GMED3009- Acute Kidney Injury (AKI) Flashcards
Definition of Acute kidney injury (AKI)
rise in the serum creatinine concentration or a decline in urine output that has developed within hours to days
- The proposed criteria for AKI include:
- an increase in serum creatinine (used to estimate GFR) by ≥0.3 mg/dL (27 micromol/L) within 48 hours or an increase to ≥1.5 times the presumed baseline value that is known or presumed to have occurred within the prior seven days, or a decrease in urine volume to <0.5 mL/kg/hour over six hours
Definition of Acute kidney injury (AKI)
rise in the serum creatinine concentration or a decline in urine output that has developed within hours to days
- The proposed criteria for AKI include an increase in serum creatinine by ≥0.3 mg/dL (27 micromol/L) within 48 hours or an increase to ≥1.5 times the presumed baseline value that is known or presumed to have occurred within the prior seven days, or a decrease in urine volume to <0.5 mL/kg/hour over six hours
What are the common causes of AKI?
Ischemia & exposure to nephrotoxic agents
Risk factors associated with AKI
o Major trauma
o Surgery
o Infection
o Haemorrhage
o Severe heart failure
o Severe liver disease
o Lower urinary tract obstruction
o Drugs
Pathophysiology of AKI
- sudden and almost complete loss of kidney function over a period of hours to days
1) Iscehmia (sepsis, trauma, hypotension, nephrotoxins) vasocontricts and causes injury to glomerular and tubular
2) decreased permeability and decrease surface area, proximal TR increased, decreased intrarenal blood flow, increased intraluminal pressure, tubular back leak causing oliguria and decreased GFR
Categories of AKI
1) Prerenal conditions occur as a result of impaired blood flow that leads to hypoperfusion of the kidney and a drop in the GFR. Main causes are hemorrhage, myocardial infarction, heart failure, sepsis or anaphylactic shock.
2) Intrarenal causes of AKI are the result of actual parenchymal damage to the glomeruli. Conditions such as burns, crush injuries, infections, and nephrotoxic agents (non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme (ACE) inhibitors), may lead to acute tubular necrosis and cessation of renal function. With burns and crush injuries, myoglobin (a protein released from muscle when injury occurs) and hemoglobin are released, causing renal toxicity, ischemia, or both.
3) Post renal causes of AKI are usually the result of an obstruction somewhere distal to the kidney. Pressure rises in the kidney tubules; eventually, the GFR decreases. Common cause include calculi (stones), tumors, benign prostatic hyperplasia, strictures and blood clots.
Signs and symptoms of AKI
- Almost every system of the body is affected when there is failure of the normal renal regulatory mechanisms.
o Decreased urine output, although occasionally urine output remains normal
o Fluid retention, causing swelling in your legs, ankles or feet
o Drowsiness
o Shortness of breath
o Fatigue
o Confusion
o Nausea
o Seizures or coma in severe cases
o Chest pain or pressure
o Anemia from blood loss due to uremic GI lesions, reduced red blood cell lifespan, and reduced erythropoietin production.
o Rise in blood urea nitrogen
o Hyperkalemia
o Muscle twitching
Aetiology of Pre-renal AKI
Pre-renal AKI represents the most common form of kidney injury and often leads to AKI if it is not promptly corrected. Pre-renal causes of AKI (“pre-renal azotemia”) are those that decrease effective blood flow to the kidney. Hypovolemia is the main source and the loss may be caused by:
Gastrointestinal
Renal
Cutaneous (eg, burns)
Haemorrhage.
Pre-renal AKI can also result from decreased renal perfusion in patients with heart failure or shock (eg, sepsis, anaphylaxis).
To summarize, volume depletion causing pre-renal AKI can be caused by the following:
* Renal losses - Diuretics, polyuria
* GI losses - Vomiting, diarrhoea
* Cutaneous losses - Burns
* Haemorrhage
* Pancreatitis
Decreased cardiac output can be caused by the following:
* Heart failure
* Pulmonary embolus
* Acute myocardial infarction
* Severe valvular disease
* Abdominal compartment syndrome - Tense ascites
Systemic vasodilation can be caused by the following:
* Sepsis
* Anaphylaxis
* Anesthetics
* Drug overdose
* Hypercalcemia
* Drugs - NSAIDs, amphotericin B, calcineurin inhibitors, norepinephrine, radiocontrast agents
Renal arterial diseases that can result in AKI include renal arterial stenosis, especially in the setting of hypotension or initiation of ACE inhibitor
Aetiology of Intrinsic AKI
Structural injury in the kidney is the main cause of intrinsic AKI (Intrinsic is within the Kidney).
