Acute Renal Injury and Failure
last authored: Jan 2012, David LaPierre
last reviewed:
Introduction
Acute renal injury, or acute renal failure, is the abrupt drop in glomerular filtration rate (GFR) sufficient to lead to retention of creatinine, urea, and other wastes, and the perturbation of extracellular fluid volume, electrolyte, and acid-base homeostasis. It occurs over a period of hours to days.
Up to 60% of people with ARF presents in community. The 40% of patients who develop ARF in hospital (5-7% of all hospitalized patients and in up to 30% of people admitted to the ICU) are more likely to have acute tubular necrosis.
The RIFLE designation describes degrees of kidney dysfunction:
- risk: abrupt GFR decrease of >25%, or serum creatinine x1.5
- injury: GFR decrease by 50%, or creatinine x2
- failure:GFR decreased by 75%, or serum creatinine x3
- loss: complete loss of function for > 4 weeks
- end-stage kidney disease >3 months
RIFLE is useful for correlating suggesting prognosis and risk for renal failure, but is problematic in that GFR determinations are valid in steady state only.
The Case of...
a simple case introducing clincial presentation and calling for a differential diagnosis to get students thinking.
Causes and Risk Factors
Acute kidney injury can result from diseases or conditions above, in, or below the kidney. Prerenal azotemia is the most important cause in hospitalized patients, while acute tubular necrosis is the most common intrinsic renal disease leading to the condition. It is characterized by an abrupt and sustained decline in GFR following an ischemic or nephrotoxic event.
prerenal
postrenal
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renalGlomerular Tubular
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Interstitial
vascular
microscopic poly-angiitis Wegners' syndrome
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Specific agents which are known to lead to acute tubular necrosis include radiographic contrast agents, aminoglycosides, vancomycin, amphoteracin B, cyclosporine, statins, acyclovir, methotrexate, NSAIDs, COX-2 inhibitors, cisplatin, ethylene glycol, and ACE inhibitors.
Pathophysiology
It appears that acute tubular necrosis is actually caused by apoptosis, with mitochondrial dysfunction, ATP depletion, elevation in cytosolic calcium, and production of free radicals all potentially being involved.
Signs and Symptoms
Current diagnostic criteria for AKI include:
- absolute increase in serum creatinine of >0.3 mg/dl (>25 mmol/L) or
- percentage increase of >50%, or
- reduction of urine output, <0.5ml/kg/hr for >6 hours
- history
- physical exam
History
Chart review is important in people with acute kidney injury, with special attention to recent changes in GFR. Other important clues include infection, nephrotoxic drugs, contrast studies, and anaesthesia.
Symptoms of renal failure itself can include:
- lethargy
- neausea
- delerium
- edema
- seizures
- fatigue
- new skin rash
- weight loss
- anorexia
- respiratory symptoms: cough, sinusitis, hemoptysis
Prerenal features include thirst.
Obstructive symptoms can include
- flank pain due to kidney stones
- urge to urinate
comorbid conditions, procedures
Past Medical History
- kidney stones
- UTI/pyelonephritis
Physical Exam
Begin, as always, with the vital signs to assess stability, especially in the context of hypovolemia or shock.
Fluid status assessment can include:
- body weight
- vital signs
- postural changes in blood pressure and pulse
- jugular venous pressure
Fever and rash suggest allergic interstitial nephritis.
Abdominal examination may reveal distended bladder of lower urinary tract obstruction.
A Foley catheter should be done to rule out bladder or below obstruction.
Investigations
- lab investigations
- diagnostic imaging
Lab Investigations
Renal function tests are necessary to demonstrate increased creatinine and BUN.
Urinalyisis should be carried out, along with thorough sediment examination. In prerenal failure, a number of hyaline and finely granular casts may be evident, while in acute tubular necrosis, dirty brown casts and renal tubular cells are present in a majority of patients.
Spot urine protein to creatinine ratio:
- a ratio of > 3 suggests acute failure
- a ratio of <3 suggests chronic disease
Urinary indices can reveal a lowered FeNa and an increased U/PCr in prerenal azotemia, while the opposite in acutue tubular necrosis. However, many factors can influence these guidelines.
Blood Tests
- uric acid
- ASOT, hep B and C screen, HIV screen
- ANA, anti ds-DNA, C3, C4, ANCA, anti-GBM
- serum protein electrophoresis (for multiple myeloma)
- calcium and phosphate (will be decreased in chronic renal failure)
Diagnostic Imaging
Renal ultrasound should be done to rule out stones or other causes of obstruction.
Other tests that may be done include:
- CT renal
- IVP
- renal pyelogram
- renal biopsy
Treatments
Prevention
Prophylaxis is the best treatment; people and situations susceptible to acute tubular necrosis (ie cardiac surgery) need to be approached with caution, and fluid deficiencies should be corrected beforehand. Nephrotoxic drugs should be used only when essential and with careful monitoring.
Contrast nephrotoxicity can be avoiding through adequate hydration and bicarbonate.
Treatment
Treat complications (K+, pH, BP, pulmonary edema.
Consider hemodynamic monitoring as required.
Provide nutrition support.
Prerenal failure should be treated with fluid hydration and cessation of offending drugs.
Renal causes should identified and treated.
- stop offending drugs and avoid drugs of the same class
- steroids
- dialysis should be considered where indications exist.
Post-renal causes may be addressed through catheterization and urology consult for shunt or stent placement.
Consequences and Course
Infection is a serious cause of death in people with acute kidney injury requiring dialysis. For those who survive, renal function returns essentially to normal.
Uremia can cause cardiac, neurologic, hematoligic, gastrointestinal, and skin signs and symptoms, including pericarditis.
Hyperkalemia can be a life-threatening complication of AKI.
Moderate acidosis is generally well tolerated and does not need treatment, unless accompanied by the need to control acidosis.
Resources and References
Topic Development
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