Flashcards in acute kidney injury Deck (51):
definition of AKI
inability of kidney to maintain homeostasis leading got a buildup of nitrogenous wastes
occurs over hours to days, there is increased baseline creatinine of more than 50%. decreased Cr clearance of more than 50% deterioration requiring dialysis.
less than 100mL/24
most common form of AKi
prerenal or functional
if it is intrarenal what is the next step?
considering whether it is tubulointerstitial or glomerular.
inadequate perfusion, need to check volume status
this is despite perfusion and excretion. check urinalysis, full blood count, and autoimmune screen
blocked outflow. check the bladder and catheter and ultrasound
types of intrinsic AKI
ATN (ischemia, toxin, tubular factors), AIN (inflammation, edema), glomerulonephritis (damage to the filtering mechanisms, depends on the presentation)
BPH, malignancy, blocked catheter, ureter
what dilates the afferent arteriole?
prostacyclin and NO.
this is why NSAIDs block the afferent dilation of auto regulatory
what constricts the afferent arteriolar
endothelin, catecholamines, thromboxane
what constricts the efferent arteriole
thus ACEi block this
what are the classifications of ATN
nephrotoxic ATN endogenous toxins
heme pigments (myoglobin and hemoglobin) myeloma light chains.
exogenous toxins nephro ATN
antibiotics (aminoglycosides), radioconstrast agents , heavy metals. poisons such as ethylene glycol
what are the phases of ATN
insult, oliguria, dialysis, polyuria, and recovery. the creatinine increases steadily and then decreases
causes of acute interstitial nephritis
allergic interstitial nephritis, due to hypersensitivity to drugs; infections from bacteria and viruses, sarcoidosis
what are the clinical characteristics of allergic interstitial nephritis
fever, rash, arthralgias, eosinophilia, urinalysis shows hematuria sterile pyuria, eosinophiluria
contrast induced AKI charateristics
very uncommon with patients that have normal function. increases significant;y with renal insufficiency
onset 24-48hrs post-exposure, duration is 5-7 days. majority are nonoliguria, dialysis is rarely needed, there is typically a low fractional excretion of sodium.
risk factors for contrast induced aki
insufficiency, DM, multiple myeloma, high osmolar contrast media, contrast medium volume
what can protect against contrast induced
IV fluid, mucomyst (N-acetylcysteine), bicarbonate.
what is not helpful for contrast induced AKI
renal disease characterized by inflammation and damage to the glomeruli. this allows for protein and blood in the urine. generally either proliferative or non.
common presentations of GN
isolated hematuria and proteinuria, nephrotic syndrome, nephritic, acute renal failure, chronic renal failure.
minimal change, membranous, focal segmental
IgA, membranoproliferative, post-infectious GN, rapidly progressive GN, good pastures, MPA, wegeners
minimal change GN
abnormal podocytes on EM, there is effacement and nephrotic syndrome. in children.
what to treat MCD with?
supportive therapy and prednisilone, most have great prognosis
focal segmental GN
segments of the glomerulus develop sclerosis. presents with nephrotic. steroids are usually worthless, 50% progress to renal failure.
thickened BM usually idiopathic 1/3 have chronic, 1/3 remission, 1/3 progress to renal failure.
most common in adults, hematuria, 24-48 hrs post URTI/GI infection. there are deposits in the membrane
immune mediated or hepatitis, usually progresses to end stage renal failure.
post infectious glomerulonephritis
occurs weeks after URTI usually strep pyogenes, supportive treatment will resolve in 2-4 weeks.
RPGN different types?
crescentic. good pastures, MPA, and wegeners
autoimmune to the GBM there is an autoantibody to the glomerulus and the lung. hematuria and hemoptyosis. treat with steroids.
vasculitis disorders that cause crescentic RPGN
MPA and wegeners
vasculitis of the lungs, kidneys, and other organs. c-ANCA, need to treat with steroids and cyclophosphamide
small vessel vasculitis, p ANCA long term steroids and cytotoxic agents.
when will you see RBC casts or dysmorphic RBCs
acute glomerulonephritis, and small vessel vasculitis.
when will you see WBC and WBC casts
acute interstitial nephritis and acute pyelonephritis
acute tubular necrosis sediment
renal tubular epithelial cells, RTE casts, pigmented granular muddy brown casts.
FENa less than 1%
prerenal, urine Na <20 because functional tubules reabsorb lots of filtered Na. ATN (rarely), glomerular or vascular injury.
prerenal sometimes, ATN sometimes,
ATN. damaged tubules cannot reabsorb Na.
clinical signs and symptoms of AKI
weight gain, peripheral edema, hypertension, hyperkalemia, NV, ascites, asterixis, encephalopathy
labs for AKI
rising Cr and urea, rising potassium, decreasing Hb. acidosis, hyponatremia, hypocalcemia.
treatment for AKI
immediate management of pulmonary edema and hyperkalemia. dialysis. restriction of water, Na, K. provision of protein intake.