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

Page created on December 16, 2018. Last updated on December 15, 2021 at 19:19

Acute kidney injury/Acute renal failure

Definition and epidemiology

Acute kidney injury (AKI), previously called acute renal failure (ARF), is a clinical syndrome which is characterised by an acute decrease in GFR (over hours or days), as evidenced by elevated creatinine. This means that the kidney filters less of the plasma than normal, causing waste products usually excreted by the kidney to accumulate.

Because there isn’t always a renal “failure” in this condition, it has been renamed from acute renal failure to acute kidney injury.

AKI can be characterised by three components:

  • There is an acute decline in kidney function (as measured by decreased GFR)
  • There is an accumulation of urinary waste products
  • There may be oliguria/anuria (but not always)

Unlike chronic kidney disease, AKI is reversible in most cases, although some end up developing chronic kidney disease afterward. Depending on its type is the mortality still high (up to 60%).


Acute kidney injury is classified according to the cause:

  • Prerenal AKI – Due to decreased perfusion of the kidneys
  • Renal (or intrinsic) AKI – Due to damage to the renal parenchyme
    • Will come back to this in topic 74 and 75
  • Postrenal AKI – Due to obstruction to the passage of urine

However, in real life there are usually multiple factors involved.

According to the internet, “extrarenal uraemia” is an ancient term for kidney injury not due to organic kidney injury, i.e. prerenal AKI and postrenal AKI.

Prerenal acute kidney injury

Most common causes:

  • Hypovolaemia/hypotension
  • Decreased RBF (heart failure, renal artery stenosis)
  • Abnormal kidney haemodynamics (sepsis, hepatorenal syndrome)

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

Hepatorenal syndrome belongs to pathophys 2, but it will be quickly explained here. It occurs when a failing liver leads to abnormal haemodynamics of the kidney. 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.

Because less plasma is filtered but the tubules still work normally the tubules will reabsorb relatively more than normal. This means that oliguria or anuria often occurs, but not always.

Those compounds that get into the filtrate exclusively by filtration (mainly urea and creatinine) will accumulate in the blood due to the low GFR, causing azotaemia. 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, the serum urea concentration will rise faster than the serum creatinine concentration. The urea:creatinine ratio in the serum increases, which is often used to distinguish prerenal acute kidney injury from other causes of AKI.

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

Postrenal acute kidney injury

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

  • Urolithiasis
  • Benign prostate hyperplasia
  • Prostate cancer
  • Gynaecological cancer

Normally the pressure inside the glomeruli is 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.

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 may contribute to oliguria.

As long as there is obstruction there will 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 kidney disease.

Clinical consequences

While there are many types, the consequences of AKI are mostly the same in all types. Independent of the cause, AKI causes products which are usually excreted by the kidney to accumulate. These products include sodium, water, potassium, urea, metabolic acids, and creatinine. The most common symptom is oliguria. Other potential signs, symptoms and laboratory alterations include:

  • Decreased excretion of sodium and water -> sodium and water retention
    • -> Oedema
    • -> Hypertension
  • Decreased excretion of potassium -> hyperkalaemia
    • -> Potentially lethal arrhythmias
  • Decreased excretion of metabolic acids -> metabolic acidosis
    • Worsens hyperkalaemia
  • Decreased excretion of urea and creatinine -> azotaemia

The non-excretory function of the kidney usually normal.

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

  1. The lectures say that during prerenal will the urine have high K+ and low Na+ concentration (I guess due to RAAS activation pga low RBF), so the hyperkalemia will only be for the postrenal type? And I also don’t really understand why there is hyperkalemia, and what metabolic acidosis has to do with this? Thank you!!

    1. From what I can find, acute kidney injury is accompanied by hyperkalaemia, not hypokalaemia. It may be that the lecture is wrong (wouldn’t be the first time), or that the decreased urine production causes a larger increase in potassium than the changes in urine electrolyte composition causes a decrease in potassium.

      But I’ll add an explanation as to why hyperkalaemia and acidosis develop.

      Bare å spørre om du lurer på noe mer

  2. Ive to say, I dont know if its the clashing colours or the unhealthy grammar, but this blog is hideous! I imply, I dont want to sound like a know-it-all or something, however may you will have possibly put slightly bit more effort into this subject. Its really interesting, however you dont characterize it properly in any respect, man. Anyway, in my language, there arent much good source like this.

  3. 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 😔)

    1. Hello! Sorry for never answering your question, I don’t know how that happened. I’m sure it’s too late for me to answer it for you but I’ll answer it in case other people might have the same question.

      Decreased Na+ reabsorption would cause the urine to contain more Na+ and higher specific gravity, yes, but that’s only if you ignore the corticomedullary gradient. This gradient is dependant on proper Na+ reabsorption, and without it the tubules can’t concentrate or dilute the urine, which is the state of hyposthenuria.

  4. 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?

  5. 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.

  6. 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.

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