2.2 Cs Exam 1: Acute Kidney Injury

Front 1

define: azotemia & uremia

Back 1

azotemia: acute retention of nitrogenous wastes

uremia: symptomatic renal failure (azotemia)

(pt needs dialysis)

Front 2

define: oliguria & anuria

Back 2

oliguria: Urine output <400-500 ml/day

anuria: Urine output <50-100 ml/day

Front 3

what is the cockcroft-gault formula?

what can't you use this formula for?

why?

Back 3

(140-age) x weight (kg)/ serum Cr x 72.

Can't use it for acute renal failure bc the renal function is not in a steady state.

you can use it for chronic kidney disease bc the renal function is steady.

Front 4

what two serum lab values are used to evaluate Acute Kidney Injury (AKI)?

what else is used?

Back 4

seum lab values: BUN and creatinine (cr is used to define acute kidney injury)

other: GFR

Front 5

what are the 3 categories of acute kidney injury?

Back 5

Pre-renal
intrinsic renal
post-renal

Front 6

what are the 4 main phases of urinary elimination of nitrogenous waste?

what category of acute kidney injury matches each phase?

Back 6

1) delivery to the glomerular capillaries via an adequate renal blood flow (pre-renal azotemia)
2) formation of plasma UF containing BUN and Cr (intrinsic azotemia)
3) normal tubular handling of the UF in its passage through the nephron into the collecting system (intrinsic azotemia)
4) excretion through a nonobstructed urinary tract (post renal azotemia)

Front 7

what is the MC cause of acute kidney injury?

Back 7

acute tubular necrosis (ATN)
approx- 45%

Front 8

what are the 3 etiologies of pre-renal azotemia?

Back 8

1. volume depletion: low intake, diarrhea, vomiting, NG tube suction, hemorrhage, burns

2. decreased effective arterial blood volume: CHF, liver dz w/ ascites, nephrotic syndrome, sepsis, 3rd spacing

3. alteration in intra-renal hemodynamics: primary renal vasoconstriction- hepatorenal syndrome or hypercalcemia, drug induced- NSAIDS & ACEI/ARB

Front 9

how do NSAIDs induce AKI?

ACE I?

Back 9

NSAIDs: inhibit Prostaglandins

--> constricts the afferent arteriole & worsens GFR.

ACEI: inhibits angiotensin II

--> dilates the efferent arteriole leading to dec back-pressure and worsening GFR.

Front 10

what are the 3 steps for pre-renal azotemia evaluation?

Back 10

hx
PE: skin turgor, dry mucous membranes, JG veins, orthostatics
Labs: FENA <1% (only reliable in oliguria)--> (UNa x PCr/ PNa x UCr) x 100, BUN/Cr ratio>20, hemoconcentration (elevated Hb and Hct)

Front 11

what are the 5 etiologies of intrinsic AKI?

Back 11

1. acute tubular necrosis- MC, ischemia, sepsis, or nephrotoxins

2. acute interstitial nephritis- drug induced, infection, systemic illness

3. acute glomerulonephritis

4. acute vascular syndromes

5. intratubular obstruction

Front 12

what 5 conditions can cause ischemi acute tubular necrosis?

Back 12

1. prolonged pre-renal azotemia
2. hypotension
3. hypovolemic shock
4. Cardiac arrest
5. cardiopulmonary bypass

Front 13

what 4 conditions can cause septic acute tubular necrosis?

Back 13

1. systemic hypotension
2. direct renal vasoconstriction
3. release of cytokines (TNF)
4. activation of neutrophils by endotoxin

Front 14

what are the 2 conditions that can cause nephrotoxic acute tubular necrosis?

Back 14

Drug induced (radiocontrast dye- very common, aminoglycosides, amphotericin B, cisplatin, acetaminophen)

pigment nephropathy (hemoglobin and myoglobin- mc : rhabdo)

Front 15

what would the labs show in a pt w/ ATN?
BUN/Cr ratio?
FENA?
urine sediment?

Back 15

BUN/Cr ration <10:1
FENA >2% (not seen in contrast nephropathy or rhabdomyolysis)
Urine sediment would show tubular epithelial cells and granular casts (muddy brown)*

*Serum Cr does NOT return to normal after fluid repletion (differentiates ATN from pre-renal disease where Cr would return to baseline)

Front 16

what causes acute interstitial nephritis?

