Term
| what is acute kidney injury? |
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Definition
| an abrupt (48 hr) reduction in kidney function, a serum creatinine increase of .3 or 50% or a reduction in urine output |
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Term
| why is inulin used to measure the GFR? what else can be used? what is the calculation? |
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Definition
| inulin is freely filterable, not reabsorbed or secreted. creatine or urea could also be used. GFR = (urine conc x urine rate)/plasma conc |
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Term
| why is this formula: ((140-age)x body weight))/(72 x creatinine mg/dl) extremely limited? |
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Definition
| creatinine comes from muscle and not from fat, and considering the obesity of much of the US, body weight is less reliable |
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Term
| b/c the levey formula calculates GFR based on a total body surface area of around 1.73, how will this squew the GFR calculated for a smaller or larger person? |
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Definition
small: overestimate
large: underestimate |
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Term
| is the serum creatinine clearance for african americans higher than caucasians? |
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Definition
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Term
| is the relationship between creatinine and GFR linear? |
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Definition
| no, the difference between 1 and 2 mg/100 mL is 50% GFR reduction, while a much smaller reduction for 2->3 |
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Term
| what are the three categories of AKI (acute kidney injury)? |
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Definition
| pre-renal, intrinsic and post-renal |
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Term
| what is functional renal failure? |
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Definition
| another category he would like to add, which is seen when certain medications are used - such as NSAIDs/other drugs interfering with RAA/aldosterone system. |
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Term
| how do NSAIDs induce functional renal failure? |
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Definition
| they impair prostaglandin production which dilate afferent arterioles and therefore reduce renal blood flow |
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Term
| how do ACEI, ARB and renin inhibitors cause functional renal failure? |
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Definition
| inducing changes in intraglomerular hemodynamics - decreased intraglomerular pressure via dilation of the efferent arteriole |
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Term
| what generates glomerular filtration? |
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Definition
| intraglomerular pressure determined by the vasomoter tone of the afferent and efferent arteriole |
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Term
| what happens when GFR goes down? |
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Definition
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Term
| what is pre-renal acute kidney injury? what can cause it? |
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Definition
| renal hypoperfusion, due to an imbalance of NO/endothelin (vasodilation/vasoconstriction), decreased intravascular volume (vomiting, diarrhea, profuse sweating or inappropriate use of diuretics, hypoalbuminemia, bowel obstruction), decreased CO (not heart failure, b/c that deals with the venous side), and occasionally increased renal/systemic vascular resistance (seen in sepsis or hepatorenal syndrome) |
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Term
| what might decrease CO which would then lead to renal hypoperfusion/prerenal AKI? |
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Definition
| severe CHF, pulm HTN (blood can't get from R to L side - difficult to fix), and pericardial disease (pericardial tamponade or constrictive pericarditis) |
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Term
| what can cause increased renal/systemic vascular resistance? |
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Definition
| sepsis or hepatorenal syndrome |
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Term
| what is hepatorenal syndrome? when is it seen? why can it be considered a functional problem? |
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Definition
| severe liver disease (acute or chronic) causes vasodilation of the splanchnic vasculature BUT constriction of the systemic and renal vasculature. it is seen in pts who have significant ascites and bad liver disease. it can be considered functional AKI b/c the kidneys are fine, at least initially. it is very difficult to treat. |
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Term
| what are clinical clues of pre-renal AKI in terms of hx? symptoms? |
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Definition
| hx: GI fluid losses, decreased fluid intake, DM, CHF. symptoms: thirst, orthostatic dizziness, dyspnea, and edema |
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Term
| what are clinical clues of pre-renal AKI in terms of a physical exam? |
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Definition
| increased heart rate, higher pulse pressure (sys - dia, and dia is lowered), +tilt test, and dry skin/mucous membranes. +JVD (but if flat supine = volume contraction), + hepatojugular reflux, rales, S3 gallop, and edema are all indicative of heart failure |
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Term
| what does a +tilt test tell you? |
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Definition
| likely volume contraction |
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Term
| what are clinical clues of pre-renal AKI in terms of lab tests? |
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Definition
| BUN/creatinine ratio >20/1, urine osmolarity >400 mosm/kg, urine Na+ <20 mEq/L, urine K+ >40 mEq/L, "bland" urinalysis. (wikipedia: GFR levels are decreased due to hypoperfusion, leading to a general greater increase in BUN than creatinine. since the kidney is functioning correctly (intrinsic renal pathology) the response to decreased GFR is to increase reabsorption rates. the increased reabsorption of Na leads to increased water and urea reabsorption from the proximal tubules of the kidney back into the blood. in contrast, creatinine is actually secreted in the proximal tubule. this generally leads to a BUN:Cr ratio > 20 and a fractional excretion of Na of < 1% and an elevated urine osmolarity.) |
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Term
| what is the most important function of the kidneys? |
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Definition
| to maintain extracellular volume via reabsorption of Na+. (180 L urine made every day, only 2 L peed out) |
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Term
| what is the fractional excretion of Na+ (FeNa)? what does it mean if it is <1% what if it is >2% |
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Definition
| the clearance of Na+ (reabsorbable) expressed as a percentage of GFR (creatinine, NON-reabsorbable). <1% = prerenal azotemia, >2% = renal azotemia |
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Term
| when is the fractional excretion of urea used as opposed to sodium? what does it mean if it is <35%? what if it is >50%? |
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Definition
