Decreased blood supply to kidneys (due to hypovolemia, hypotension, or renal vasoconstriction) → failure of renal vascular autoregulation to maintain renal perfusion → decreased GFR → activation of renin-angiotensin system → increased aldosterone release → increased reabsorption of Na+, H2O → increased Urine osmolality → secretion of antidiuretic hormone → increased reabsorption of H2O and urea
Creatinine is still secreted in the proximal tubules, so the blood BUN:creatinine ratio increases.
Intrinsic
Damage to a vascular or tubular component of the nephron → necrosis or apoptosis of tubular cells → decreased reabsorption capacity of electrolytes (e.g., Na+), water, and/or urea (depending on the location of injury along the tubular system) → increased Na+ and H2O in the urine → decreased Urine osmolality
Postrenal
Four phases of AKI
Initiating event (kidney injury)
Oliguric or anuric phase (maintenance phase)
1–3 weeks
Polyuric/diuretic phase
∼ 2 weeks
Glomerular filtration returns to normal, which increases urine production (polyuria), while tubular reabsorption remains disturbed.
Generally, the glomeruli recover faster than the tubular system
Complications: loss of electrolytes and water (dehydration, hyponatremia, and hypokalemia)
Recovery phase
Clinical features
Subtypes and variants
Acute tubular necrosis
Epidemiology: causes ∼ 85% of intrinsic AKIs
Location
The straight segment of the proximal tubule and the straight segment of the distal tubule (i.e., the thick ascending limb) are particularly susceptible to ischemic damage.
They are in medulla and they have high metabolic activity.
The convoluted segment of the proximal tubule is particularly susceptible to damage from toxins.
First encounters toxins
Etiology
Ischemic: Injury occurs secondary to decreased renal blood flow.
Severe hypotension, especially in the context of shock: hypovolemic (e.g., hemorrhage, severe dehydration), septic, cardiogenic (e.g., heart failure), or neurogenic shock
Cholesterol embolism (atheroemboli)
Toxic: Injury occurs directly due to nephrotoxic substances.