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GU > Acute Kidney Injury - Exam 1 > Flashcards

Acute Kidney Injury - Exam 1 Flashcards

1
Q

What are the normal culprits behind an acute kidney injury?

A

inability to manage: fluid, electrolytes and acid base balance

decreased excretion of urea and creatinine

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2
Q

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

A

serum Cr

GFR

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3
Q

What criteria for dx AKI is used most commonly?

A

KDIGO

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4
Q

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

A

normal: 800-2000 mL/day

**anuria: less than 50mL

**oliguria: less than 400mL

polyuria: excessive urine 2500-3000mL +

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5
Q

What does anuria make you think is the underlying cause?

A

Acute obstruction, cortical necrosis, aortic dissection

aka very bad finding!!

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6
Q

Define azotemia

Define uremia

A

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)

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7
Q

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

A

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

intra-renal

post-renal

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8
Q

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

A

intrinsic kidney: direct injury

postrenal obstruction- LEAST common
caused by obstruction of urinary flow

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9
Q

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

A

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
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10
Q

What arteriole does angiotensin II prefer?

A

works on both but prefers Efferent arteriole

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11
Q

What affect do NSAIDs have on the kidney?

A

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

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12
Q

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

A

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

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13
Q

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

A

Tamm-Horsfall mucoprotein

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14
Q

What is the treatment for prerenal azotemia?

A

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

Maintain euvolemia
Correct abnormal electrolytes
Avoid nephrotoxic drugs

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15
Q

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

A

BPH

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

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16
Q

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?

A

post renal obstruction

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

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17
Q

What am I?

A

renal US showing hydronephrosis

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18
Q

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

A

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

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19
Q

In postrenal AKI where is the obstruction more common?

A

in the lower abdomen

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20
Q

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

A

tubular injury

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

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21
Q

What are the 3 major causes of acute tubular necrosis?

A

ischemia
nephrotoxins
sepsis

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22
Q

in ATN, what is ischemia characterized by?

A

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

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23
Q

endogenous or exogenous more commonly cause ATN?

A

Exogenous more commonly cause damage

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24
Q

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

A
  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

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25
Q

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

A

Can remain in renal tissues up to 1 month

Trough levels are most useful to predict toxicity

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26
Q

Give some examples of endogenous nephrotoxins

A

myoglobinuria due to rhabdomyolysis

hemoglobinuria

hyperuricemia

bence jones protein

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27
Q

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

A

due to rhabdomyolysis, muscle necrosis

Crush injury, muscle necrosis from prolonged unconsciousness

CK >20,000-50,000 IU/L

28
Q

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

A

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

**rehydration

29
Q

______, ______ and ______ may also occur with myoglobinuria

A

Hyperkalemia, hyperphosphatemia, hyperuricemia may also occur

30
Q

When is hemoglobinuria commonly seen? What is the tx?

A

Seen in transfusion reactions and hemolytic anemia

Tx - Reversal of underlying disorder, hydration

31
Q

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?

A

in rapid cell turnover and lysis

Usual cause - chemo

Serum uric acid often > 15-20 mg/dL

gout: uric acid between 6-7

32
Q

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

A

directly toxic, obstructs tubules

Seen in association with multiple myeloma

33
Q

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

A

￬ 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

34
Q

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

A

Treatment - remove cause, avoid complications

avoid: volume overload and hyperkalemia (loop diuretics or dialysis)

protein restrict

35
Q

Why do you need to restrict protein in ATN?

A

Protein restriction - to prevent metabolic acidosis

36
Q

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

A

nonoliguric ATN has been long term outcomes

37
Q

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

A

False!! some may never fully recover baseline kidney function

38
Q

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

A

5%

nephritic in nature so inflammation is involved

nephrotic: minimal inflammation with proteinuria (think chronic cases)

39
Q

Almost all acute glomerulonephritis involves the development of _______

A

inflammatory glomerular lesions

40
Q

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

A

severe breaks in glomerular walls

acute glomerulonephritis

41
Q

HTN, edema, and urine containing protein, RBCs, WBCs, and RBC casts

What am I?

A

Acute Glomerulonephritis

42
Q

Name 5 types of glomerulonephritis?

A

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

43
Q

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

A

Immune Complex Deposition

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

44
Q

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

A

Post-infectious (especially seen with endocarditis and streptococcus

lupus

45
Q

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?

A

Anti-GBM-associated

lungs

Goodpasture’s Syndrome - renal + pulmonary involvement

46
Q

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

A

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

47
Q

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

A

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

48
Q

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

A

Pauci-Immune Glomerulonephritis

cell-mediated immune processes

49
Q

What is ANCA?

A

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

50
Q

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?

A

Pauci-Immune Glomerulonephritis

lungs, skin, upper airway

51
Q

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

A

HTN and edema

scrotum and periorbital

52
Q

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

A

Urine sediment - RBCs, WBCs, RBC casts

Urinalysis - hematuria, moderate proteinuria

53
Q

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

A

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

54
Q

What is the tx for AG?

A

treat the underlying disease process!

High-dose corticosteroids
Cytotoxic agents may be used
Plasma exchange - Goodpasture disease, pauci-immune glomerulonephritis

55
Q

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

A

Goodpasture disease and pauci-immune glomerulonephritis

56
Q

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

A

inflammation of the interstitium that surrounds the tubules

cell-mediated immune reactions predominate

57
Q

Must _____ in order to confirm acute interstital nephritis

A

bx!! but not done regularly because it is painful

58
Q

What is the biggest cause of AIN? Give some examples

A

medications!!

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

59
Q

What are some infectious causes of AIN?

A

Bacterial - strep, staph, diphtheria, legionella, rickettsia (RMSF)

Viral - CMV, EBV

Fungal - histoplasmosis

60
Q

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

A

SLE, Sjogren’s, sarcoidosis, etc.

More commonly cause glomerulonephritis

61
Q

Fever
rash
eosinophilia
WBCs (95%), RBCs, eosinophiluria, WBC casts

What am I?
What will they NOT have if it is NSAID related?

A

acute interstitial nephritis

fever commonly absent if it is NSAID related

62
Q

What is the classic triad of AIN?

A

fever, rash, arthralgia

All 3 only present in 10-15% of pts

63
Q

What is the tx for AIN?

A

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

64
Q

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

A

acute interstitial nephritis because the nephrons are spared

65
Q

Draw the Jensen chart about types of kidney injury

A
66
Q

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

A

large: Acute interstitial nephritis

small/cystic: Hx of CKD

67
Q
A

GU (13 decks)

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