Tutorial 41 - Acute Kidney Injury Flashcards
An AKI is defined as a reduction in kidney function that has developed within hours to days. What parameters are commonly used to determine if a patient has an AKI?
- Rise in serum creatinine concentration
- Decline in urine output
What is the commonly accepted criteria for an AKI for the following:
- serum creatinine concentration
- urine output
Serum creatinine concentration:
- increase ≥0.3 mg/dL (27 micromol/L) within 48 hours OR
- increase to ≥1.5 times the baseline value (either known or presumed to have within prior 7 days)
Urine output:
- decrease in urine volume to <0.5 mL/kg/hour for more than six hours
What are signs and symptoms of an AKI?
- Decreased urine output
- Hypertension
- Edema
NOTES:
- Symptoms result directly from decreased kidney function.
- Some patients may be asymptomatic!
What are the general causes of pre-renal AKIs? (x3)
Dr. Yusuf: please review (from UpToDate article) - how would you test this information? -CZ
Also - how do you want to test information in the notes - see following question.
- Decreased renal artery perfusion.
- Renal venous congestion
- Drugs affecting glomerular hemodynamics
NOTES:
- Can occur with total body volume depletion (diarrhea, vomiting, acute bleeding, unreplenished insensible losses, excessive diuretic therapy, third-space sequestration (eg, crush injury or acute pancreatitis)
- Can occur in euvolemic patients due to low arterial blood pressure (occurs different types of distributive shock (eg, sepsis or anaphylaxis), or any loss of arteriolar vasomotor tone (eg, overtreatment with antihypertensive medication).
- Can occur in patients with total body volume overload who have reduced kidney perfusion due to a low effective circulating volume (severe heart failure with reduced ejection fraction or decompensated liver disease with portal hypertension and ascites (ie, hepatorenal syndrome)).
- Prerenal: hypovolemia, hemorrhage, distributive shock, congestive hear
What conditions can lead to an AKI in a hypervolemic (volume overloaded) patient?
Low effective circulating blood volume.
- Severe heart failure
- Hepatorenal syndrome (Decompensated liver disease with portal hypertension and ascites)
What are renal (intrinsic) causes of AKI?
**1. Renal vascular disease **
* Small vessel disease (atheroembolic disease, and thrombotic microangiopathies, such as thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP/HUS), scleroderma, and malignant hypertension)
* Large vessel diseaes (renal infarction from aortic dissection, systemic thromboembolism, renal artery abnormality (such as aneurysm), and acute renal vein thrombosis)
2. Glomerular Disease
3. Tubular and interstitial disease (acute tubular necrosis, acute interstitial nephritis)
Acute tubular necrosis - typically from ischemia (cardiac surgery, sepsis, and/or shock) or nephrotoxic exposure.
- May occur in conjunction with use of NSAIDs or radiocontrast (esp in patients with decreased kidney perfusion)
- May occur after exposure to nephrotoxic medications (amphotericin, cisplatin)
Acute interstitial nephritis - often drug-induced (NSAIDs, various antibiotics, and checkpoint inhibitors for cancer immunotherapy)
What is the most common etiology of a post-renal cause of AKI?
Obstruction along the urinary tract.
Commonly:
- prostatic disease (hyperplasia or cancer)
- urothelial carcinoma
- gynecologic/metastatic cancer
What is the most common cause of an obstruction along the urinary tract causing AKI?
Prostatic disease (hyperplasia or cancer).
For hospitalized patients who develop AKIs, what are the indications that a patient should be assessed for urgent dialysis?
Dr. Yusuf - should this be included? From UpToDate article.
- refractory pulmonary edema
- life-threatening hyperkalemia or metabolic acidosis,
- encephalopathy
- pericardial rub
You are seeing a hospitalized patient who was admitted two days ago due to septic shock. They have now developed an AKI since being in the hospital. What is the most likely classification (pre-renal, renal, or post-renal) and cause of their AKI?
Dr. Yusuf - please reword/rephrase. Also - should their be more questions about the approach to AKI outlined in the UpToDate article?
Renal.
Acute tubular necrosis (ischemic damage to the proximal and distal tubule due secondary to decreased perfusion from septic shock).
What serum potassium level is used to define hyperkalemia?
Serum [K+] of > 5.5 mmol/L
What are the symptoms of hyperkalemia, and at what serum potassium level do these symptoms usually begin to develop?
arrhythmias, muscle weakness and paralysis, (and even death)
Symptoms start to develop when serum [K+] of > 6.5 mmol/L**
** Not a hard and fast rule.
What are the two major mechanisms of hyperkalemia?
Impaired potassium excretion
* common in acute or chronic kidney disease when glomeruli can’t dispose of serum potassium)
* can occur with decreased aldosterone secretion/response
Increased potassium release from cells (intracellular potassium shift).
What are causes of intracellular potassium shift?
- Cellular injury leading to potassium leak from cells (rhabdomyalysis, excessive exercise, other hemolytic processes)
- Metabolic acidosis (DKA, increased EtOH consumption, sepsis)
- Insulin deficiency
- Tumour lysis syndrome
- Medications (e.g., digoxin, succinylcholine, beta blockers, calcium channel blockers, tacrolimus, mannitol)
What is the occurence of hyperkalemia in hospitalized patients?
1-10%