Acute tubular necrosis

Question 1

What is acute tubular necrosis (ATN)?

Answer 1

Acute tubular necrosis (ATN) is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys. ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI.

Question 2

What causes ATN?

Answer 2

This condition is usually the result of a combination of factors which have caused renal ischaemia and toxicity, e.g. hypotension and dehydration or sepsis with associated nephrotoxic drugs.

Question 3

How is ATN diagnosed?

Answer 3

The histology of ATN does not usually show frankly necrotic cells but sloughing of the renal tubular epithelium causing dilation and obstruction of tubules and some mild leukocyte infiltration. The presence of “muddy brown casts” of epithelial cells found in the urine during urinalysis is pathognomonic for ATN.

Question 4

How is ATN classified?

Answer 4

ATN may be classified as either toxic or ischaemic. Toxic ATN occurs when the tubular cells are exposed to a toxic substance (nephrotoxic ATN). Ischemic ATN occurs when the tubular cells do not get enough oxygen, a condition that they are highly sensitive and susceptible to, due to their very high metabolism.

Question 5

How is ATN managed?

Answer 5

Management relies on aggressive treatment of the factors that precipitated ATN (e.g. hydration and cessation of the offending drug). Because the tubular cells continually replace themselves, the overall prognosis for ATN is quite good if the cause is corrected, and recovery is likely within 7 to 21 days

There is a high mortality associated with ATN (approx. 50%), but this is usually because of the associated illnesses (e.g. septic shock), age etc. Once recovered only a very small proportion of people are left with chronic kidney disease. The severity of this illness is the reason such effort is made to recognise risk factors and prevent this disease.

Question 6

What are the 3 phases of ATN?

Answer 6

1. Oliguric phase:
   The kidneys produce less than 500mls of urine per day. Patients in this phase are vulnerable to fluid overload and electrolyte imbalance especially potassium. Creatinine levels usually rise quite rapidly during this phase.
2. Maintenance phase:
   The patient is no longer oliguric, and this increased urinary output helps maintain fluid and electrolyte balance. Creatinine level are usually stable or rise very slowly.
3. Polyuric recovery phase:
   In this phase the kidneys produce large quantities of dilute urine, so large in fact patients can become hypovolaemic and unwell. There are a number of causes for this phase postulated, but one explanation is that the distal tubules and collecting ducts recover last and in particular their aquaporin channels. These damaged aquaporin channels do not allow water to be reabsorbed and therefore high quantities of dilute urine are produced. Patients are also susceptible to electrolyte loss (e.g. hypokalaemia) in this phase. Creatinine levels falls swiftly in this phase.