Acute tubular necrosis

Introduction

Acute kidney injury is a common clinical problem in hospitals and particularly in ICUs. The two leading causes of acute kidney injury in hospitals are prerenal renal failure and acute tubular necrosis (ATN). Prerenal kidney failure due to poor renal perfusion with decrease in GFR and potesielt fast reversible upon correction of renal perfusion. Being perfusjonsvikten standing over longer ischemic damage of tubular cells arise and ATN occurs. ATN can also result from nefrotoksiner and sepsis and will not be off immediately reversible.

Causes

Tubular cells have a very high metabolic activity as ion pumps are energy intensive. Although the kidney normally has a high blood flow (20-25% of the cardiac output goes to the kidneys) is the meddulære through bleeding vulnerable. Ischemia of tubular cells will lead to death, shedding of cells into tubules and acute decline in GFR. Nefrotoksiner may cause ATN by direct damage or influence of peritubulær circulation with ischemic injury of tubular cells as a result.

Table of common causes of ATN:

Causes Examples
Prerenal causes Dehydration
Hypotension
Reduced circulating volume
Selective renal ischemia
NSAIDs
ACE inhibitors in combination with the above
Sepsis
Nefrotoksiner Aminoglycosides
Freedom of myoglobin and hemoglobin
Cisplatin
Iodine-containing X-ray contrast
Antiviral drugs

Causes	Examples
Prerenal causes	Dehydration
	Hypotension
	Reduced circulating volume
	Selective renal ischemia
	NSAIDs
	ACE inhibitors in combination with the above
Sepsis
Nefrotoksiner	Aminoglycosides
	Freedom of myoglobin and hemoglobin
	Cisplatin
	Iodine-containing X-ray contrast
	Antiviral drugs

Clinical presentation

Affected patients present with acute kidney injury with rapidly rising creatinine. Kidney failure can be both oligurisk and non-oligurisk

Urinary Findings

Unlike the prerenal kidney failure where urine sediment classic will be normal and the patient acknowledges a concentrated urine with sodium reabsorbed patient will at ATN have a urinary sediment with abundant granular cylinders and tubulicellesylindre because shedding of dead tubule. By ATN will tubular function be affected and classical is fractional excretion of sodium high as signs of this. (Photo by ATN on urine microscopy).

Histopathology

It is seen necrosis of epithelial cells in the tubules, interstitial hemorrhage and leukocyte infiltration

Course and treatment

Treatment consists of discontinuation of nephrotoxic substances that are not essential for life and strive to restore renal perfusion. Tubule has a good potential to regenerate and the prognosis is good. Classic renal function be normal in 6-12 weeks after an episode with ATN, but chronic renal injury may be composed by severe episodes with ATN.