Kidney Flashcards
kidney is not responsible for release of
angiotensin
kidney is responsible for
synthesis of renin
acidbase balance
reabsorption of electrolytes
regulation of extracellular fluid
although kidneys constitute 0.5% of total body mass how much of the resting cardiac output do they recieve
20-25%
one of the reasons they are so susceptible
risk factors for acute kidney injury include
dehydration
advance age
cirrhosis
are all nsaids nephrotoxic
yes
glomerulus function
formation of ultrafiltrate
proximal function
bulk reabsorption of solute and water
80%
distal function
controls urine concentration
up to 25% of water and solute reabsorbed
loop on henle function
reabsorbs solute
collecting duct function
fine tuning in the balance between excretion and reabsorption of water
kidney responsible for synthesis and release of which hormones
1,25-dihydroxy vit D
renin
erythropoietin
what makes the kidney susceptible to toxicity
lots of blood flow so toxins in circulation delivered to kidney in large amounts
concentrate toxicants in tubular fluid
metabolism of xenobiotics occurs in kidney
glomeruli and interstitium are susceptible to attack by the immune system
what defines acute kidney injury
abrupt decline in GFR
srcr increase? >0.3mg/dl in 48hr
srcr >1.5 x baseline within 7 days
urine volume <0.5ml/kg/hr for 6 hr
mechanism of prerenal AKI
impaired renal perfusion
reduced renal blood flow through vasoconstriction, volume depletion and decreased cardiac output
drugs that cause prerenal AKI
bleeding - anticoagulant
volume depletion - diuretic, cathartic
CV dysfunction - beta blocker
vasoconstriction - nsaid, cyclosporin
mechnism of renal aki
intrinsic damage in the kidney
vascular, glomerular, and tubular
drugs causing vascular renal aki
vascular - cyclosporin, tacrolimue, quinine, clopidogrel
drugs causing glomerular renal AKI
acei
nsaid
drugs causingacute tubular necrosis (ischemic injury in tubules)
acetaminophen aminoglycoside antifunal chemo agents iodinated contrast dye
drugs causing acute interstitial nephritis (hypersensitivity)
antimicrobials nsaid diuretic antihistamine PPI
mechanism of post renal aki
obstruction of urine flow
not common
kidneys fail rapidly
due to bladder dysfunction, crystals forming, retroperitoneal fibrosis
drugs causing bladder dysfunction the post renal aki
anticholinergic
antipsychotic
drugs that form crystal and cause post renal aki
acyclovir
ciprofloxacin
methotrexate
sulfonamides
drugs that cause retroperitoneal fibrosis and cause post renal aki
beta blockers
hydralazine
methyldopa
bromocriptine
risk factors for AKI
preexisting renal impairment dehydration (diuresis, vomiting, diarrhea, hemorrhage) cirrhosis, heart faillure, diabetes multiple nephrotoxic agents seriously ill advanced age
cause of chronic kidney disease
deterioration of renal function due to DM, HTN, AKI, nephrotoxic chemicals
chronic interstitial nephritis
how do nsaids damage the kidney
prerenal - decrease prostaglandins causes vasoconstriction and decreased renal blood flow
also acute interstitial nephritis
clinical manifestation of nsaid kidney damage
increased plasma creatinine
decreased renal blood flow and GFR
oliguria
how do you prevent nsaid kidney damage
avoid nsaids amoung high risk patients
creatinine should be monitored closely
avoid nsaids prior to procedures involving radiocontrast
mechanism of aminoglycoside kidney damage
proximal tubular necrosis - freely filtered and accumulate in proximal tubule, bind to phospholipids within the plasma membrane
interstitial nephritis
type of kidney damange with aminoglycosides
interstitial nephritis
proximal tubular necrosis
clinical manifestations of AG renal damamge
increased plasma creatinine
increased BUN
non oliguric - polyuria bc lose concentrating ability
electrolyte abnormalities
prevention of aminoglycoside renal damage
adjust dose for renal function correct hypokalemia and hypomagnesemia limit duration to 7-10days minimize concomitant nephrotoxic meds monitor therapy choose one with less nephrotoxicity once daily regimen
additional risk factors for AG toxicity
elevated plasma drug concentrations - get peak and trough levels daily
prolonged duration of therapy
type: gent>tobra>amikacin
frequency of dosing
why is once daily dosing less toxic
uptake of the drug is saturable
aki indidence in iodinated contrast media
almost never when no risk factors
50% in high risk
iodinated contrast medica mechanism of renal damage
high osmolality
acute tubular necrosis and vasocontraction
first gen media
ionic monomers
highly hyperosmolal
second gen media
nonionic monomers
lower osmolality
newest generation media
nonionic, dimers
iso-osmolal
least risk but costly
range osmolality of iodinated contrast media
ionic monomers >nonionic monomers > nonionic dimers
clinical manifestations of iodinated contrast media damage
rapid decline within 24-48hr mild increase in serum creatinin non-oliguric hyperkalemia acidosis hyperphosphatemia
additional risk factors for contrast media
dose - higher is more toxicity type - higher osmolarity more toxicity intraarterial more toxic than IV interventional angiography higher than diagnostic PCI reduced renal perfusion heart failure, multiple myeloma
patients at risk of kidney damage with contrast media
<60 GFR and proteinuria >500mg/d
<60 GFR and comorbidities (diabetes, liver fialure, heart failure)
GFR <45
prevention of kidney damage with contrast media
avoid volume depletion
withhold nsaids 24-48hr before
use smallest dose
use iso-osmolal agent or nonionic low osmolal agent
hydration wiht IV isotonic saline
premedicate with acetylcysteine (NAC) for antioxidant properties
tubule most commonly affected by drug induced renal toxicity
proximal
analgesic nephropathy
renal papillary necrosis and chronic interstitial nephritis caused by acetaminophen, nsaid, asa
