Acute kidney injury: Clinical (To be retired)
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Acute kidney injury: Clinical (To be retired)
Medical and surgical emergencies
Cardiology, cardiac surgery and vascular surgery
Advanced cardiac life support (ACLS): Clinical (To be retired)
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Coronary artery disease: Clinical (To be retired)
Heart failure: Clinical (To be retired)
Syncope: Clinical (To be retired)
Pericardial disease: Clinical (To be retired)
Valvular heart disease: Clinical (To be retired)
Chest trauma: Clinical (To be retired)
Shock: Clinical (To be retired)
Peripheral vascular disease: Clinical (To be retired)
Leg ulcers: Clinical (To be retired)
Aortic aneurysms and dissections: Clinical (To be retired)
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympathomimetics: Direct agonists
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Positive inotropic medications
Antiplatelet medications
Dermatology and plastic surgery
Blistering skin disorders: Clinical (To be retired)
Bites and stings: Clinical (To be retired)
Burns: Clinical (To be retired)
Endocrinology and ENT (Otolaryngology)
Diabetes mellitus: Clinical (To be retired)
Hyperthyroidism: Clinical (To be retired)
Hypothyroidism and thyroiditis: Clinical (To be retired)
Parathyroid conditions and calcium imbalance: Clinical (To be retired)
Adrenal insufficiency: Clinical (To be retired)
Neck trauma: Clinical (To be retired)
Insulins
Mineralocorticoids and mineralocorticoid antagonists
Glucocorticoids
Gastroenterology and general surgery
Abdominal pain: Clinical (To be retired)
Appendicitis: Clinical (To be retired)
Gastrointestinal bleeding: Clinical (To be retired)
Peptic ulcers and stomach cancer: Clinical (To be retired)
Inflammatory bowel disease: Clinical (To be retired)
Diverticular disease: Clinical (To be retired)
Gallbladder disorders: Clinical (To be retired)
Pancreatitis: Clinical (To be retired)
Cirrhosis: Clinical (To be retired)
Hernias: Clinical (To be retired)
Bowel obstruction: Clinical (To be retired)
Abdominal trauma: Clinical (To be retired)
Laxatives and cathartics
Antidiarrheals
Acid reducing medications
Hematology and oncology
Blood products and transfusion: Clinical (To be retired)
Venous thromboembolism: Clinical (To be retired)
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Thrombolytics
Infectious diseases
Fever of unknown origin: Clinical (To be retired)
Infective endocarditis: Clinical (To be retired)
Pneumonia: Clinical (To be retired)
Tuberculosis: Pathology review
Diarrhea: Clinical (To be retired)
Urinary tract infections: Clinical (To be retired)
Meningitis, encephalitis and brain abscesses: Clinical (To be retired)
Bites and stings: Clinical (To be retired)
Skin and soft tissue infections: Clinical (To be retired)
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Antimalarials
Anti-mite and louse medications
Nephrology and urology
Hypernatremia: Clinical (To be retired)
Hyponatremia: Clinical (To be retired)
Hyperkalemia: Clinical (To be retired)
Hypokalemia: Clinical (To be retired)
Metabolic and respiratory acidosis: Clinical (To be retired)
Metabolic and respiratory alkalosis: Clinical (To be retired)
Toxidromes: Clinical (To be retired)
Medication overdoses and toxicities: Pathology review
Environmental and chemical toxicities: Pathology review
Acute kidney injury: Clinical (To be retired)
Kidney stones: Clinical (To be retired)
Adrenergic antagonists: Alpha blockers
Neurology and neurosurgery
Stroke: Clinical (To be retired)
Seizures: Clinical (To be retired)
Headaches: Clinical (To be retired)
Traumatic brain injury: Clinical (To be retired)
Neck trauma: Clinical (To be retired)
Lower back pain: Clinical (To be retired)
Spinal cord disorders: Pathology review
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Nonbenzodiazepine anticonvulsants
Migraine medications
Osmotic diuretics
Antiplatelet medications
Thrombolytics
Opioid agonists, mixed agonist-antagonists and partial agonists
Opioid antagonists
Pulmonology and thoracic surgery
Asthma: Clinical (To be retired)
Chronic obstructive pulmonary disease (COPD): Clinical (To be retired)
Venous thromboembolism: Clinical (To be retired)
