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56 Cards in this Set
- Front
- Back
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Acute kidney injury definition
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>25% reduction in GFR over hours to days
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Oliguric
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<0.5 ml/kg/hr of urine production
30 ml/hr |
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Diagnostic categories of acute kidney injury
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Pre-renal (hemodynamic)
Renal glomerular, tubular-interstitial, vascular Post-renal (obstructive) |
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Pathogenesis of hemodynamic acute kidney injury
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Decreased circulating volume
Resulting sympathetic and RAA response results in reduced blood to kidney and redistribution of low w/in kidney |
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Relationship of GFR and renal perfusion
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Kidney is perfused by efferent arteriole
So if GFR goes down, so does perfusion |
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Why is renal perfusion a big deal?
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Metabolically active cells
Always at a relatively low oxygen tension, so a fall is problem |
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What happens when renal perfusion drops?
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Mild/moderately - "pre-renal" tubular cells can make it, work to concentrate urine, result is small amt of concentrate urine with urea as osmole
Severe- acute tubular necrosis Urine is similar to plasma osmolality |
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Acute tubular necrosis pathology
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Tubular epithelial cells die
Slough off into urine forming casts Can regenerate over days to weeks |
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Pre-renal acute kidney injury treatment?
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Restore volume
If just pre-renal, will response |
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Acute tubular necrosis treatment
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Nothing will speed up regeneration
Don't fluid overload Minimize K+ Monitor neurologic fnc May need dialysis until regeneration |
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Difference in urine between pre-renal oliguria and ATN
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Pre-renal will have concetration > plasma, FENA < 1%, Na < 20, high BUN/creatinine ratio, bland urine appearance
ATN - isosthenuria, FENA > 2%, urine sodium 50-150, low BUN/creatinine ratio, granular casts |
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Why is BUN/creatinine high in pre-renal oliguria?
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In proximal tubule, BUN is reabsorbed with Na
Na reabsorption is maximized in pre-renal oliguria Other things that change the BUN are protein intake and liver fnc |
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Patients at increased risk for hemodynamic acute kidney injury
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Chronic kidney disease
Elderly Reduced blood to kidneys heart failure, atherosclerosis, renal stenosis, ACEIs Concurrent tubular insult (amphotericin) |
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Working up hemodynamic acute kidney injury
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History
Figure out when the injury happened Test urine and blood to decide if its oliguria or ATN Remove causative factors If its ATN, support for 4 days to 4 weeks |
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Is golmerulonephritis a common cause of acute kidney injury
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No
<5% More common in kids |
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Tubulointerstitial acute kidney injury
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Direct injury to renal tubular cells
Allergic interstitial nephritis Endogenous toxins Exogenous toxins Crystals |
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Allergic interstitial nephritis causes
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Penicillins and cephalosporins
PPIs Sulfa containing meds NSAIDs |
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Pathology of allergic interstitial nephritis
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Inflammatory cells in the interstitium
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Clinical presentation of allergic interstitial nephritis
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Increased creatinine
Rash NOT oliguric, not too much protein WBCs in urine, eosinophils Rare - systemic, desquamating rash, eosinophila |
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Allergic interstitial nephritis + nephrotic syndrome
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Rare toxicity of NSAIDs
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Managing allergic interstitial nephritis?
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Remove offending agent
Severe cases benefit from steroids |
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Myoglobin and the kidney
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Bad
Constriction of afferent arteriole 2/2 decreased EDRF Directly damages tubular cells when they are hypoxic Urine turns pink |
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Where does myoglobin come from?
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Heme protein released from skeletal muscle in a crush injury
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Multiple myeloma and the kidney
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Light chains are freely filtered
Taken up by proximal tubular cells (Have a specific receptor) Accumulate in lysosomes and are toxic in excess |
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Urine acid and the kidney
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Uric acid reabsorbed in PCT
high concentration in interstital space Crystals produce intense inflammatory response and peritubular giant cells |
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Hyperuricemia, how?
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Tumor lysis syndome
Lesch nyhan Gout ? |
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NSAIDs effect on kidney
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Inhibit vasodilatory prostaglandins
Afferent arteriole vasoconstriction fall in GFR, can lead to ATN Chronic renal damage from medullary ischemia type IV RTA, interstital fibrosis |
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Radiocontrast and kidney
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Constricts afferent arteriole
Directly toxic to tubular cells Prevent by adequately hydrating, using a lower dose |
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Who gets renal toxicity from contrast?
