Acute tubular necrosis
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Acute tubular necrosis
Renal
Renal
Renal system anatomy and physiology
Hydration
Renal clearance
Regulation of renal blood flow
Tubular reabsorption and secretion
Tubular reabsorption of glucose
Renin-angiotensin-aldosterone system
Sodium homeostasis
Phosphate, calcium and magnesium homeostasis
Potassium homeostasis
Antidiuretic hormone
Free water clearance
Erythropoietin
Vitamin D
Physiologic pH and buffers
The role of the kidney in acid-base balance
Respiratory acidosis
Metabolic acidosis
Plasma anion gap
Respiratory alkalosis
Metabolic alkalosis
Hyperphosphatemia
Hypophosphatemia
Hypernatremia
Hyponatremia
Hypermagnesemia
Hypomagnesemia
Hyperkalemia
Hypokalemia
Hypercalcemia
Hypocalcemia
Acute tubular necrosis
Prerenal azotemia
Renal azotemia
Postrenal azotemia
Chronic kidney disease
Renal artery stenosis
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Osmotic diuretics
Loop diuretics
Potassium sparing diuretics
Thiazide and thiazide-like diuretics
Carbonic anhydrase inhibitors
ACE inhibitors, ARBs and direct renin inhibitors
Key Takeaways
Acute tubular necrosis (ATN) is a type of acute kidney injury (AKI) that results in the sudden and rapid death of tubular cells in the kidneys. This can lead to a decrease in urine production and an increase in the levels of creatinine and urea in the blood.
ATN may be caused by sepsis leading to hypotension and renal hypoperfusion; ischemia due to renal hypoperfusion, like in hypovolemic shock; but it can also be due to exposure to toxins and nephrotoxic drugs which cause damage to the tubular cells. Such drugs include nephrotoxic antibiotics, contrast agents used during imaging studies, amphotericin B, and toxic heavy metals.