What is the classic clinical triad associated with it?

Back 16

AKI d/t lymphocytic infiltration of the interstitium

clinical triad: fever+ rash+ eosinophilia (only found in 10%)

Front 17

what is the MC cause of acute interstitial nephritis?

what infections and systemic illnesses can cause acute interstitial nephritis?

Back 17

MC= drugs (71%)

infection: bacterial, viral, tb

systemic: sarcoid, sjogren's and TINU (tubulointerstitial nephritis and uveitis)

Front 18

what are the 3 steps for an acute interstitial nephritis evaluation?

Back 18

hx: involving a preceding illness or drug exposure
PE: fever, rash
Lab data: eosinophilia, eosinophiluria, and analysis of urine sediment- WBC's or WBC casts in the absence of a urine infection.

Front 19

what are the 3 indications for a renal biopsy of a pt w/ acute interstitial nephritis?

Back 19

-uncertainty of diagnosis
-advanced renal failure
-lack of recovery once drug is discontinued

Front 20

what is the tx of acute interstitial nephritis?

Back 20

discontinue offending drug,

tx underlying infection,

tx systemic illness

(^remove cause)

*steroid therapy in those pts who do not respond to conservative measures. Taper once serum Cr returns to baseline

Front 21

what 5 conditions or group of conditions fall under the category of acute glomerulonephritis?

Back 21

- postinfectious (post-streptococcal or endocarditis- associated)
- systemic vasculitis (ANCA-associated such as wegner's granulomatosis and microscopic polyangiitis) and mixed cryglobulinemia.
- Goodpasture's syndrome
- Lupus nephritis
- Rapidly progressive GN (crescentic GN)

Front 22

what are the four steps for acute glomerulonephritis evaluation?

Back 22

- analysis of urine sediment (dysmorphic RBC's, RBC casts)
- variable degree of proteinuria
- serologies (ANA, complement, hepatitis panel ANCA, anti-GBM, ASO titers, RPR)
- renal biopsy for definitive diagnosis***

Front 23

what 6 conditions cause hypocomplementemia in glomerular dz?

Back 23

postinfectious GN
lupus nephritis
membranoproliferative GN
mixed cryoglobinemia
atheroembolic renal dz
thrombotic thrombocytopenic purpura (last two are non-immune complex mediated renal dzes)

Front 24

what five vascular syndromes cause acute kidney injury?

Back 24

-renal artery thromboembolism
-renal vein thrombosis
-renal artery dissection
-atheroembolic renal dz
-thrombotic microangiopathies (HUS-TTP, scleroderma renal crisis and malignant HTN)

Front 25

what 2 conditions cause intratubular obstruction that can lead to acute kidney injury?

Back 25

- intratubular crystal deposition
* tumor lysis syndrome (uric acid)
* Ethylene glycol toxicity (calcium oxalate)
* Medication-associated (acyclovir and indinavir)

- intratubular protein deposition
* multiple myeloma (filtered light chains--> cast)

Front 26

what four conditions can cause in intrinsic upper tract obstruction leading to postrenal acute kidney injury?

extrinisc?

Back 26

intrinsic:

-nephrolithiasis
-papillary necrosis
-blood clot
-transitional cell cancer

extrinsic:

-retroperitoneal or pelvic malignancy

-retroperitoneal fibrosis

-endometriosis

-AAA

Front 27

what are the 7 conditions that can cause a lower tract obstruction that may lead to post renal AKI?

Back 27

BPH,

prostate CA,

transitional cell CA,

urethral stricture,

bladder stones,

blood clot,

neurogenic bladder

Front 28

what are the 2 steps for evaluating a postrenal AKI?

Back 28

- post void residual bladder volume: >100 ml c/w voiding dysfunction
- radiologic studies: Ultrasound*, CT, nuclear, retrograde pyelography, antegrade nephrostogram

Front 29

how do you tx a lower tract obstruction?

upper tract?

Back 29

lower: bladder catheter
upper: ureteral stents and/or percutaneous nephrostomies (straight into the bladder and drain the bladder from there)

Front 30

what are the tubular defects associated w/ obstructive nephropathy?

Back 30

-impaired concentrating ability
-impaired sodium reabsorption
-type 1 RTA (renal tubular acidosis): hyperkalemic acidosis d/t diminished distal hydrogen and potassium secretion

Front 31

what are the six risk factors for contrast nephropathy that leads to ATN (w/i 48 hrs of contrast)?

