The causes of acute renal failure (ARF) are conventionally and conveniently divided into 3 categories : prerenal, renal, and postrenal.
- Prerenal ARF involves an essentially normal kidney that is responding to hypoperfusion by decreasing the glomerular filtration rate (GFR).
- Renal or intrinsic ARF refers to a condition in which the pathology lies within the kidney itself.
- Postrenal ARF is caused by an obstruction of the urinary tract. Acute tubular necrosis (ATN) is the most common cause of ARF in the renal category.
Prerenal ARF represents the most common form of kidney injury and often leads to intrinsic ARF if it is not promptly corrected.
- Volume loss from GI, renal, cutaneous (eg, burns), and internal or external hemorrhage can result in this syndrome.
- Prerenal ARF can also result from decreased renal perfusion in patients with heart failure or shock (eg, sepsis, anaphylaxis).
- Special classes of medications that can induce prerenal ARF in volume-depleted states are angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), which are otherwise safely tolerated and beneficial in most patients with chronic kidney disease.
- Arteriolar vasoconstriction leading to prerenal ARF can occur in hypercalcemic states, with the use of radiocontrast agents, nonsteroidal anti-inflammatory drugs (NSAIDs), amphoter
eicin, calcineurin inhibitors, norepinephrine, and other pressor agents.
- The hepatorenal syndrome can also be considered a form of prerenal ARF because functional renal failure develops from diffuse vasoconstriction in vessels supplying the kidney.
Structural injury in the kidney is the hallmark of Renal or Intrinsic ARF, and the most common form is acute tubular injury (ATN), either Ischemic or Cytotoxic. Frank necrosis is not prominent in most human cases of ATN and tends to be patchy.
Intrarenal Vasoconstriction is the dominant mechanism for the reduced glomerular filtration rate (GFR) in patients with ATN. The mediators of this vasoconstriction are unknown, but tubular injury seems to be an important concomitant finding.
Urine backflow and intratubular obstruction (from sloughed cells and debris) are causes of reduced net ultrafiltration. The importance of this mechanism is highlighted by the improvement in renal function that follows relief of such intratubular obstruction.
Apart from the increase in basal renal vascular tone, the stressed renal microvasculature is more sensitive to potentially vasoconstrictive drugs and otherwise-tolerated changes in systemic blood pressure. The vasculature of the injured kidney has an impaired vasodilatory response and loses its autoregulatory behavior.
- A physiologic hallmark of ATN is a failure to maximally dilute or concentrate urine (isosthenuria). This defect is not responsive to pharmacologic doses of vasopressin. The injured kidney fails to generate and maintain a high medullary solute gradient because the accumulation of solute in the medulla depends on normal distal nephron function.
- Failure to excrete concentrated urine, even in the presence of oliguria, is a helpful diagnostic clue to distinguish prerenal from intrinsic renal disease, in which urine osmolality is less than 300 mOsm/kg. In prerenal azotemia, urine osmolality is typically more than 500 mOsm/kg.
- Glomerulonephritis can be a cause of ARF and usually falls into a class referred to as rapidly progressive glomerulonephritis (RPGN). The pathologic correlation of RPGN is the presence of glomerular crescents (glomerular injury) on biopsy; if more than 50% of glomeruli contain crescents, this usually results in a significant decline in renal function. Although comparatively rare, acute glomerulonephritides should be part of the diagnostic consideration in cases of ARF.
Mechanical obstruction of the urinary collecting system, including the renal pelvis, ureters, bladder, or urethra, results in obstructive uropathy or postrenal ARF.
If the site of obstruction is unilateral, then a rise in the serum creatinine level may not be apparent due to contralateral renal function. Although the serum creatinine level may remain low with unilateral obstruction, a significant loss of GFR occurs, and patients with partial obstruction may develop progressive loss of GFR if the obstruction is not relieved. Causes of obstruction include stone disease; stricture; and intraluminal, extraluminal, or intramural tumors.
Bilateral obstruction is usually a result of prostate enlargement or tumors in men and urologic or gynecologic tumors in women.
Patients who develop anuria typically have obstruction at the level of the bladder or downstream to it.
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