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43 Cards in this Set
- Front
- Back
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What is the definition of AKI?
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A deterioration of renal function that has lasted less than three months
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What is the definition of Chronic Kidney Disease?
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A persistent deterioration of renal function that has lasted greater than 3 months
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What is the general diagnostic approach to AKI? (3)
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Pre-renal - secondary to decreased renal plasma flow
Renal - due to dysfunction of the renal parenchyma Post-renal - secondary to an inability to pass urine from the kidneys out through the urethra |
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What are 3 pathophysiologic causes of pre-renal AKI?
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Decreased ECF volume
Decreased effective ECF volume - decreased cardiac output, decreased plasma oncotic pressure Disruption of renal hemodynamics - Drugs (NSIADs, ACEi/ARBs), Endogenous mediators (vasoactive compounds in liver failure) |
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What are signs/symptoms of pre-renal AKI?
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Hypotension, tachycardia, orthostatic changes, low JVP
Heart Failure Liver Failure |
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What are serum abnormalities found in pre-renal AKI?
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Hemoconcentration - Elevated hemoglobin and albumin
Low urinary flow - Elevated Urea:Creatinine ratio |
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What are urine abnormalities found in pre-renal AKI?
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Bland urine sediment
Low [Na+] |
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What are the main things that urine dipstick measures? (3)
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Albumin (protein)
Hemoglobin WBC's |
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What 3 things can be found on urine microscopy?
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Casts
Crystals Cells |
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What are the signs and symptoms of Renal AKI?
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Systemic involvement - pulmonary, joint, rashes, neurologic
Hypertension Mild-moderate ECF volume overload Anemia or thrombocytopenia Abnormal urine sediment - Blood or WBC or Protein or abnormal casts |
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How do you classify parenchymal kidney disease? (3)
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Tubulo-interstitial - Allergic/Acute interstitial neprhitis (AIN), Acute tubular necrosis (ATN), Tubular obstruction
Glomerular - primary or secondary, proliferative or non-proliferative Vascular - Arterial or venous |
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What are 3 types of tubulo-interstitial kidney disease are there?
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Allergic/acute interstitial nephritis
Acute tubular necrosis Tubular obstruction |
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What is the definition of Interstitial Nephritis?
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Interstitial inflammation resulting in AKI
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What causes AIN? (3)
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Drug Reaction: antibiotics, NSAIDs, PPIs
Autoimmune disease: Sjogren's, Sarcoidosis Infectious: legionella, TB, EBV, CMV, HIV |
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What is the classic triad seen drug-induced AIN?
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Rash
Fever Eosinophilia |
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What are Urinary Findings in Drug-induced AIN?
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Dipstick: +/- blood, +/- protein, +/- WBCs (eosinophils)
Microscopy: WBC casts |
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How long after drug exposure does AIN occur?
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7-10 days
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What are the first and second most common causes of AKI?
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1) pre-renal failure
2) ATN |
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What is the definition of ATN?
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Injury and death of renal tubular cells
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What are causes of ATN? (2)
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Ischemia: pre-renal AKI, etc.
Toxin: endogenous (myoglobin, hemoglobin), exogenous (aminoglycosides, IV contrast agents) |
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What are risk factors for ATN? (4)
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Pre-existing chronic kidney disease
Pre-existing cardiovascular disease ECF volume depletion Multiple renal insults |
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What do you find on urinalysis in ATN?
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Dipstick: blood and protein
Microscopy: Hemegranular casts (aka muddy brown casts) |
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What is the definition of tubular obstruction in renal AKI?
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Acute kidney injury due to intratubular obstruction
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What are causes of tubular obstruction in renal AKI? (2)
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Endogenous: Tumour lysis syndrome (uric acid crystals), Myeloma Cast Nephropathy (immunoglobulin cas formation)
Exogenous: Drugs (Septra, Acyclovir or methotrexate crystals) |
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What do you find on urinalysis in tubular obstructive renal AKI?
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Dipstick: normal or abnormal
Microscopy: Crystals |
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What are 2 kinds of glomerular disease and which one typically results in AKI?
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Proliferative - AKI
Non-proliferative |
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What types of cells proliferate in proliferative glomerular disease?
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Mesangial cells
Endothelial cells Epithelial cells |
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What causes glomerular disease? (2 main classifications with examples)
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Primary: idiopathic
Secondary: Autoimmune (SLE), malignancy, infections, drugs/toxins (NSAIDs, etc) |
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What are signs and symptoms of proliferative glomerulonephritis?
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Rapid decline in GFR
Hypertension Anemia Elevated inflammatory markers ECF volume normal or expanded |
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What is found on urinalysis in proliferative glomerulonephritis?
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Dipstick: blood, protein
Microscopy: Dysmorphic RBC's, RBC casts |
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What are signs and symptoms of non-proliferative glomerulopathies?
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Peripheral edema (severe)
Nephrotic Range proteinuria (>3.5g/day) Hypoalbuminemia Hyperlipidemia Slow deterioration in renal function |
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What do you find on urinalysis in non-proliferative glomerulopathies?
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Dipstick: +++protein (>3.5g/day), +/- blood
Microscopy: oval fatty bodies, fatty casts |
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Why are patients with non-proliferative glomerulopathies at risk for thrombosis?
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Because they lose anti-thrombin III in their urine
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What can cause vascular AKI?(4)
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Arterial: Renal artery disease
Arteriolar: Cholesterol embolic disease Capillary: thrombotic microangiopathies (TTP, HUS, malignant HTN, drug induced, HIV, preeclampsia, etc) Venous: Renal vein thrombosis |
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What are causes of post-renal AKI? (7 categorized anatomically)
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Urethral obstruction (stone, stricture, etc)
Prostate (hypertrophy, malignancy) Gynecological or colorectal malignancy Bladder (mass/tumour, stone, neurogenic) Ureteric (stricture, stone, malignancy) - bilateral Retroperitoneal mass (infections, malignant) - bilateral Retroperitoneal fibrosis (idiopathic, radiation induced, drug induced) - bilateral |
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How do you diagnose post-renal AKI?
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Imaging - U/S is first line, CT abdo
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What are general principals for treating AKI? (4)
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Remove offending nephrotoxin
Avoid further nephrotoxic therapies/investigations (ex IV contrast dyes) Treat ECF volume depletion Avoid complications: ECF volume overload, hyperkalemia, medication toxicity |
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How do you treat pre-renal AKI?
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IV fluids to replete ECF volume
Improve cardiac output if needed |
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How do you treat renal AKI? (ATN, AIN, Glomerulonephritis)
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ATN: remove offending agent, correct ECF volume depletion, supportive care
AIN: remove offending agent, consider corticosteroid therapy Glomeruloneprhitis: immunosuppressive therapy |
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How do you treat complications of AKI? (3)
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ECF volume overload: restrict Na+ intake, use high dose diuretics
Hyperkalemia: restrict K+ intake, promote K+ loss (diuretics, laxatives), shift K+ intracellularly (insulin, beta 2 agonist) |
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What are indications for dialysis in AKI?
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Hyperkalemia that is unresponsive
ECF volume overload that is unresponsive Metabolic acidosis that is unresponsive Uremic encephalopathy Uremic Pericarditis Intoxications: ethanol, methanol |
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What is uremia?
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Accumulation of urea in blood when kidney failure occurs that leads to encephalopathy, uremic pericarditis, etc
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Draw a flow chart for the approach to diagnosis of AKI along with findings on urinalysis
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See lecture
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