Back 31

- underlying renal failure
- DM nephropathy
- heart failure or other cause of reduced renal perfusion (hypovolemia)
- multiple myeloma
- high total dose of contrast
- high osmolality ionic agents

Front 32

what are the 3 ways used to prevent contrast nephropathy?

Back 32

low or iso-osmolal nonionic agents
isotonic saline (pre and post procedure)
acetylcysteine (harmless and inexpensive)

Front 33

what are the clinical manifestations of rhabdomyolysis?

Back 33

Renal failure
Muscle pain and weakness
Elevated CK (creatine kinase) level
Myoglobinuria
U/A: +blood but no RBC’s
Hyperkalemia and hyperphosphatemia
Hypocalcemia
Hyperuricemia
Elevated transaminases (ALT and AST)

Front 34

what are the 9 causes of rhabdomyolysis?

Back 34

Trauma or compression
Drugs (statins, fibrates, colchicine, coaine, heroin, opiods, alcohol)
Extreme exertion
Seizures
Alcoholism
Malignant hyperthermia
Neuroleptic malignant syndrome
Electrolyte abnormalities
Myopathies

Front 35

how do you tx rhabdomyolysis?

Back 35

isotonic saline (incr urine flow to protect kidney tubules from myoglobinuric damage)

Front 36

how do aminoglycosides cause nephrotoxicity? When does this usually occur?

Once discontinuing the drug, how long does renal recovery take?

Back 36

d/t accumulation and storage in the proximal tubular cells which induces damage.
AKI usually occurs after 5-7 days of therapy.
3 weeks.

Front 37

what are the 5 renal manifestations of hypercalcemia?

Back 37

-direct renal vasoconstriction
-volume contraction
-chronic hypercalcemic nephropathy (nephrocalcinosis)
-nephrolithiasis
-nephrogenic diabetes insipidus

Front 38

in ambulatory pts, what is the etiology of hypercalcemia?

How about in hospitalized pts?

Back 38

ambulatory: primary hyperparathyroidism
hospitalized: malignancy

Front 39

how do you tx hypercalcemia?

Back 39

-isotonic saline (for volume deficiency)
-loop diuretics (for volume overload)

-calcitonin (limited to first 40 hrs)
-bisphosphonates (zolendronate over pamidronate)** definitive tx

Front 40

Pt presents to your office after mitral valve replacement surgery.

He has cyanotic digits, livedo reticularis and his kidneys are failing. dx:

and what is the pathognomic sign for this disease?

Back 40

Atheroembolic renal dz

Pathognomonic: biconvex cholesterol clefts.

Can also have Ischemic bowel, eosinophilia, eosinophiluria and hypocomplementemia.

Front 41

how do you tx the ANCA positive vasculitis?

Which ANCA positive vasculitis involves the respiratory tract?

which one causes pauci-immune glomerulonephritis?

Back 41

cyclophosphamide and steroids

Respiratory tract: Wegener's granulomatosis polyangitis

pauci-immune glomerulonephritis: Microscopic polyangiitis.

Front 42

pt presents which hemoptysis and kidney failure. You draw blood and find Anti-GBM ab in serum. Renal biopsy shows linear deposition of IgG along the glomerular capillaries.

Dx,

tx,

what are the circulating Abs directed against?

Back 42

Dx: Rapidly progressive crescentic glomerulonephritis---- Goodpasture's syndrome

tx: plasmapheresis combined w/ cyclophosphamide and steroids

Circulating abs are directed against the alpha 3 chain of type 4 collagen found in the alveolar and glomerular basement membranes.

Front 43

what are the 3 hep C associated renal diseases? and how do you tx them?

Back 43

-Mixed cryglobulinemia
-membranoproliferative glomerulonephritis
-membraneous nephropathy

Tx: aimed against Hep C virus. If CrCl> 50 (give pegylated interferon alpha and ribavirin), if CrCl <50 (give nonpegylated interferon alpha)

Front 44

what are the 3 types of lupus nephritis that require tx?

WHat is the tx?

Back 44

severe focal proliferation
diffuse proliferative
membranous

tx: immunosuppressive tx

cyclophosphamide and steroids (mycophenolate may be more efficacious than cyclophosphamide)

Front 45

what are the 5 indications for dialysis?

