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CPR II Exam 3 > Approach to Proteinuria, Oliguria, and Polyuria > Flashcards

Approach to Proteinuria, Oliguria, and Polyuria Flashcards

1
Q

What are the criteria for CKD?

A

Markers or kidney damage OR decreased GFR

for greater than 3 months

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2
Q

What is the criteria for AKI?

A

GFR less than 60 and/or markers of kidney damage

less than 3 months

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3
Q

In the absence of kidney damage neither GFR category stage 1 or stage 2 can fulfill the criteria for what condition?

A

CKD

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4
Q

What are the risk factors for CKD?

What is the major cause?*

A

DM*

HTN*

CVD

AKI

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5
Q

What are some s/s of CKD?

A

often asymptomatic

Edema

HTN

decreased UOP

Foamy urine (proteinuria)

uremia (n/v/confusion, metalic taste)

Pericardial friction rub

asterixis

uremic frost

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6
Q

What are the three simple tests to ID most CKD pt’s?

A

eGFR

urine-albumine-to-creatinine ratio or urine protien-to-creatinine ratio

urinalysis

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7
Q

What renal U/S findings are significant for CKD?

A

atrophic or small kidneys

cortical thinning

increased echogenicity

elevated resistive indices

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8
Q

What is renal replacement therapy?

A

hemodialysis

peritoneal dialysis

renal transplantation

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9
Q

What are the indications for dialysis?

AEIOU

A

A-severe acidosis

E-Electrolyte disturbance

I-Ingestion

O-volume Overload

U-Uremia

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10
Q

staging of AKI is based on what two things?

A

Serum Creatinine

or

Urine Ouput

(whichebver is worse)

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11
Q

What will a prerenal etiology of AKI look like?

A

hypotension

hypovolemia

reduced cardiac output with HF, tamponade or PE

systemic vasodilation (sepsis, SIRS, hepatorenal)

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12
Q

What will a postrenal etiology of AKI look like?

A

bladder outlet obstruction (BPH, cancer)

ureteral obstruction (stones, malig., fibrosis)

renal pelvis issues (stones, necrosis)

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13
Q

What are the three intrinsic etiologies of AKI?

A

ATN (ischemia > toxins)

Interstitial nephritis

Glomerulonephritis

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14
Q

What are the s/s of AKI?

A

Same as CKD

(duration is shorter)

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15
Q

What are the common diagnostic tests for AKI?

A

UA with micro

Urine alb/cr ratio or protein/cr ratio

Renal US

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16
Q

What BUN/Cr ratio is suggestive of PRerenal Azotemia?

A

>20:1

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17
Q

What FENA score indicates prerenal azotemia and ATN?

A

<1% prerenal azotemia

>2% ATN

18
Q

What FeUrea indicates prerenal azotemia and aTN?

A

<35% prerenal azotemia

>50% ATN

19
Q

If you see renal tubular epithelial cells, transitional cells, granular or waxy casts in the urine, what is the cause?

A

ATN

20
Q

If you see WBC, WBC casts, or urine eosinophils int he urine what is the cause?

A

AIN or pyelonephritis

21
Q

IF you see dysmorphic RBCs or RBC casts in the urine what is the cause?

A

vasculitis or glomerulonephritis

22
Q

If you see proteinuria <3.5g/day, hematuria, dysmorphic RBCs and casts what is the cause?

A

NEphritic syndrome

23
Q

If you see heavy proteinuria >3.5g/day, lipiduria, minimal hematuria, what is the cause?

A

NephrOtic syndrome

24
Q

What is the cause of hyaline casts?

A

nonspecific, prerenal azotemia

25
Q

What is the cause of WBCs, RBCs, bacteria in urin?

A

UTI

26
Q

What is the treatment of AKI?

A

depends on etiology

correct underlying issue

supportive (fluids, renal replacement, avoid hypotension and nephrotxins)

27
Q

What are the key features of NephrOtic syndrome?

A

>3.5g/day of Protein

hypoalbumemia

edema

hyperlipidemia

lipiduria

*if albumin is normal, pt does not have nephrotic syndrome

28
Q

How is nephrOtic syndrome diagnosed?

A

Renal biopsy

29
Q

How is nephrItic syndrome defined?

What key feature is seen in urine?

A

Hematuria

HTN

minimal proteinuria

renal failure common

*Active urinary sediment (casts)

30
Q

How is nephrItic syndrome diagnosed>

A

renal biopsy

31
Q

What is a common urinary symptom of diabetes inspidus?

A

Polyuria (solute diuresis or water diuresis)

32
Q

What can cause solute diuresis?

A

glucosuria (hyperglycemia)

urea (resolution of aztoemia)

sodium (IVF)

mannitol (tx of ICP)

33
Q

What can cause water diuresis?

A

primary polydipsia

central or nephrogenic Diabetes inspidus

34
Q

How is ADH released in response to increased serum osmolality?

How is ADH released in response to decreased BP or increased BV?

A

serum osmolality is detected by osmoreceptors in the anterior hypothalamus which causes ADH release

These are sensed by the arterial baroreceptors and atrial stretch receptors leading to ADH release

35
Q

When ADH is released, what does it bind to?

How does this relate to dehydration?

A

binds to V2R and increased cAMP leading to insertion of AQP2 and urea transporters on the apical membrane

In dehydration, this is why urea levels increase

36
Q

What is central diabetes insipidus?

A

caused by decreased release of ADH

usually idiopathic

37
Q

What is nephrogenic diabetes inspidus?

A

caused by decreased response to antidiuretic hormone (ADH)

rare hereditary form seen in children

can be caused by lithium or hypercalcemia

38
Q

how does hypercalcemia lead to polyuria?

Then how does it cause nephrogenic DI?

A

basolateral calcium sensor (CaSR) in TAL leads to inactivation of luminal K channel which inactivates NKCL2 transporter (like a loop diuretic)

in the CD on the apical membrane, the CaSR is activated by high Ca levels. The CaSR induces degradation of the AQP2 channels leading to nephrogenic DI

39
Q

How is DI diagnoseD?

A

24hr urine volume collection

urine osm <300

water deprivation test

40
Q

how is DI treated?

how is hypernatremia treated?

A

central-give vasopressin

nephrogenic-decrease solute intake, thiazide diuretics, NSAIDs, vasopressin

hypernatremia-replace free water deficit with water or IV D5W

CPR II Exam 3 (17 decks)

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