Acute Kidney Injury - Exam 1

Question 1

What are the normal culprits behind an acute kidney injury?

Answer 1

inability to manage: fluid, electrolytes and acid base balance

decreased excretion of urea and creatinine

Question 2

In an acute kidney injury, by the time _____ rises, ____ usually has already fallen significantly!

Answer 2

serum Cr

GFR

Question 3

What criteria for dx AKI is used most commonly?

Answer 3

KDIGO

Question 4

What is normal urine output? **What is anuria? **oliguria? polyuria?

Answer 4

normal: 800-2000 mL/day

**anuria: less than 50mL

**oliguria: less than 400mL

polyuria: excessive urine 2500-3000mL +

Question 5

What does anuria make you think is the underlying cause?

Answer 5

Acute obstruction, cortical necrosis, aortic dissection

aka very bad finding!!

Question 6

Define azotemia

Define uremia

Answer 6

Azotemia - ￪ nitrogenous wastes in the blood (no symptoms present)

Uremia - nonspecific SYMPTOMS caused by elevated nitrogenous waste (especially urea) in the blood (symptoms will be vague and basically the pt does not feel well)

Question 7

What are the 3 broad categories of acute kidney injury? What is the MC cause of AKI? What is the underlying cause?

Answer 7

**Pre-renal azotemia- MC due to renal hypoperfusion

intra-renal

post-renal

Question 8

What is intrinsic kidney injury due to? What is the LEAST common cause of AKI? What is the underlying cause?

Answer 8

intrinsic kidney: direct injury

postrenal obstruction- LEAST common
caused by obstruction of urinary flow

Question 9

What is the underlying cause of prerenal azotemia? Give 3 examples

Answer 9

inadequate renal perfusion aka anything that changes the blood flow to the kidneys

1. hypovolemia due to dehydration, hemorrhage, GI loss, diuresis, pancreatitis, burns, peritonitis.
2. Decreased cardiac output - decompensated HF, cardiogenic shock, PE, pericardial tamponade, arrhythmias, liver failure
3. Changed vascular resistance
   ￬ - sepsis, anaphylaxis, anesthesia
   ￪ - epinephrine, high-dose dopamine, renal artery stenosis
   Meds that interfere with renal vascular autoregulation
   NSAIDs, iodinated contrast, ACEIs/ARBs

Question 10

What arteriole does angiotensin II prefer?

Answer 10

works on both but prefers Efferent arteriole

Question 11

What affect do NSAIDs have on the kidney?

Answer 11

NSAIDs work on the Afferent arteriole by blocking the action of prostaglandins that would normally dilate the afferent arteriole. Blocking this action harms the kidney because it leads to decreased perfusion

Question 12

In prerenal azotemia what is the BUN/Cr ratio? What should the FENa+ be? Describe the urinary sediment? What is the urine osmolality

Answer 12

BUN:Cr ratio > 20:1 usually

If oliguric, there should be a low fractional excretion of sodium (FENa+) in the urine - <1%

urine sediment is usually normal, may see some hyaline casts

urine osmolality is normal

Question 13

In prerenal azotemia, hyaline casts are formed from ______ secreted by tubule

Answer 13

Tamm-Horsfall mucoprotein

Question 14

What is the treatment for prerenal azotemia?

Answer 14

treat the underlying cause to why the kidneys are having decreased blood flow

Maintain euvolemia
Correct abnormal electrolytes
Avoid nephrotoxic drugs

Question 15

What is the MC cause of postrenal obstruction in men? What are some generic causes?

Answer 15

BPH

devices such as an obstructed foley catheter, medications, cancer, retroperitoneal fibrosis, neurogenic bladder

Question 16

Anuria or polyuria possible
May have lower abdominal pain
May see large prostate, distended bladder, pelvic/abdominal mass

What am I?
What are the dx studies/procedure of choice?

Answer 16

post renal obstruction

Bladder catheterization and/or abdominopelvic US can be helpful to look for hydroureter and obstruction

Question 17

What am I?

Answer 17

renal US showing hydronephrosis

Question 18

What is the BUN/Cr ratio in postrenal obstruction? What is the urine osmolality? What may be seen in the urine sediment?

Answer 18

Lab Findings:

￬ GFR and ￪ BUN/Cr with BUN:Cr > 20:1 usually

Urine sodium - varies

Urine osmolality - 400 mosm/kg or less

Urine sediment - often normal; may see RBCs, WBCs, crystals

Question 19

In postrenal AKI where is the obstruction more common?

Answer 19

in the lower abdomen

Question 20

In many cases, what does prerenal azotemia lead to ? What are 3 forms of intrinsic kidney injury? Which one is MC?

Answer 20

tubular injury

**Acute Tubular Necrosis- MC
Acute Glomerulonephritis
Acute Interstitial Nephritis

Question 21

What are the 3 major causes of acute tubular necrosis?

