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Flashcards in acute kidney injury Deck (51):
1

definition of AKI

inability of kidney to maintain homeostasis leading got a buildup of nitrogenous wastes

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AKI characteristics

occurs over hours to days, there is increased baseline creatinine of more than 50%. decreased Cr clearance of more than 50% deterioration requiring dialysis.

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anuria

less than 100mL/24

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oliguria

<500mL

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polyuria

>2.5L

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most common form of AKi

prerenal or functional

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if it is intrarenal what is the next step?

considering whether it is tubulointerstitial or glomerular.

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prerenal causes

inadequate perfusion, need to check volume status

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renal causes

this is despite perfusion and excretion. check urinalysis, full blood count, and autoimmune screen

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post-renal causes

blocked outflow. check the bladder and catheter and ultrasound

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types of intrinsic AKI

ATN (ischemia, toxin, tubular factors), AIN (inflammation, edema), glomerulonephritis (damage to the filtering mechanisms, depends on the presentation)

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post-renal causes

BPH, malignancy, blocked catheter, ureter

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what dilates the afferent arteriole?

prostacyclin and NO.
this is why NSAIDs block the afferent dilation of auto regulatory

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what constricts the afferent arteriolar

endothelin, catecholamines, thromboxane

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what constricts the efferent arteriole

angiotensin II
thus ACEi block this

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what are the classifications of ATN

nephrotoxic, ischemic

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nephrotoxic ATN endogenous toxins

heme pigments (myoglobin and hemoglobin) myeloma light chains.

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exogenous toxins nephro ATN

antibiotics (aminoglycosides), radioconstrast agents , heavy metals. poisons such as ethylene glycol

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what are the phases of ATN

insult, oliguria, dialysis, polyuria, and recovery. the creatinine increases steadily and then decreases

20

causes of acute interstitial nephritis

allergic interstitial nephritis, due to hypersensitivity to drugs; infections from bacteria and viruses, sarcoidosis

21

what are the clinical characteristics of allergic interstitial nephritis

fever, rash, arthralgias, eosinophilia, urinalysis shows hematuria sterile pyuria, eosinophiluria

22

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.

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risk factors for contrast induced aki

insufficiency, DM, multiple myeloma, high osmolar contrast media, contrast medium volume

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what can protect against contrast induced

IV fluid, mucomyst (N-acetylcysteine), bicarbonate.

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what is not helpful for contrast induced AKI

diuretics, mannitol

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glomerulonephritis definiton

renal disease characterized by inflammation and damage to the glomeruli. this allows for protein and blood in the urine. generally either proliferative or non.

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common presentations of GN

isolated hematuria and proteinuria, nephrotic syndrome, nephritic, acute renal failure, chronic renal failure.

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nonproliferative types

minimal change, membranous, focal segmental

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proliferative types

IgA, membranoproliferative, post-infectious GN, rapidly progressive GN, good pastures, MPA, wegeners

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minimal change GN

abnormal podocytes on EM, there is effacement and nephrotic syndrome. in children.

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what to treat MCD with?

supportive therapy and prednisilone, most have great prognosis

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focal segmental GN

segments of the glomerulus develop sclerosis. presents with nephrotic. steroids are usually worthless, 50% progress to renal failure.

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membranous glomerulonephritis

thickened BM usually idiopathic 1/3 have chronic, 1/3 remission, 1/3 progress to renal failure.

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IgA nephropathy

most common in adults, hematuria, 24-48 hrs post URTI/GI infection. there are deposits in the membrane

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membranoproliferative GN

immune mediated or hepatitis, usually progresses to end stage renal failure.

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post infectious glomerulonephritis

occurs weeks after URTI usually strep pyogenes, supportive treatment will resolve in 2-4 weeks.

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RPGN different types?

crescentic. good pastures, MPA, and wegeners

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good pastures

autoimmune to the GBM there is an autoantibody to the glomerulus and the lung. hematuria and hemoptyosis. treat with steroids.

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vasculitis disorders that cause crescentic RPGN

MPA and wegeners

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wegeners

vasculitis of the lungs, kidneys, and other organs. c-ANCA, need to treat with steroids and cyclophosphamide

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MPA

small vessel vasculitis, p ANCA long term steroids and cytotoxic agents.

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when will you see RBC casts or dysmorphic RBCs

acute glomerulonephritis, and small vessel vasculitis.

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when will you see WBC and WBC casts

acute interstitial nephritis and acute pyelonephritis

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acute tubular necrosis sediment

renal tubular epithelial cells, RTE casts, pigmented granular muddy brown casts.

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FENa less than 1%

prerenal, urine Na <20 because functional tubules reabsorb lots of filtered Na. ATN (rarely), glomerular or vascular injury.

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FENa 1-2%

prerenal sometimes, ATN sometimes,

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FENa >2

ATN. damaged tubules cannot reabsorb Na.

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clinical signs and symptoms of AKI

weight gain, peripheral edema, hypertension, hyperkalemia, NV, ascites, asterixis, encephalopathy

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labs for AKI

rising Cr and urea, rising potassium, decreasing Hb. acidosis, hyponatremia, hypocalcemia.

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treatment for AKI

immediate management of pulmonary edema and hyperkalemia. dialysis. restriction of water, Na, K. provision of protein intake.

51

indications for acute dialysis

AEIOU
acidosis, electrolytes, ingestion of drugs/ischemia, overload, uremia