acute kidney injury

Question 1

definition of AKI

Answer 1

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

Question 2

AKI characteristics

Answer 2

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

Question 3

anuria

Answer 3

less than 100mL/24

Question 4

oliguria

Answer 4

<500mL

Question 5

polyuria

Answer 5

> 2.5L

Question 6

most common form of AKi

Answer 6

prerenal or functional

Question 7

if it is intrarenal what is the next step?

Answer 7

considering whether it is tubulointerstitial or glomerular.

Question 8

prerenal causes

Answer 8

inadequate perfusion, need to check volume status

Question 9

renal causes

Answer 9

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

Question 10

post-renal causes

Answer 10

blocked outflow. check the bladder and catheter and ultrasound

Question 11

types of intrinsic AKI

Answer 11

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

Question 12

post-renal causes

Answer 12

BPH, malignancy, blocked catheter, ureter

Question 13

what dilates the afferent arteriole?

Answer 13

prostacyclin and NO.

this is why NSAIDs block the afferent dilation of auto regulatory

Question 14

what constricts the afferent arteriolar

Answer 14

endothelin, catecholamines, thromboxane

Question 15

what constricts the efferent arteriole

Answer 15

angiotensin II

thus ACEi block this

Question 16

what are the classifications of ATN

Answer 16

nephrotoxic, ischemic

Question 17

nephrotoxic ATN endogenous toxins

Answer 17

heme pigments (myoglobin and hemoglobin) myeloma light chains.

Question 18

exogenous toxins nephro ATN

Answer 18

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

Question 19

what are the phases of ATN

Answer 19

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

Question 20

causes of acute interstitial nephritis

Answer 20

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

Question 21

what are the clinical characteristics of allergic interstitial nephritis

Answer 21

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

Question 22

contrast induced AKI charateristics

Answer 22

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.

Question 23

risk factors for contrast induced aki

Answer 23

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

Question 24

what can protect against contrast induced

Answer 24

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

Question 25

what is not helpful for contrast induced AKI

Answer 25

diuretics, mannitol

Question 26

glomerulonephritis definiton

Answer 26

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

Question 27

common presentations of GN

Answer 27

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

Question 28

nonproliferative types

Answer 28

minimal change, membranous, focal segmental

Question 29

proliferative types

Answer 29

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

Question 30

minimal change GN

Answer 30

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

Question 31

what to treat MCD with?

Answer 31

supportive therapy and prednisilone, most have great prognosis

Question 32

focal segmental GN

Answer 32

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

Question 33

membranous glomerulonephritis

Answer 33

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

Question 34

IgA nephropathy

Answer 34

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

Question 35

membranoproliferative GN

Answer 35

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

Question 36

post infectious glomerulonephritis

Answer 36

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

Question 37

RPGN different types?

Answer 37

crescentic. good pastures, MPA, and wegeners

Question 38

good pastures

Answer 38

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

Question 39

vasculitis disorders that cause crescentic RPGN

Answer 39

MPA and wegeners

Question 40

wegeners

Answer 40

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

Question 41

MPA

Answer 41

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

Question 42

when will you see RBC casts or dysmorphic RBCs

Answer 42

acute glomerulonephritis, and small vessel vasculitis.

Question 43

when will you see WBC and WBC casts

Answer 43

acute interstitial nephritis and acute pyelonephritis

Question 44

acute tubular necrosis sediment

Answer 44

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

Question 45

FENa less than 1%

Answer 45

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

Question 46

FENa 1-2%

Answer 46

prerenal sometimes, ATN sometimes,

Question 47

FENa >2

Answer 47

ATN. damaged tubules cannot reabsorb Na.

Question 48

clinical signs and symptoms of AKI

Answer 48

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

Question 49

labs for AKI

Answer 49

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

Question 50

treatment for AKI

Answer 50

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

Question 51

indications for acute dialysis

Answer 51

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