Answer 21

ischemia
nephrotoxins
sepsis

Question 22

in ATN, what is ischemia characterized by?

Answer 22

by inadequate GFR and inadequate blood flow to maintain perfusion
Prolonged hypotension or hypoxemia

Question 23

endogenous or exogenous more commonly cause ATN?

Answer 23

Exogenous more commonly cause damage

Question 24

Name the top 3 common exogenous nephrotoxins. Give a few others

Answer 24

1. Aminoglycosides : examples -> gentamicin, tobramycin, amikacin, plazomicin, streptomycin, neomycin, and paromomycin (gentamicin is the WORST and streptomycin in the least harmful)
2. Amphotericin B (hurts kidneys after 2-3 grams)
3. Vanc

sulfonamides, cephalosporins, tetracycline, acyclovir, foscarnet, IV contrast, methotrexate, cyclosporine, cisplatin, heavy metals, ethylene glycol, insecticides, herbicides

Question 25

For aminoglycosides, how long does the medication remain in the renal tissue? What is used to predict toxicity?

Answer 25

Can remain in renal tissues up to 1 month Trough levels are most useful to predict toxicity

Question 26

Give some examples of endogenous nephrotoxins

Answer 26

myoglobinuria due to rhabdomyolysis hemoglobinuria hyperuricemia bence jones protein

Question 27

When is myoglobinuria commonly seen? What is the CK lab value?

Answer 27

due to rhabdomyolysis, muscle necrosis Crush injury, muscle necrosis from prolonged unconsciousness CK >20,000-50,000 IU/L

Question 28

What will the urine dipstick read like in myoglobinuria? What is the tx for myoglobinuria?

Answer 28

Urine dipstick will read false + for hemoglobin Urine appears dark brown, but has no RBCs on microscopy **rehydration

Question 29

______, ______ and ______ may also occur with myoglobinuria

Answer 29

Hyperkalemia, hyperphosphatemia, hyperuricemia may also occur

Question 30

When is hemoglobinuria commonly seen? What is the tx?

Answer 30

Seen in transfusion reactions and hemolytic anemia Tx - Reversal of underlying disorder, hydration

Question 31

When is hyperuricemia commonly seen? What is the usual cause? What is the serum uric acid level? What is common uric acid level for gout?

Answer 31

in rapid cell turnover and lysis Usual cause - chemo Serum uric acid often > 15-20 mg/dL gout: uric acid between 6-7

Question 32

What is the Bence Jones Protein? What dz is it associated with?

Answer 32

directly toxic, obstructs tubules Seen in association with multiple myeloma

Question 33

In acute tubular necrosis, what is the normal BUN/Cr ratio? urine sodium? What is seen the urinary sediment? _____ and ____ are also common

Answer 33

￬ GFR and ￪ BUN/Cr with BUN:Cr < 20:1 usually Urine sodium is often elevated Urinary sediment - pigmented granular casts or “muddy brown” casts, renal tubular cells, epithelial cell casts Hyperkalemia and hyperphosphatemia are common

Question 34

What is the tx for ATN? What do you need to avoid?

Answer 34

Treatment - remove cause, avoid complications avoid: volume overload and hyperkalemia (loop diuretics or dialysis) protein restrict

Question 35

Why do you need to restrict protein in ATN?

Answer 35

Protein restriction - to prevent metabolic acidosis

Question 36

Which has better long-term outcomes in ATN, oliguric or non-oliguric?

Answer 36

nonoliguric ATN has been long term outcomes

Question 37

T/F: In ATN, pts will regain baseline kidney function.

Answer 37

False!! some may never fully recover baseline kidney function

Question 38

Acute Glomerulonephritis is approximately ____ of intrinsic AKI cases. Most are ______ in nature. Few are ____

Answer 38

5% nephritic in nature so inflammation is involved nephrotic: minimal inflammation with proteinuria (think chronic cases)

Question 39

Almost all acute glomerulonephritis involves the development of _______

Answer 39

inflammatory glomerular lesions

Question 40

What are crescent lesions? What type of AKI are they associated with?

Answer 40

severe breaks in glomerular walls acute glomerulonephritis

Question 41

HTN, edema, and urine containing protein, RBCs, WBCs, and RBC casts What am I?

Answer 41

Acute Glomerulonephritis

Question 42

Name 5 types of glomerulonephritis?

Answer 42

Immune Complex Deposition Anti-GBM-associated C3 Glomerulopathy Monoclonal Ig-Mediated Pauci-Immune Glomerulonephritis

Question 43

What types of acute glomerulonephritis: ______ when antigen excess over antibody production occurs. What happens next?

