Proteinuria, Oliguria and Polyuria Flashcards

1
Q

Anuria

A

UOP <50-100 ml/day

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2
Q

Oliguria

A

UOP <400-500 ml/day

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3
Q

Polyuria

A

UOP >3000 ml/day

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4
Q

Azotemia

A

Elevated BUN without symptoms

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5
Q

Uremia

A

Elevated BUN w/ symptoms such as:

  • N/V
  • Confusion
  • Pruritus
  • Metallic Taste
  • Fatigue
  • Anorexia
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6
Q

CKD Criteria

A
  1. Markers of Kidney damage: Albuminuria, increased urine sediment, electrolyte/Renal Tubular disorder, kidney transplant
  2. Decreased GFR <60 ml/min/1.73m^2

Either or both for minimum 3 months

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7
Q

How would you distinguish CKD from AKI?

A

Time of symptoms:
<3 months= AKI
>3months= CKD

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8
Q

Briefly describe the stages of CKD

A

1-5: 1 is mild with >90 GFR; 5 is ESRD with <15 GFR

If GFR is between 60-90 (stage 1-2) but no symptoms, it’s not CKD

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9
Q

Top 4 RF for CKD

A
  1. DM
  2. HTN
  3. CVD
  4. AKI

Notable: NSAID use, Age>65, AA population

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10
Q

Clinical presentation of CKD

A
Edema
HTN
Oliguria/Anuria
Proteinuria
Uremia
Asterixis
Uremic Frost
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11
Q

3 tests to identify CKD

A
  1. eGFR
  2. Urine Albumin:Creatinine Ratio or PRO:Creatinine Ratio
  3. Urinalysis
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12
Q

What U/S findings are indicative of CKD?

A

Atrophic/small kidneys (normal= fist)
Cortical thinning (normal= >1cm)
Increased echogenicity
Elevated resistive index (renal artery stenosis)

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13
Q

Indications for dialysis

A
AEIOU: 
Acidosis
Electrolyte disturbance
Ingestion of toxins (GOLDMARK and ME DIE)
Overload volume
Uremia
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14
Q

2 tests to determine AKI

A

Serum Creatinine- increased
Urine Output- decreased

do not need to memorize stages, but know that Serum creatinine 1.5-1.9x starts and/or UO <0.5ml/kg/h starts stage 1

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15
Q

Common causes of prerenal AKI

A

Hypotension
Hypovolemia
Reduced CO (HF)
Systemic vasodilation (sepsis)

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16
Q

Causes of Postrenal AKI

A

Any obstruction

17
Q

What causes 85% of intrinsic AKI

A

ATN- ischemic or toxic

18
Q

What labs should you obtain on ALL AKI patients?

A

Urinalysis with microscopy

Urine albumin:creatinine ratio or pro:creatinine ratio

19
Q

How can FeNa help determine cause of AKI?

A

FeNa<1% is prerenal

FeNa>2% is ATN (intrinsic)

20
Q

When is FeUrea used over FeNa?

A

In patients on diuretics/fluids

21
Q

Urine Microscopy findings in ATN

A

epithelial cells, granular casts, waxy casts

22
Q

Urine Microscopy findings in AIN

A

WBC/WBC casts, eosinophils

23
Q

Complications associated with AKI

A

Hypervolemia
Electrolyte imbalance
Hyperuricemia
Acidosis

24
Q

Nephrotic syndrome definition

A
Proteinuria >3.5 g/day
Hypoalbuminemia
Edema
Hyperlipidemia
Lipiduria
25
Q

Important pathogenic cause of Nephrotic syndrome

A

Low renal perfusion leads to over activation of RAAS and increased Na+ and H2O retention

26
Q

Nephrotic Syndrome Ddx

A
  1. Diabetic Nephropathy
  2. Minimal Change Dz (children)
  3. FSGS (adults and some children)
  4. Membranous Nephropathy (adults)
27
Q

Nephritic Syndrome definition

A

Proteinuria <3.5 g/day
Hematuria
HTN
Active urinary sediment (RBC and casts)

28
Q

Nephritic Syndrome Ddx

A
  1. IgA nephropathy
  2. Thin BM Nephropathy
  3. MPGN
  4. Lupus Nephritis
  5. RPGN
  6. APGN (post-infectious)
29
Q

What labs would you order???

A

Just wanted to put in here that I’m sure we’ll get questions that lead us to a diagnosis and then ask what lab test to order.
For example: Pt looks like they have FSGS and are sexually active, order and HIV test

30
Q

Describe the 2 types of Diabetes Insipidus

A
  1. Central- lack of ADH in circulation. Corrects with administration of Vasopressin.
  2. Nephrogenic- lack of response to ADH. Does NOT correct with Vasopressin.
31
Q

MoA of ADH

A

Binds V2R on basolateral collecting duct cell and increases cAMP which drives insertion of AQP2 and Urea channels on apical membrane.
Effect: Increased Water resorption & urea (BUN:creatinine increased)

32
Q

Allison is prescribed Lithium because she’s unhinged. What can this possibly lead to?

A

Nephrogenic Diabetes Insipidus due to increased degradation of AQP2 channels.

33
Q

How does Calcium levels affect resorption?

A

Hypercalcemia leads to activation of Ca-sensor on basolateral membrane of TAL. This inhibits ROM-K channel which decreased NKCC2.
Similar to loop diuretic and Bartter Syndrome

34
Q

Explain results of Water Deprivation test for central and nephrogenic Diabetes Insipidus

A

Central: low urine osmolality that corrects with ADH
Nephrogenic: low urine osmolality that does not correct
Normal person: high urine osmolality that does not change with ADH administration.

35
Q

Treatment for Nephrogenic DI

A

Decrease solute intake
Thiazide diuretic
NSAIDs (inhibit PG’s because PG’s inhibit ADH)