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Heme/Onc/Renal > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

Chronic kidney disease is the presence of kidney damage for 3 months or more, usually detected as which lab value?

A

Urinary albumin greater than 30 mg/day

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2
Q

There are three characteristic “failures” in chronic kidney disease. These are?

A
  1. ) Excratory failure (accumlination of excess nitrogen)
  2. ) Regulatory failure (abnormal conservation or excretion of fluids and electrolytes)
  3. ) Biosynthetic failure (inadequate production of ammonia, Vit. D, or EPO
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3
Q

Measures the amount of plasma filtered across glomerular capilaries (mL/min)

A

GFR

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4
Q

A normal GFR is?

A

120 ml/min/1.73 m2

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5
Q

A product of muscle breakdown produced at a relatively constant rate

  • freely filtered by glomeruli
  • Minimal to no reabsorption
  • 10% secretion
A

Creatinine

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6
Q

Overestimates GFR slightly

A

Creatinine

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7
Q

GFR declines with age, but creatinine tends not to change due to parallel decrease in?

A

Muscle mass

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8
Q

What is the Schwartz equation for estimating GFR in children ages 1 to 17?

A

eGFR = 0.413 x height

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9
Q

A cysteine protease produced by all cells that is completely filtered by the glomeruli

  • New method for GFR calculation
  • Not readily available
A

Cystatin C

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10
Q

The BUN to creatinine ratio is usually 10-15:1. This ratio is disproportionally increase in which 6 situations?

A

Volume depletion, GI bleeding, Corticosteroid use, High protein diet, Obstruction, or any catabolic state

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11
Q

BUN is disproportionally decreaed in which 3 situations?

A

Low protein diet, Liver disease, Malnutrition

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12
Q

Increased glomerular permeability to macromolecules and is a marker of kidney damage when persistently elevated

A

Proteinuria in CKD

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13
Q

Increased Urinary Albumin Excretion is a sensitive marker for CKD due to which three diseases?

A

DM, GN, and HTN

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14
Q

A history of prior abnormal renal function/progression is of utmost importance in the evaluation of?

-i.e. prior abnormal urinalyses to distinguish from AKI

A

CKD

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15
Q

In addition to prior history of kidney damage, two other important factors of evaluating CKD are?

A

GFR estimate (eGFR) and Albuminuria/Proteinuria

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16
Q

Ultrasound of kidneys in CKD typically shows?

A

Small and echogenic kidneys

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17
Q

What are 5 major laboratory findings in CKD?

A

Elevated BUN and creatinine, Anemia, Metabolic Acidosis, and Hypocalcemia/hyperphosphatemia

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18
Q

In CKD, we may see a urinary sediment containing red blood cells, leukocytes, and casts, which may indicate

A

GN, tubulointerstitial disease, vascular disease, or urologic disorders

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19
Q

In the progression of renal disease, we see endothelial damage in the form of detachment of

A

Glomerular epithelial cells

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20
Q

In the progression of renal disease, we see production of

A

Cytokines

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21
Q

This results in further nephron dropout setting up a cycle leading to

A

ESRD

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22
Q

In CKD, we want to reduce blood pressure to?

  1. ) Normal Case?
  2. ) With significant proteinuria?
A
  1. ) Less than 140/80

2. ) Less than 130/80

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23
Q

Have benefits beyond their degree of BP lowering and are more effective with low salt diet or addition of diuretics

A

ACE inhibitors

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24
Q

In type II DM with CKD, we especially want to treat with

A

ARBs

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25
Q

Is it recommended to use ACEi’s and ARBs?

A

NO

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26
Q

7-10 days following initiatin of ACEi or ARB, we need to check BMP for?

A

Creatinine, and K+

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27
Q

Inhibition of agiotension II (by use of ACE inhibitors) slows deterioration in CKD by?

-This decreases proteinuria

A

Decreasing intraglomerular hypertension and changing glomerular barrier size

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28
Q

The benefit of ACEi’s is mostly seen in patients with significant

A

Proteinuria

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29
Q

We want to recommend a low protein diet in CKD patients with GFR values of

A

Less than 30-60

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30
Q

May play a role in the hyperfilitration seen in recently giagnosed DM

A

IGF-1

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31
Q

In DM, we can prevent progression to CKD with?

-Prevents transition to macroalbuminuria

A

RAS inhibition

32
Q

A major risk factor for long-term loss of kidney function is?

A

Acute Kidney Injury (AKI)

33
Q

An episode of AKI increases risk of developing CKD

A

4x

34
Q

Metabolic Acidosis is one thing that can cause CKD progression, we can slow this with

A

NaHCO3 suplementation

35
Q

Normally, we filter about 25,000 mEq of Na per day and excrete about 100-150 mEq. So normal FENa is

A

Less than 1%

36
Q

We need to excrete progressively larger fractions of filtered load to stay in balance on usual intake as

A

GFR decreases

37
Q

In CKD, urine osmolarity may be fixed at

A

300 mOsm/kg

38
Q

In CKD, we see an increase in stool excretion of

A

K+

39
Q

K+, Na+, and Water restriction are all important in

A

CKD

40
Q

In HYPERkalemia, we can stabilize cardiac conduction by treating with

A

Calcium Gluconate

41
Q

In HYPERkalemia, we can help move K+ INTO cells, by treating with which three things?