The most common form is Acute Tubular necrosis (ATN), either ischemic or cytotoxic.
Glomerulonephritis can be a cause of AKI and usually falls into a class referred to as rapidly progressive (RP) glomerulonephritis.
To summarize, vascular (large- and small-vessel) causes of intrinsic AKI include the following:
* Renal artery obstruction - Thrombosis, emboli, dissection, vasculitis
* Renal vein obstruction - Thrombosis
* Microangiopathy - disseminated intravascular coagulation (DIC), preeclampsia
* Malignant hypertension
* Scleroderma renal crisis
* Transplant rejection
* Atheroembolic disease
Tubular aetiologies may include ischemia or cytotoxicity. Cytotoxic aetiologies include the following:
* Rhabdomyolysis
* Seizures, ethylene glycol poisoning, megadose vitamin C, acyclovir, methotrexate
* Drugs - Aminoglycosides, lithium, amphotericin B, radiocontrast agents
Interstitial causes include the following:
* Drugs - Penicillins, cephalosporins, NSAIDs, proton-pump inhibitors, allopurinol, rifampin, sulfonamides
* Infection - Pyelonephritis, viral nephritides
* Systemic disease - lupus, lymphoma, leukemia,
Aetiology of Post renal AKI
Mechanical obstruction of the urinary collecting system, including the renal pelvis, ureters, bladder, or urethra, results in obstructive uropathy or post-renal AKI. Causes of obstruction include the following:
* Stone disease
* Stricture
* Intraluminal, extraluminal, or intramural tumours
* Thrombosis or compressive hematoma
* Fibrosis
Pathophysiology of the 3 stages of AKI
Pre-renal failure, GFR is depressed by compromised renal perfusion. Tubular and glomerular function remains normal.
Intrinsic renal failure includes diseases of the kidney itself, predominantly affecting the glomerulus or tubule, which is associated with the release of renal afferent vasoconstrictors. Ischemic renal injury is the most common cause of intrinsic renal failure. Patients with chronic kidney disease may also present with superimposed AKI from prerenal failure and obstruction, as well as intrinsic renal disease.
Post-renal/Obstruction of the urinary tract initially causes an increase in tubular pressure, which decreases the filtration driving force. This pressure gradient soon equalizes, and maintenance of a depressed GFR then depends on renal efferent vasoconstriction.
3 phases of AKI
Oliguria- low urea output less than 400ml per
Diuretic- 1-3 L per day
Recovery- GFR increases allowing urea and creatine levels to plateu and decrease can take up to 12 months
typical signs and symptoms of AKI
- Decreased urine output, although occasionally urine output remains normal
- Fluid retention, causing swelling in your legs, ankles or feet
- Drowsiness
- Shortness of breath
- Fatigue
- Confusion
- Nausea
- Seizures or coma in severe cases
- Chest pain or pressure
clinical manifestations of AKI
- Critical illness and lethargy with persistent nausea, vomiting, and diarrhea.
- Skin and mucous membranes are dry.
- Central nervous system manifestations: drowsiness, headache, muscle twitching, seizures.
- Urine output scanty to normal; urine may be bloody with low specific gravity.
- Steady rise in blood urea nitrogen (BUN) may occur depending on degree of catabolism; serum creatinine values increase with disease progression.
- Hyperkalemia may lead to dysrhythmias and cardiac arrest.
- Progressive acidosis, increase in serum phosphate concentrations, and low serum calcium levels may be noted.
- Anemia from blood loss due to uremic GI lesions, reduced red blood cell lifespan, and reduced erythropoietin production.
Diagnostic investigations
- Kidney function studies: Increased levels of blood urea nitrogen (BUN) and creatinine
- Complete/Full blood count
- Serologic tests
- Electrolytes
- bladder pressure: Patients with a bladder pressure above 25 mm Hg should be suspected of having AKI caused by abdominal compartment syndrome
- Ultrasonography: Renal ultrasonography is useful for evaluating existing renal disease and obstruction of the urinary collecting system
- CT scan- to identify masses, lesions or obstructions
- Renal Biospy: Of masses/lesions to confirm intra-renal causes
- Aortorenal angiography: Can be helpful in establishing the diagnosis of renal vascular diseases, such as renal artery stenosis, renal atheroembolic disease, atherosclerosis with aortorenal occlusion, and certain cases of necrotizing vasculitis (eg, polyarteritis nodosa)
- Urinalysis- sediment can indicate intra-renal disorders, but can be present in Pre and post renal. Check for Haematuria and pyuria which may be present in intra-renal.
