize
(sometimes, kidney function is permanently compromised)