A

Glucose and insulin, NEbuized albuterol, and HCO3-

42
Q

We can also treat HYPERkalemia with cation exchange resins such as?

A

Kayexelate (Na+ polystyrene sulfonate), and Veltassa (patiromer)

43
Q

Common in CKD when eGFR is less than 25ml/min

-Due to decreased ammonia excretion

A

Metabolic Acidosis

44
Q

In patient’s with normal renal function, even a SLIGHT decrease in plasma HCO3- induces tubular cells to

A

Increase NH4 production and H+ secretion

45
Q

For patient’s withg CKD, we need to maintain HCO3- in normal range using non K+ containing HCO3- cupplements or citrate salts such as

A

Bicitra or Shohl’s

46
Q

In CKD, we can also see problems with bone and mineral metabolism due to

A

Hyperparathyroidism and renal osteodystrophy

47
Q

A systemic disorder of mineral and bone metabolism due to CKD

A

Mineral bone disease

48
Q

Characterized by abnormalities of Ca2+, phosphorus, PTH, Vit D, bone turnover, etc

A

Mineral bone disease

49
Q

In serum of patients with Mineral Bone Disease, we will often see a

A

Lower serum Ca2+, Elevated serum PO4, and Elevated PTH

50
Q

Secreted by osteocytes and promotes renal phosphate excretion

A

Fibroblast Growth Factor 23 (FGF 23)

51
Q

Levels increased early in CKD, stimulated by elevated serum PO

A

FGF 23

52
Q

Increases renal PO4 excretion, stimulates PTH, supresses 1,25 di(OH) Vit. D, diminishing PO4 absorption from intestine

A

FGF 23

53
Q

What are the three major types of Mineral Bone Disease (MBD)?

A

Osteitis fibrosa cystica, Adynamic bone disease, Osteomalacia

54
Q

Most common form of MBD due hyperparathyroidism and osteoclast simulating efects of PTH

-high turnover type

A

Osteitis fibrosa cystica

55
Q

Characterized by low turnover, spontaneously low PTH procution or iatrogenic suppression

-Sometimes caused by aluminum toxicity

A

Adynamix bone disease

56
Q

Lack of bone mineralization. In the past was associated with Al toxicity, hypovitaminosis D

A

Osteomalacia

57
Q

Frequently asymptomatic, but may manifest as joint pain and stiffness, spontaneous tendon rupture, and predisposition to fracture

A

CKD MBD

58
Q

We also see extra skeletal calcifications in

A

CKD MBD

59
Q

With stage 3-5 CKD, our goals we want to:

  1. ) Correct?
  2. ) Control?
A
  1. ) 25OH Vit D deficiency

2. ) Control Phosphorus

60
Q

We can treat with calcium carbonate and calcium acetate which are

A

Phosphate binders

61
Q

Sevelamer carbonate; lanthanum carbonate; ferric

citrate (Auryxia); and sucoferric oxyhydroxide (Velphoro) are

A

Noncalcium phosphate binders

62
Q

To help increase Vit. D, we can take which three things?

A

Calcitriol, Doxacaldiferol, and paricalcitol

63
Q

Increases sensitivity of parathyroid calcium sensing receptor to suppressive effect of calcium

A

Cincacalet (ESRD)

64
Q

Almost universal with severe CKD when creatinine is greater 2-3 mg/dl

A

Anemia

65
Q

CKD anemia is classified as

A

Nomorchromic and normocytic

66
Q

CKD anemia is multifactorial but the major component is decreased

A

EPO production

67
Q

Binds to erythroid progenitors causing differentiation to erythrocytes

A

EPO

68
Q

Impairs activity, nutrition, quality of life, and contributes to LVH, and high output CHF

A

Anemia

69
Q

Pre-dialysis (mean hemoglobin 10.1), we can treat with

A

EPO stimulating agent

70
Q

Worsened if hematocrit is raised too quickly

A

Hypertension

71
Q

Our goal Hgb 10-12 g/dL because studies show that in CKD we have increased risk of stroke and higher CV with

A

Hgb above 13

72
Q

Clinical manifestation of severe kidney failure characterized by accumulation of organic waste products normally cleared by the kidney

A

Uremia

73
Q

The surrogate markers for uremia are

A

BUN/creatinine

74
Q

We refer patient for transplant evaluation when GFR is

A

Less than 20

75
Q

Nausea, anorexia, uncontrolled hyperkalemia, and uncontrolled volume overload are some indications for

A

Dialysis

76
Q

What are 4 modalities for ESRD?

A
  1. ) Hemodialysis
  2. ) Peritoneal dialysis
  3. ) Conservation management
  4. ) Transplant

Heme/Onc/Renal (3 decks)

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