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image ATN is not synonymous with AKI; it is a cause of AKI.


The presentation ranges from asymptomatic (with discovery of an increased creatinine on routine laboratory testing) to symptoms of volume overload (edema and dyspnea) and symptoms of uremia (such as anorexia, nausea, delirium, fatigue, and pruritus).


  1. Etiology

    1. Ischemia due to renal hypoperfusion prolonged enough to cause tubular cell damage

      1. Patients with normal kidneys and normal renal arteries maintain normal renal blood flow and GFR with mean arterial pressures (MAPs) as low as 80 mm Hg, via autoregulatory mechanisms.

      2. As renal arterial pressure decreases, afferent arterioles vasodilate due to renal prostaglandins, whereas efferent arterioles vasoconstrict via angiotensin II effects, thus, maintaining glomerular capillary pressure and GFR.

      3. If renal artery pressure drops below the autoregulatory range, endogenous vasoconstrictors increase afferent arteriolar resistance, leading to reduced glomerular capillary pressure and GFR.

      4. If low renal perfusion persists, prolonged ischemia leads to tubular injury and cell death.

      5. Patients with the conditions or exposures listed in Table 28-3, all of which impair autoregulation, are at higher risk for developing ATN.

    2. Toxin exposure (medications [such as aminoglycosides, amphotericin B, cisplatin], hemoglobin, myoglobin, myeloma light chains)

    3. Contrast-induced AKI

      1. Defined as a rise in serum Cr ≥ 0.5 mg/dL or a 25% increase from baseline, assessed 48 hours after a radiologic procedure

      2. Serum Cr peaks at 3 days and may return to baseline by 10 days.

      3. Risk factors for contrast-induced AKI include CKD, diabetes mellitus, intravascular volume depletion, HF, anemia, hypotension, and the volume of contrast used.

      4. The Mehran Risk Score for contrast-induced AKI after coronary angiography can be calculated online at

  2. Epidemiology and prognosis of ATN

    1. ATN accounts for 55–60% of AKI in hospitalized patients and for 11% in outpatients.

    2. Postoperative ATN and contrast-induced AKI are the most common causes.

    3. Can be oliguric (urinary output < 400 mL/day) or nonoliguric.

    4. Mortality in hospitalized patients with ATN is 15–30%; in ICU patients, mortality is about 40–60%.

    5. Risk factors for increased mortality include

      1. Male sex

      2. Advanced age

      3. Comorbid illness

      4. Malignancy

      5. Oliguria

      6. Sepsis

      7. Mechanical ventilation

      8. Multiorgan failure

      9. Severity of illness

    6. 60% of patients who survive recover kidney function over 1–2 weeks; a “post ATN diuresis,” during which urinary output transiently increases, may be seen.

    7. CKD is more likely to develop in patients with normal kidneys who have recovered from ATN; those with preexisting CKD are more likely to need future dialysis.

Table 28-3.Factors affecting autoregulation of glomerular pressure and glomerular filtration rate.

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