Answer 43

Immune Complex Deposition Antigen-antibody complexes lodge in glomerular basement membrane (GBM) Complement activation to resolve complexes → destruction of GBM

Question 44

**What are the 3 MC causes of immune complex deposition AG?

Answer 44

Post-infectious (especially seen with **endocarditis** and **streptococcus** **lupus**

Question 45

What types of acute glomerulonephritis: ______ Autoantibodies against glomerular basement membrane (GBM). What other organ is likely to be involved? What is it called when both are involved?

Answer 45

Anti-GBM-associated lungs Goodpasture’s Syndrome - renal + pulmonary involvement

Question 46

What types of acute glomerulonephritis: ______ deposition in the glomerulus +/- Ig deposition. What is it caused by? What can be helpful to identify?

Answer 46

C3 glomerulopathy, C3 Caused by abnormalities in the alternative complement pathway Low serum C3 levels can help identify, but normal C3 does not rule out

Question 47

What types of acute glomerulonephritis: ______ deposited in GBM and/or tubular basement membrane. What is NOT seen? ____ can be used to identify this type of AG

Answer 47

Monoclonal Ig-Mediated, Monoclonal Ig No excess amounts of antigen as seen in immune complex GN Serum Protein Electrophoresis (SPEP), Associated with monoclonal gammopathies multiple myeloma

Question 48

What types of acute glomerulonephritis: ______ small-vessel vasculitis associated with ANCAs. What is the tissue injury secondary to?

Answer 48

Pauci-Immune Glomerulonephritis cell-mediated immune processes

Question 49

What is ANCA?

Answer 49

Antineutrophil Cytoplasmic Antibodies, which are proteins produced by the immune system that mistakenly attack healthy white blood cells called neutrophils

Question 50

Which type of AG has no immune complexes or direct Ig or complement deposition or binding? Name 3 additional parts of the body that it can also effect?

Answer 50

Pauci-Immune Glomerulonephritis lungs, skin, upper airway

Question 51

Name the 2 major s/s of acute glomerulonephritis. Where do they often show up first?

Answer 51

HTN and edema scrotum and periorbital

Question 52

**What does the urine sediment look like in AG? What does the urinalysis look like?

Answer 52

Urine sediment - RBCs, WBCs, RBC casts Urinalysis - hematuria, moderate proteinuria

Question 53

Name 5 additional tests that can be ordered to determine what type of AG is present?

Answer 53

ASO titers - help evaluate for recent strep infection anti-GBM antibodies SPEP P-ANCA and C-ANCA levels Complement levels: C3 and C4 low in immune complex GN C3 alone low in C3 glomerulonephropathy

Question 54

What is the tx for AG?

Answer 54

treat the underlying disease process! High-dose corticosteroids Cytotoxic agents may be used Plasma exchange - Goodpasture disease, pauci-immune glomerulonephritis

Question 55

In ______ and ____ types of AG you would want to tx with a plasma exchange.

Answer 55

Goodpasture disease and pauci-immune glomerulonephritis

Question 56

In acute interstitial nephritis, what is happening? _______ immune reactions predominate

Answer 56

inflammation of the interstitium that surrounds the tubules cell-mediated immune reactions predominate

Question 57

Must _____ in order to confirm acute interstital nephritis

Answer 57

bx!! but not done regularly because it is painful

Question 58

What is the biggest cause of AIN? Give some examples

Answer 58

medications!! PCNs (β-lactams), cephalosporins, rifampin, sulfonamides, HIV drugs Others - diuretics, NSAIDs, rifampin, anticonvulsants, allopurinol, PPIs, H2 blockers

Question 59

What are some infectious causes of AIN?

Answer 59

Bacterial - strep, staph, diphtheria, legionella, rickettsia (RMSF) Viral - CMV, EBV Fungal - histoplasmosis

Question 60

What are some immunologic causes of AIN? What do they more commonly cause?

Answer 60

SLE, Sjogren’s, sarcoidosis, etc. More commonly cause glomerulonephritis

Question 61

Fever rash eosinophilia WBCs (95%), RBCs, eosinophiluria, WBC casts What am I? What will they NOT have if it is NSAID related?

Answer 61

acute interstitial nephritis fever commonly absent if it is NSAID related

Question 62

What is the classic triad of AIN?

Answer 62

fever, rash, arthralgia All 3 only present in 10-15% of pts

Question 63

What is the tx for AIN?

Answer 63

Treatment - removal of cause, supportive care May use course of IV or oral corticosteroids if renal injury persists after agent is removed Urgent dialysis may be necessary in up to ⅓ of all pts

Question 64

Which type of intrarenal AKI has the best prognosis? Why?

Answer 64

acute interstitial nephritis because the nephrons are spared

Question 65

Draw the Jensen chart about types of kidney injury

Answer 65

Question 66

What type of AKI will you see an enlarged kidney on US? may see small or polycystic kidney

Answer 66

large: Acute interstitial nephritis small/cystic: Hx of CKD