72. Acute renal failure. Occurrence, general features – extrarenal uremia. Prerenal azotemia. Postrenal failure

Last updated on March 9, 2020 at 22:02

Acute renal failure

In acute renal failure (ARF) will acute injuries cause failure of excretory functions even though the kidneys were originally healthy. Unlike chronic renal failure can it be cured and reversed without consequences (in almost all cases).

Depending on its type is the mortality still high (up to 60%), and in around 5% of cases will CRF or cortical necrosis develop.

We can divide acute renal failure into three types:

  • Prerenal – Due to reduced RBF. Nephrons are intact
  • Renal parenchymal – Due to damage to the parenchyme. Will come back to this in topic 74 and 75
  • Postrenal – Due to obstruction to the passage of urine
Prerenal acute renal failure


  • Heart failure -> Cardiac output redistribution
  • Hypovolaemia
  • Liver cirrhosis
  • Hepatorenal syndrome
  • Renal artery obstruction (often by atherosclerosis)

Hepatorenal syndrome occurs when factors released from failing livers cause vasodilation in the splanchnic circulation, causing less blood to enter the kidneys. The kidney will respond by activating RAAS which vasoconstricts renal arteries. However, RAAS can’t overcome the vasodilation of the splanchnic circulation and instead just further limits the renal blood flow.

All these disorders cause significant decrease in renal blood flow, which leads to a decrease in GFR as well. Decreased filtration means less work for the tubules, so the tubules don’t need too much oxygen. This means that despite the decreased perfusion will they not normally be hypoxic and will work as normal. Of course, if the RBF is severely decreased will damage occur.

Because less plasma is filtered but the tubules still work normally will the tubules reabsorb relatively more than normal. This means that oliguria occurs.

Those compounds that get into the filtrate exclusively by filtration (mainly urea and creatinine) will accumulate in the blood due to the low GFR. Azotaemia occurs. Urea reabsorption is enhanced (idk why) but creatinine reabsorption is non-existent. Urea accumulates in the blood by increased reabsorption and less filtering, while creatinine just accumulates because of less filtering. Because of this will the serum urea concentration rise faster than the serum creatinine concentration. The urea:creatinine ratio in the serum increases, which is often used to diagnose prerenal acute renal failure.

I know the blue book disagrees here, but I believe the book is wrong. All other sources indicate that urea rises more than creatinine.

Hyperkalaemia occurs due to low GFR. Acidosis worsens this hyperkalaemia by causing potassium to be exchanged out of cells in exchange for protons.

Postrenal acute renal failure

Postrenal ARF occurs when something blocks the outflow of urine. Common causes include:

  • Urolithiasis
  • Prostatic hyperplasia/adenoma

Normally is the pressure inside the glomeruli higher than in the tubule. It is this filtration pressure difference that causes substances and fluid to be filtered out. The result of a blockage that the pressure inside the bladder/ureter/pelvis (depending on where the blockage is) causes a 20 – 300 mmHg pressure increase in the Bowman space. The filtration pressure therefore decreases, which reduces the GFR. This causes azotaemia.

The increased pressure damages the tubule cells and even forces substances in the filtrate to be forced back in to the circulation by the tubules, so-called “back-leak”. This causes oliguria.

As long as there is obstruction will there of course be little to no urine excretion. When the obstruction is removed the GFR normalize quickly, but the damaged tubular cells need a lot of time to recover. During this period is Na+ reabsorption low, which disrupts the cortico-medullary osmotic gradient, causing hyposthenuria with polyuria. The ADH sensitivity is also decreased due to damage, which contributes to polyuria.

Repeated obstruction may cause permanent damage and chronic renal failure.

Symptoms of acute renal failure

While there are many types are the symptoms mostly the same in all types.

  • Salt and water retention -> Oedema, hypertension
  • Hyperkalaemia -> Rhythm abnormalities (Ventricular fibrillation)
  • Metabolic acidosis
    • -> Worsens hyperkalaemia
    • -> hyperventilation -> hypocapnia -> cerebral vasoconstriction -> decreased cerebral blood flow
  • Hyperosmolarity
  • Azotaemia -> vomiting, diarrhoea
  • Uraemic toxins -> Histotoxic hypoxia -> encephalopathy

Despite these are the non-excretory function of the kidney usually normal.

Previous page:
71. Uremic coma

Next page:
73. Renal circulation. Cardiorenal syndrome

7 thoughts on “72. Acute renal failure. Occurrence, general features – extrarenal uremia. Prerenal azotemia. Postrenal failure”

  1. If there is more Na+ being absorbed, then I guess due to the TGF, the RAAS will be activated and this is the reason for the hyperkalemia?

    1. Your explanation doesn’t really make sense as aldosterone causes potassium loss and not hyperkalaemia.

  2. It is hyperkalemia due to the oliguria. Even though the tubules are able to excrete a concentrated urine, there is a maximum of about 1,035mOsm/kg. Thereby we need a higher amount of urine to excrete all the extra K+, that’s also why the daily rise is only 0,5mmol/L.

  3. hi there
    sry ya mentioned in pre renal less RBF and less work for tubules
    but further say tubules reabsorb more than normal to cause oliguria
    how is it possible?

  4. Hi greek doctor.
    Can you explain a little more about how decreased na reabsorption lead to hyposthenuria with polyuria ?
    Thanks .
    ( I’m so weak in kidney , the reason i asked is because, if less na is reabsorbed , it means that more na in urine , which increases the specific gravity of urine , am i wrong ? It’s so confusing for me 😔)

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