Monday, November 24, 2014

Acute Kidney Injury: Understanding the Causes

Acute kidney injury (AKI), previously known as acute renal failure, is a rapid reduction in kidney function that can represent a spectrum of injuries that involve failure to maintain fluid, electrolyte and acid-base balances. A variety of patients suffering from a variety of medical conditions can develop AKI. Patients with urological issues often experience AKI as a result of their disease, or occasionally treatments thereof. 

A prior blog reviewed the "Basics of Renal Failure and Acute Kidney Injury," click here to read the prior blog.

This blog will review the causes of AKI, specifically as they may affect urological patients.

In general, AKI is grouped into three categories that describe the etiology (cause) and subsequent management:

  • Pre-renal
  • Intra-renal
  • Post-renal
Most patients who develop AKI in the community do so as a result of a pre-renal etiology. In contrast, of the patients who develop AKI in the hospital, upwards of 45%, do so as a result of acute tubular necrosis (ATN) – a form of intra-renal AKI. For surgical patients, there are 11 established pre-operative predictors of AKI following surgery:
  • Age ≥ 56 years
  • Male Sex
  • Congestive Heart Failure (CHF)
  • Diabetes Mellitus on oral medications or requiring insulin
  • Hypertension
  • Emergency Surgery
  • Intraperitoneal (Abdominal) Surgery
  • Ascites (fluid in the abdomen)
  • Mild or moderate renal insufficiency preoperatively
The strongest predictors of post-operative AKI are intraperitoneal (abdominal) surgery, pre-existing renal insufficiency and abdominal ascites.[1]

From Kheterpal etal. [1]


All causes of pre-renal AKI result from decreased perfusion of the kidney. Common causes include decreased blood volume, dehydration, heart failure and other disease states that decrease blood flow to the kidneys. Most commonly, pre-renal AKI is due to transient hypoperfusion (or decreased blood flow to the kidney over a short period of time). Pre-renal AKI can be further classified into three causes of hypoperfusion:
  • Volume depletion: not enough blood volume to perfuse the kidney
    • Traumatic or surgical blood loss
    • Gastrointestinal losses (dehydration) from vomiting, diarrhea, etc.
    • Dehydration due to kidney disease (overdiuresis, salt-wasting diseases)
  • Cardiac: blood volume is normal, but the heart cannot "pump" the blood effectively
    • Acute causes: myocardial infarction (heart attack), arrhythmia
    • Chronic causes: valvular disease, cardiomyopathy
  • Redistribution of fluid: blood volume is normal, the hear can pump effectively, but the body cannot keep fluid in the blood vessels
    • Hypoalbuminemia (low body protein): liver disease, malnutrition/starvation
    • Physical injury: burns, crush injury
    • Vascular:
      • Vasodilation (opening of blood vessels all over the body, preventing blood from reaching the kidneys): serious infections, sepsis, anti-hypertensive medications
      • Obstruction of the renal blood vessels: artherosclerotic disease, renal artery stenosis
Hallmarks of pre-renal AKI include a reversible state, lack of structural damage to the kidney or the nephron (microscopic filtering apparatus of the kidney), and response to replacement of fluids. Often patients will return to normal kidney function within 24-72 hours of fluid replacement.



Intra-renal AKI can be further classified into diseases that affect either: (1) the microscopic blood vessels of the kidney, (2) the glomerulus, or filtering mechanism of the kidney), (3) the tubules of the kidney that resorb fluids and electrolytes, or (4) the interstitium (the space between strictures) in the kidney.
Microscopic blood clots and a number of diseases termed microangiopathies can affect the small blood vessels in the kidney. The glomerulus is most often affected by a number of autoimmune disease states including: anti-glomerular basement membrane disease, glomerulonephritis (inflammation of the glomerulus) related to SLE (systemic lupus erythematosus) or Wegener's (ANCA-associated). In addition, glomerulonephritis can occur after a number of serious bacterial infections – termed post-infectious glomerulonephritis.
The most common cause of tubular injury is ATN (Acute Tubular Necrosis) caused by a combination of renal hypoperfusion and ischemic (no blood flow) injury, usually in combination with a toxic exposure to medication, prolonged surgery or disease-state that makes the kidney more sensitive to injury. ATN usually presents as oliguria (very low urine output, 150-300cc/day; normal is 800-2,000cc/day). During the early phases of ATN, the serum creatinine will rise (see "Basics of Renal Failure and Acute Kidney Injury" for description of serum creatinine and its relationship to AKI) while the patient continues to make an unconcentrated form of urine. Most patients will recover from ATN, however due to the tubular injuries patients can experience serious fluid and electrolyte abnormalities – about 25% of deaths related to AKI occur in the initial phases of ATN.
Interstitial diseases of the kidney are often caused by medications, infections and autoimmune diseases (similar to glomerulonephritis). AIN (Acute Interstitial Nephritis) is a rare but serious cause of drug-induced AKI. The most common meidcations to cause AIN are antibiotics, non-steroidal anti-inflammtory medications (ibuprofen, aspirin), diuretics and proton-pump inhibitors for gastroesophageal reflux. Patients may develop a fever, demonstrate white blood cells (specifically eosinophils, inflammatory cells associated with allergy-like reactions) in their urine without infection, and have a rising serum creatinine.



Post-renal AKI refers to any obstruction of the urinary system. Obstructions can occur in the kidney, ureter(s) or at the level of the bladder, prostate (in men) or urethra. The obstruction is usually mechanical in nature and can be caused by a variety of benign and malignant conditions. Kidney stones, blood clots, stricture disease and malignancy can obstruct the ureters. Obstruction should involve both ureters to cause AKI; however in some circumstances, when pre-existing renal insufficiency is present, obstruction of one ureter can cause AKI. Similar causes including bladder stones, urethral strictures, benign growth (benign prostatic hyperplasia in men, uterine disease or prolapse in women) and pelvic malignancies can cause obstruction of the bladder and/or urethra. Post-renal AKI is easily treated with resolution of the obstruction. The obstruction can be relieved with a catheter in the bladder or nephrostomy tubes in the kidneys until the offending cause can be treated.



  • AKI can be grouped into three etiologies that describe the cause and management of the injury:
    • Pre-renal
    • Intra-renal
    • Post-renal
  • Pre-renal AKI refers to hyoperfusion or not enough blood flow to the kidney.
  • Intra-renal AKI is usually due to disease states that affect the kidney and its micropscopic filtering unit, the nephron.
  • Post-renal AKI is caused by mechanical obstruction of the urinary system and is treated by drainage until the offending obstruction can be removed.





[1] Kheterpal S et al. Development and validation of an acute kidney injury risk index for patients undergoing general surgery: Results from a national data set. Anesthesiology 2009; 110 (3): 505-15.


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