renal final exam

what is incremental cost effectiveness ratio

is is the cost divided by the effectiveness of treatment

what are cost

direct medical cost (hospitilization), negative cost from savings in healthcare, the cost would not occur if patient died, and indirect cost is not the value of lost life years

what are time horizons

shows the cost effectiveness of a patient over there life, if we did assume until trail ended that would mean patients died

what is ambiguity with cost 

cost is hard to determine which lens to look through such as cost to consumer vs cost paid by insurance company

what are QALYs

give credit to interventions that improve quality of life but not life expectancy, discount the value of life when disabilities are present., and was first mentioned by klaraman in 1968 when he analyzed treatment of renal disease 

what is the range of QALYs

each year is weight between 0-1 1 is perfect health 0 is death 

how are QALYs calculated

the quality of life multiplied by the time in that health state it represent the amount of time spent in full health

what are the issues with QALYs

hard to measure and can be different on different people such as patient, partner and physician 

who has the lowest to highest perspective of QALYs

partner has lowest than physician in middle and patient has the highest

what is the visual analogue scale

best measurement tool to measure QALYs

what is a standard gamble

option A is relative safe but not the best and then B has two outcomes one a lot better than A and one a lot worse than  the goal is to find the percent chance the good thing will happen vs the bad 

what is the time trade off

would you rather spend a loner time in bad health or a shorter time in good health

how is time trade off calculated

using a scale and the patient plots a point take the point and divide it by the end number

how does who we interview effect hoe basd the disease is perceived 

the public always thinks it the worse and long term patients are use to it so dont perceive it as bad

what is the cost effecitveness cut off

50,000/QALY was when ESKD coverage was mandated in medicare in the 1970s so the gov said if less than we need to cover

what is an example of cost effectivness

lifetime cost 281,640 mean QALYS 35 so incremental costeffectivness 75,000 +

what is the value of human life 

depends on what your looking at can be anywhere between 80,000 to 10 million 

what is the compensating wage differentials 

the more dangerous the job the higher paying it is 

what is the willingness to pay for safety equipment

how much a group will be willing to pay to save one life by adding a safety precaution

who was the first person to get dialysis

clyde shields was very expensive but successful

at the start of dialysis who tended to get it

white males that were below 55 years of age with most patients were refused treatment 

what are death panels

panels that no longer exist would determine which patients get dialysis and the others would die 

how was ESKD covered by medicare

henry jackson friend got CKD in 11965 was approved in 1972

what are the increase life expectancy from dialysis and donors

dialysis 5-10 years, deceased donor 8-12 and living donor 15-20

how many people are waiting for a kidney

102,000

what is the solution to love ones wanting to donate but not matching

kidney paired donations

what are nead chains

a bunch of people are involved matching patients with love ones that want to donate kidneys with those that match

what is the epidemiology of CKD

more than 1 in 7 adults have CKD 15% is about 37 millions 

what is ESKD epidemiology

808,000 have eskd, 549,440 are on dialysis, and 258,560 have had transplants

how many people start dialysis or have a transplant a day

360 people

what are ESKD causes

diabetes, high blood pressure, and glmerulonephritis

what are the risk factor rates with diabetes and HTN

1/3 of diabetes have CKD, and 1/5 patient with HTN have CKD

what is the most common aes for ESKD

45-64 most die before getting older

what is the annual cost of ESKD

52.3 billion,, for patient is 260,00 in first year and 17,000 starting after first year for transplant, and 95,000 for hemodialysis and 70,000 for peritoneal per year 

what is the value of life

EPA 10$ million dollars, lifetime earing for college graduates 2.4 million, median wrongful death 2.2 million, 9-11 compensation 1.7 million, life insurance 165,000$, average net worth 80,000

how many people are waiting for a transplant

102,000

what is AKI

rapid reduction in kidney function as measured by increase creatinine or decrease urine output 

what may AKI result in

acute accumulation of nitrogenous and other waste products, and may dysregulate extracellular volume, electrolytes, and/or the acid/bade content of the blood