Acute respiratory distress syndrome: Clinical (To be retired)
Pleural effusion: Clinical (To be retired)
Pneumothorax: Clinical (To be retired)
Chest trauma: Clinical (To be retired)
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Pulmonary corticosteroids and mast cell inhibitors
Rheumatology and orthopedic surgery
Joint pain: Clinical (To be retired)
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Axilla
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Anatomy clinical correlates: Bones, joints and muscles of the back
Anatomy clinical correlates: Hip, gluteal region and thigh
Anatomy clinical correlates: Knee
Anatomy clinical correlates: Leg and ankle
Anatomy clinical correlates: Foot
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Glucocorticoids
Opioid agonists, mixed agonist-antagonists and partial agonists
Antigout medications
Assessments
Acute kidney injury: Clinical (To be retired)
USMLE® Step 2 questions
0 / 4 complete
Questions
USMLE® Step 2 style questions USMLE
of complete
| Laboratory value | Result |
| Hemoglobin | 10.7 g/dL |
| Leukocyte Count | 7,300/mm3 |
| Platelet Count | 80,000/mm3 |
| Blood Urea Nitrogen | 35 mg/dL |
| Creatinine, Serum | 2.0 mg/dL |
Memory Anchors and Partner Content
Transcript
Content Reviewers
Rishi Desai, MD, MPHContributors
Anca-Elena Stefan, MD
Alex Aranda
With acute kidney injury, or AKI, there’s a decrease in kidney function that typically happens over a few days.
This leads to the retention of urea and other nitrogenous waste products- such as ammonia and uric acid and dysregulation of extracellular volume and electrolytes.
The most commonly used diagnostic criteria for AKI are the Kidney Disease: Improving Global Outcomes or KDIGO guidelines.
The KDIGO guidelines define AKI as an increase in serum creatinine of at least 0.3 milligrams per deciliter within 48 hours or as an increase in serum creatinine by 1.5 times the baseline serum creatinine within the last 7 days or when the urine volume has been less than 0.5 milliliters per kilogram per hour for six hours.
Based on these criteria, there are three stages of AKI, where stage 1 is mild and stage 3 is severe AKI.
In stage 1 AKI, there’s an increase in serum creatinine to 1.5 to 1.9 times the baseline serum creatinine or an increase in serum creatinine by 0.3 milligrams per deciliter or a decrease in urine output to below 0.5 milligrams per kilogram per hour for 6 to 12 hours.
In stage 2 AKI, there’s an increase in serum creatinine to 2 to 2.9 times the baseline serum creatinine or a decrease in urine output to less than 0.5 milligrams per kilogram per hour for more than 12 hours.
In stage 3 AKI, there’s an increase in serum creatinine to 3 times the baseline serum creatinine or an increase in serum creatinine to more than 4 milligrams per deciliter or a decrease in urine output to less than 0.3 milligrams per kilogram per hour for more than 24 hours or anuria- meaning less than 100 milliliters per day of urine- for more than 12 hours or where renal replacement therapy has been initiated.
All individuals are classified according to whichever criteria places them in the most severe stage of injury.
Once diagnosed, the causes of AKI can be split into prerenal, intrarenal, and post-renal causes.
In prerenal AKI, there’s decreased blood flow into the kidneys.
This can happen in hypovolemic states like an acute hemorrhage, gastrointestinal losses- like with diarrhea and vomiting, renal losses- like with diuretics or osmotic diuresis in hyperglycemia, dermal losses- like with burns and finally sequestration of fluid- also known as third-spacing- like with acute pancreatitis or sepsis.
Summary
Acute kidney injury (AKI) is a sudden, potentially reversible decline in renal function. AKI results in the accumulation of water, nitrogenous wastes, sodium, and other metabolic wastes in the body, and can also lead to electrolyte imbalances. Common causes include dehydration, sepsis, and some drug therapy.
AKI often presents with reduced urine output, but there can be other signs such as edema, and those associated with the accumulation of metabolic wastes such as anorexia, seizures, and altered mental status. Left untreated, it can lead to chronic kidney disease (CKD)
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