Back 45

uremic syndrome
uncontrollable hyperkalemia
severe metabolic acidosis
refractory fluid overload
severe renal failure (BUN > 100 or Cr>10)

Front 46

What are the associated signs and sxs of uremic syndrome?

Back 46

signs: pericardial friction rub or pericardial effusion, tremors, asterixis (flapping tremor or liver flap), myoclonus, wrist or foot drop, seizures, and bleeding tendency (diathesis)

sxs: N/V, poor appetite, fatigue/lethargy, pruritis and altered mentation

Front 47

what is winter's formula?

Back 47

respiratory compensation for a metabolic acidosis

PCO2= 1.5 x (HCO3) + 8 (+/-2)

eg:
HCO3= 20, expected PCO2= 36-40

Front 48

what is the pathophysiology of hepatorenal syndrome?

Back 48

-portal HTN
-splanchnic vasodilatation
-arterial underfilling and systemic vasodilatation
- hepatorenal reflex- stim of vasoconstrictor systems
-renal vasoconstriction

Front 49

pt presents in your ICU which rapidly progressive renal failure. The pt is oliguric and anuric. Dx

Back 49

Hepatorenal syndrome type I, median survival 2 weeks

Front 50

pt presents in your ICU which slowly progressive and indolent renal failure over months. His ascites is resistant to diuretics. Dx

Back 50

type II hepatorenal syndrome

Front 51

what is the criteria for hepatorenal syndrome?

Back 51

-acute/chronic liver dz w/ portal HTN
-low GFR
-r/o other causes* dx of exclusion
- lack of renal improvement despite diuretic withdrawal and volume expansion
-oliguria
-urine Na <10 mEq/L
-proteinuria <500 mg/day

Front 52

how do you tx hepatorenal syndrome?

Back 52

midodrine (selective alpha 1 agonist--- systemic vasoconstriction)
octreotide (somatostatin analog, inhibitor of endogenous vasodilator release)
albumin and vasopressin
liver transplant in appropriate candidates

Front 53

what are the 5 components of tumor lysis syndrome?

Back 53

hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia and AKI

Front 54

when do you usually see tumor lysis syndrome?

when do you usually see AKI associated w/ these circumstances?

Back 54

in lymphomas and leukemias

both spontaneously (AKI d/t acute uric acid nephropathy w/ a lack of hyperphosphatemia) and post-chemotherapy (AKI d/t severe hyperphosphatemia)

Front 55

what are the 3 ways you can prevent tumor lysis syndrome in your pt? How do you tx tumor lysis syndrome?

Back 55

Prevent:

allopurinol
rasburicase
0.9 NS IVF (hydration-->high urine output)

tx: IVF hydration and diuretics (to wash out obstructing uric acid crystals),

rasburicase, hemodialysis if oligoanuric (removes uric acid), and CRRT (continuous renal replacement therapy)-- preferred in hyperphosphatemic renal failure, will avoid the rebound hyperphosphatemia seen w/ intermittent hemodialysis.

Front 56

what is the most common renal diagnosis in pts w/ multiple myeloma?

what does it cause?

Back 56

Cast nephropathy- binding of Tamm-Horsfall mucoprotein (normally synthesized in the TAL of loop of henle) causing direct tubular injury w/ intratubular cast formation and obstruction

Front 57

what is the difference between AL amyloidosis assoc w/ multiple myeloma and light chain deposition disease?

Back 57

In AL Amyloidosis--> Light chain fragments form Congo red Positive B-pleated fibrils,

in LCDD they do not form fibrils and their deposits are congo red negative.

Front 58

what are the three signs of fanconi syndrome? what is fanconi syndrome d/ t?

Back 58

proximal RTA
phosphate wasting
hypouricemia

d/t: reabsorption of filtered light chain in proximal tubules-->

intracellular crystal formation-->

impaired proximal tubular function.

Front 59

what are the 5 features associated w/ TTP-HUS?

Back 59

-microangiopathic hemolytic anemia*
-thrombocytopenia*
- AKI
- neurologic abnormalities
- fever

Front 60

what are the causes of TTP-HUS?

Tx?

Back 60

MC- idiopathic
shiga-toxin producing E. coli
Drugs: quinine, ticlid, cyclosporine, mitomycin
pregnancy/ post partum
HIV
sepsis
postcardiac bypass

Tx: plasma exchange