what can be done to prevent AKI

limit harmful diagnostic/therapeutic procedures or medications to avoid AKI, tend to use supportive therapies to help treat AKI

what is done if AKI present

stop offending drug, maintain BP and fluid/electrolyte homeostasis

what is the definition of AKI

increase of serum creatinine of 0.3 or higher in 48 hours or a serum creatinine increase of 1.5 fold from baseline from a measurement within seven days, or decreased urine output of less than 0.5 mL/kg/hr for over six hours 

what are risk factors for aki

critical illness, sepsis, circulatory shock, hypovolemia, burns, trama, surgery, diabetes, CKD, CLD, HF, vascular disease, HTN, cancer, anemia, medication and older age 

what are the categories of AKI

prerenal, intrinsic, postrenal, and pseudo-renal

what is a prerenal AKI

hypoperfusion of kidneys with undamaged parenchymal tissue is due to intravascular volume depletion, hypotension, and reduced cardiac output

how does the body respond to prerenal AKI

sympathetic nervous system activation leading to vasoconstriction, RAAS activation, stimulation of thirst, intrarenal autoregulatory response (afferent vasocontraction and efferent constriction )

what limits the autoregulatory response and predioses to pre renal AKI

atherosclerosis, CKD, ACE/arbs, NSAIDS, and calcineurin inhibitors

how do nsaid prevent autoregulatory response

vasoconstricts afferent arteriole is what calcineurin inhibitors do 

what is intrinsic AKI

damage to kidney parenchyma occurs is categorized based on structure affected

what is the types of intrinsic AKI

tubular (acute tubular necrosis, crystal induced nephropathy), glomerular disease, reno-vascular disease, and interstitial injury

what is ATN

most common cause of intrinsic AKI, involves injury of the renal tubular cells, is due to sepsis, prolonged ischemia and toxins 

what are the endogenous nephrotoxins (cause ATN))

myoglobin (release is caused by rhabdomyolysis), uric acid (massive release from tumor cells during chemo leads to uric acid precipitation in renal tubules), and hypercalcemia (due to intense renal vasoconstrictions and volume depletion)

what are the exogenous nephrotoxins for (ATN

aminoglycosides (accumulates in proximal tubules damages mitochondria), vancomycin (has direct tubular toxicity and cast formation), amphotericin B,  Cisplatin/carboplatin, tenofovir, foscarnet, radiocontrast media (causes vasoconstriction and oxidative stress reduce oxygen to tubular cells)

when is radiocontrast media used

IV admin for CT scan and Intra-arterial admin for angiography

what is crystal-induced nephropathy

drugs can crystallize within renal tubules leading to obstruction local inflammation and tubular cell injury, 

what is the mechanism of crystal-induced nephropathy

drug precipitation occurs when urinary solubility thresholds are exceeded worse with acidic urine or rapid infusions, leads to intratubular blockage, increase tubular pressure and secondary ischemic injury

what drugs cause crystal induced nephropathy

acyclovir/valacyclovir, methotrexate, triamterene, and foscarnet 

what are clinical feature of crystal induced neropathy

usually a day to three days of exposure, flank pain, hematuria, dark or cloudy urine or reduced urine output, drug crystals in urine mild proteinuria or granular casts 

how are crystal induced neuropathy prevented

hydration, slow infusion rates, urine alkalization, and monitor renal function and avoid concurrent nephrotoxins

what is Acute interstitial nephritis

delayed T cell-mediated hypersensitivity will have eosinophils, intersitium of kidney is inflamed and edematous

what causes AIN

beta lactam class (cillins), cephalosporins (cef or ceph) (two most common), fluoroquinolones, antimicrobial sulfonamides, firampin, NSAIDs, PPIs, allopurinol, some diuretics including loop and thiazide, cimetidine, 

how are AIN prevented/ treamtnet

avoid unnecessary chronic exposure and monitor renal function, treatment is stop offending agent and consider corticosteroids

what is postrenal AKI

due to obstruction of urine flow, extrarenal (BPH, retroperitoneal fibrosis, kidney stones and malignancy/tumor, intrarenal obstructions, crystals blood clots and tumors