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CKD
High doses, frequent studies HTN, diabetes, CHF -- less able to keep kidney perfused |
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Aminoglycoside renal toxicity
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Filtered and then selectively take up by PCT cells
Concentrates in PCT cells Interferes with mitochondrial fnc and inositol phospholipid signal transduction |
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Presentation of aminoglycoside renal toxicity
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Usually 3-5 days later
Non-oliguric May also have RTA Can occur after just one dose |
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Amphotericin B toxicity
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Distal nephron
Inserts ion channel into cell membrane Shorts Na/K ATPase Increases O2 requirements Decreased GFR, RTA |
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Cisplatin renal toxicty
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Direct tubular toxin
Proximal and distal nephron Decreased GFR HypoK, hypoMg, neprhogenic DI |
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Drugs that from crystals that can cause damage in tubule
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Resolve quickly
Acyclovir Quinolones Long-term damage Indinavir MTX sodium phosphate |
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Typical clinical presentation of toxic tubular injury
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Creatinine rises
No systemic illness Often not oliguric Little protein Pretty bland urine |
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Effect of damage tubular cells on GFR
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Tubuloglomerular feedback leads to reduced GFR with tubular dysfnc
High tubular Na or Cl reaching distal causes macula densa to release adenosine, which constricts the nearby afferent arteriole Back leak Back pressure |
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Instrinsic acute kidney caused by vascular problems
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Either renal artery/vein problems or microangiopathies
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Renal artery occulusion
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Happens in pts with pre-existing renal stenosis who have a sudden loss of perfusion from ACEI, thrombus, severe dehydration
Previous normal renal artery thrombosis in pts with clotting disorders Causes acute kidney injury |
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Renal vein thrombosis
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Gross hematuria
Acute kidney injury Not oliguric Usually bilateral See in cancer, other hypercoagulable states (including membraneous glomerulopathy) Dull loin pain, or none |
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Thrombotic microangiopathies that can cause acute kidney injury
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HUS/TTP
Scleroderma renal crisis Malignant HTN DIC Preeclampsia Gemcitamin Cyclosporine, tacrolimus |
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Presentation of thrombotic microangiopathies w/ renal involvement
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Systemic for that disease
Oliguric w/ bland urine Renal biopsy shows endothelial damage and proliferation, plt and fibrin thrombi |
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Post renal causes of acute kidney injury
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Obstruction from renal pelvis to urethra
Congenital Prostate enlargement Pelvic/retroperitoneal malignancy Stones |
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Pathogenesis of acute kidney injury in obstruction
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Higher pressure in renal pelvis
Reduces blood flow to medulla Ischemic medullar results in Lower GFR from TG feedback Dilute urine (ADH resistant) Type IV RTA Not oliguric |
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Most common cause of acute renal failure in community
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Obstruction 50-60%
Drug induced 30-40% Hemodynamic 20% |
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Diagnosing obstructive GU lesions
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US is most sensitive
CT is best for looking at stones |
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What does GFR mean in acute kidney injury
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Proportional to functioning nephrons
So is creatinine |
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Cause of type IV RTA
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Obstruction
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Complicaitons of a reduced GFR
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Reduced ability to clear Na and H2O
edema, HTN Reduced ability to excrete K Reduced ability to excrete acid load Accumulation of Mg PO4 Uremia |
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Uremic encephalopathy
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Fatigue
Altered consciousness Hiccups Puritis Asterixsis Seizure |
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Oliguria means?
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SEVERE nephron injury
Clearing even 8 mL/min gets you out of this category |
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Sequelae of an episode of acute kidney injury
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2-5 fold increased risk of death during this admission
Increased risk of death up to 2 years after Increased lifetime risk of ESRD and dialysis |
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Most common causes of acute kidney injury in hospital?
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Hemodynamic - 80%
surgical blood loss, sepsis, cardiac failure Toxic - 20% |
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Diagnostic approach to ARF in outpatient
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1. Plot creatinine over time
2. Careful history 3. UA 4. Put in a catheter / US 5. If hematuria, consider GN |
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Diagnostic approach to ARF in hospital
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1. Plot creatinine/events
2. Med history, history 3. UA 4. Determine if its ATN |
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Indications for dialysis in acute kidney injury
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Volume overload unresponsive to diuretics
HyperK - unresponsive Acidosis - unresponsive Uremic encephalopathy Uremic bleeding Uremic pericarditis |
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Goals of dialysis
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Regulation of ECF vol
Regulation of ECF composition (K, acids, toxins, drugs) Administraiton of blood products, nutrition |