| when pts are using antibx that involve obligatory Na+ loss b/c they have a sodium moiety attached (ie. sodium-penicillin). <35% = prerenal azotemia and >50% = renal azotemia |
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Term
| what does it tell you if Na+ is high and Cl- is low? |
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Definition
| something, such as an antibiotic is obligating some of the Na+ |
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Term
| what are post-renal causes of AKI? |
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Definition
| urethra: valve pathology, strictures, phimosis, or tumor. bladder outlet (more common): prostate (important cause), tumor, stone, infection, clot, neurologic, drugs |
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Term
| what can post-renal causes of AKI become? |
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Definition
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Term
| what is prostatic hypertrophy treated with? |
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Definition
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Term
| what are intraureteral causes of post-renal AKI? |
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Definition
| stones, clots, crystals (sulfonamides urate), edema, papillary necrosis (seen w/ sickle cells, NSAIDs, pyelonephritis), and pyogenic debris |
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Term
| what are extraureteral causes of post-renal AKI? |
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Definition
| tumor (*cervix*/prostate/endometriosis), periureteral (retroperitoneal) fibrosis, abscess, accidental |
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Term
| what are renal causes of post-renal AKI? |
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Definition
| intratubular crystals (sulda, triamterene, indinavir, acyclovir, mannitol, ethylene glycyol) and intratubular proteins (light chains, myoglobin, and hemoglobin) |
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Term
| what are clinical clues for post renal AKI gathered via hx? |
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Definition
| lower tract disease/symptoms, GU sx, and nephrolithiasis, drugs (crystals/outlet dysfunction), and GYN disease |
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Term
| where should you look for post renal AKI clinical clues on the physical exam? |
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Definition
| lower abdominal area, check for pelvic masses, phimosis |
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Term
| what are good imaging techniques for diagnosing post renal AKI? |
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Definition
| renal ultrasound (first tool to use), duplex doppler ultrasound, resistive index <.7, contrast studies (DO NOT use if creatinine elevated), CT, and MRI (sometimes use gadolinium, but NOT if creatinine is elevated) |
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Term
| what are the various kinds of intrinsic AKIs and their prevalence? |
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Definition
| vascular, glomerular 5%, interstitial 10% and tubular (ATN) 85% |
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Term
| what are the 2 kinds of acute tubular necrosis (ATN)? |
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Definition
| nephrotoxic and ischemic (ischemic: more common and due to extreme hypoperfusion or infarctions like cortical necrosis) |
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Term
| what are some things that can cause ATN via nephrotoxicity? |
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Definition
| heavy metals (mercury,arsenic, lead), carbon tetracholoride, ethylene glycol, ax-ray contrast media, MRI contrast media, pesticides, antibx (aminoglycosides/amphotericin), CA, chemotherapy (cisplatin, methotrexate), immunosuppressive agents (cyclosporine), and NSAIDs |
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Term
| what is the pathogenesis of acute AKI? |
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Definition
| renal ischemia leads to endothelial and tubular injury. endothelially, there is activation of vasoactive compounds and especially vasoconstrictors and vasodilation, increased leukocyte-endothelial adhesion, release of adhesion molecules to set up impaired blood flow in the area, which perpetuates the ischemia. in terms of tubular injury, the cytoskeleton is disrupted which leads to tubular obstruction & backleak |
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Term
| after renal injury, and thus cell injury, what kinds of problems an reperfusion cause? |
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Definition
| persistent intrarenal vasoconstriction and congestion of vessels in the outer medulla - which both lead to persistent hypoxis of the outer medulla, and persistent dysfunction/progressive necrosis of cells affecting predominately the pars recta w/some involvement of mTAL segments as well |
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Term
| after cell death due to necrosis and apoptosis in AKI, can the tubular cells regenerate? |
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Definition
| yes, perhaps not 100%, but the dead cells should slough off and make way for the new layer coming underneath. this can take hrs to mos to occur. |
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Term
| what are risk factors for acute tubular necrosis? |
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Definition
| pre-existing renal disease, age (start to lose renal function @ 35), infection (sepsis), other systemic diseases, nephrotoxins and hypovolemia (less blood to start with) |
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Term
| what are systemic diseases associated with increased risk of acute tubular necrosis? |
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Definition
| diabetic nephropathy, CHF,COPD, cirrhosis with ascites, hyperbilirubinemia, rhabdomyolysis - hemolysis, multiple myeloma, hypercalcemia, and significant vascular disease |
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Term
| how is acute tubular necrosis lab work distinguished from pre renal AKI? |
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Definition
| in acute tubular necrosis, the BUN/creatinine is not high (BUN does not go up disproportionately to creatinine b/c this is filtration and not related to the tubular reabsorption/secretion), the urine osmolarity is low (b/c tubules are damaged and cannot concentrate as they should - higher Na, lower K in urine), and urinalysis will be grossly abnormal - RBC/WBC/casts, RBC casts are bascially pathognomonic. |
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Term
| what are muddy brown casts? |
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Definition
| cellular debris caught up in tamm-horsefall protein which are highly suggestive of acute tubular necrosis |
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Term
| what is tx for acute tubular necrosis? |
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Definition
| avoidance is the key (avoid nephrotoxins, don't let pts get dehydrated/volume contracted), once pts have it, optimize hemodynamics, make sure perfusion as good as possible, and decrease possible obstructions. supportive care consists of good electrolyte/acid+base balance, nutrition, and infection prevention |
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Term
| what are indications for dialysis? |
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Definition
| Acid/base disturbances, Electrolyte abnormalities (high K/low Na), Intoxications, Overload (fluid), and Uremia (AEIOU) |
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