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?

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
What is the cause of WBCs, RBCs, bacteria in urin?
UTI
26
What is the treatment of AKI?
depends on etiology correct underlying issue supportive (fluids, renal replacement, avoid hypotension and nephrotxins)
27
What are the key features of NephrOtic syndrome?
\>3.5g/day of Protein hypoalbumemia edema hyperlipidemia lipiduria **\*if albumin is normal, pt does not have nephrotic syndrome**
28
How is nephrOtic syndrome diagnosed?
Renal biopsy
29
How is nephrItic syndrome defined? What key feature is seen in urine?
Hematuria HTN minimal proteinuria renal failure common \*Active urinary sediment (casts)
30
How is nephrItic syndrome diagnosed\>
renal biopsy
31
What is a common urinary symptom of diabetes inspidus?
Polyuria (solute diuresis or water diuresis)
32
What can cause solute diuresis?
glucosuria (hyperglycemia) urea (resolution of aztoemia) sodium (IVF) mannitol (tx of ICP)
33
What can cause water diuresis?
primary polydipsia central or nephrogenic Diabetes inspidus
34
How is ADH released in response to increased serum osmolality? How is ADH released in response to decreased BP or increased BV?
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
When ADH is released, what does it bind to? How does this relate to dehydration?
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
What is central diabetes insipidus?
caused by decreased release of ADH usually idiopathic
37
What is nephrogenic diabetes inspidus?
caused by decreased response to antidiuretic hormone (ADH) rare hereditary form seen in children can be caused by lithium or hypercalcemia
38
how does hypercalcemia lead to polyuria? Then how does it cause nephrogenic DI?
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
How is DI diagnoseD?
24hr urine volume collection urine osm \<300 water deprivation test
40
how is DI treated? how is hypernatremia treated?
**central**-give vasopressin **nephrogenic**-decrease solute intake, thiazide diuretics, NSAIDs, vasopressin **hypernatremia**-replace free water deficit with water or IV D5W