what is hydronephrosis

dilation and distension of renal collecting system due to urinary obstruction outflow distal to the renal pelvis 

what needs to be avoided in postrenal AKI

anticholinergics

what are signs of pseudo-renal AKI

a rise in BUN and/or SCr when GFR did not change the meds are cimetidine, pyrimehtamine, trimethoprim, and fenofibrate

how is AKI diagnosed

patient meets the AKI criteria need to check if they have baseline renal insufficiency

are equations used for dosing in AKI

no as they lag so they are inacurrate 

what type of AKI has an elevated BUN 20 to 1

pre-renal block may be elevated due to other factors unrelated to renal function such as upper GI bleeding, TPN< increase tissue catabolism and glucocorticoid use 

what is anuria

failure of the kidney to produce urine is very uncommon may occur with severe sepsis, sever ischemia or complete urinary blockage

what is oliguria

reduce urine output is common in prerenal AKI is less than 500ml per day in adults

what are the components of urine microscopy in AKI

renal tubular cell, cast, white cell cast, granular cast,, and muddy brown cast

renal tubular cell

suggest acute tubular injury

what are cast

(solidification of protein matric in the nephron which may contain white red blood cell renal epithelial cells, fat globules, bacteria and degenerated form of any of the above

what are urinary electrolytes

includes urine sodium creatine and urea, is if under one is sign of pre renal AKI as the body is trying to retain water and sodium 

what are other forms of diagnostic for AKI

CBC to check for infection as well a serum potassium and phosphorous as AKI can increase these electrolytes, renal imaging and catheterization and renal biopsy

what is the prevention of AKI

avoid nephrotoxic agents as much as possible use normal saline,

when is normal saline used with radiocontrast

when gfr below 30 or risk factors below 45 and may hold metformin

what is treatment of AKI

manage precipitating event, avoid hypotension, stop nephrotoxins, look for etiology of AKI, know baseline function, and supportive care

how is prerenal AKI treated

minimize drugs that diminish renal blood flow,. if due to failure of cardiovascular treat cardiovascular, for volume depletion

amphotericin B

TOxic ATN, is a direct tubular membrane injury and afferent vasoconstriction, present with rising creatine, electrolyte wasting, risk factors are high cumulative dosing dehydration and CKD, prevent with lipid  formulation and saline loading, what to do is swith to liposomal form 

radio contrast media

vasoconstriction and oxidative stree reduce oxygen to tubular cells, has peak creatine at 48-72 hours , risk factors CKD diabetes, high contrast volume, dehydration, prevent with saline, and minimize contrast volume, supportive care and monitor, resolve within a week

how is intrinsic treated

if possible stop treatment, maintain adequate cardiac output and blood pressure to allow for tissue perfusion, fluid overload can happen use furosemide

what can be given to overcome diuretic resistance

reduce sodium intake, increase loop dose, switch loop dose to IV, optimize renal blood flow and may combine with thiazides 

what is postrenal treatment

relieve obstruction if present can use urinary catheter, subreapubic catherer, ureteral stent, percutaneous nephrostomy tube, and manage underlying cause and avoid anticholinergic medications

what are the anticholinergic agents

chlorpheniramine, diphenhydramine, doxepin, hydroxyzine, meclizine, benztropine, trihexyphenidyl, oxybutynin, solifenacin, tolterodine, atropine, dicyclomine, glycopyrrolate, scopolamine, promethazine, chlorpromazine, clozapine, and tricyclic antidepressants 

what are complications of AKI

uremia hyper or hypovolemia, hyperkalemia, metabolic acidosis, hyperphosphatemia, and hypocalcemia 

how are electrolyte management for aKI

sodium and fluid retention, hyperkalemia as most is renally eliminated, hyperphospatemia, hypermagnesemia, (last two restrict from diet)

what may be indicated in severe AKI

RRT

what are indication for RRT

acid-base abnormalities, electrolyte imbalances, intoxications, fluid overload and uremia

who was the first dialysis patient

Clyde shields