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PHAR 255 > Kidney's > Flashcards

Kidney's Flashcards

1
Q

What are the Functions of the kidney’s? (3)

A

Excretory:
- filtration, secretion, excretion
Endocrine:
- renin, prostaglandins, kinins, erythropoeitin
Metabolic:
- Vit D activation, gluconeogenesis, insulin metabolism

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2
Q

What excretory functions do the kidneys have?

A

REgulate fluids, electrolytes, and acid-base balance
Remove metabolic waste products and foreign chemicals from blood for urinary excretion.

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3
Q

Explain the filtration process of the kidneys.

A

Blood enters glomerulus through afferent arteriole
Blood filtered by hydrostatic pressure through capillaries that for from the glomerulus into the bowman capsule
Blood leaves kidney through efferent arteriole

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4
Q

What is the filtrate composed of?

A

~20% of plasma entering glomerulus, mainly fluids, electrolytes, small molecules
Excludes proteins and large molecules

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5
Q

What arteriole does unfiltered blood enter in the kidneys?

A

Afferent

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6
Q

What arteriole does filtered blood leave the kidney from?

A

Efferent

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7
Q

What are some examples of filtrates in the urine?

A

Glucose
Electrolytes
AA’s
Water
Urea
Uric acid
Creatinine
Protein (some not alot)

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8
Q

What is reabsorption?

A

Movement of substances out of rena tubules back into the blood capilaries

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9
Q

What is secretion?

A

Substances move out of the blood and into the tubules to be converted into urine

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10
Q

How are substances secreted?

A

Active transport or
Difusion across the membrane

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11
Q

Which organs regulate acid-base balance? How?

A

Kidneys: hydrogen ion secretion, bicarbonate reabsorption, phosphate and ammonia buffer systems
Lungs: alveolar ventilation of CO2

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12
Q

What is acidosis?

A

In response to excess acid, kidneys reabsorb all filtered bicarbonate and produces new bocarbonate

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13
Q

What is alkalosis?

A

In response to little acid, kidneys excrete bicarbonate to restore H+ [ ] to normal

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14
Q

What kinds of waste do the kindeys excrete?

A

Waste products from protein metabolism and muscle contraction,
Certain drugs

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15
Q

What hormones to the kidney’s produce?

A

BP control
RBC production

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16
Q

What BP control mechanisms are in place?

A

RAAS
Antidiuretic hormone
Atrial natriuretic peptide

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17
Q

Where is renin released from?

A

renal juxtaglomerular cells b/c of decreased BP

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18
Q

What can renin indirectly lead too?

A

Vasoconstriction amd Na/ water rentention

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19
Q

What are the effects of Angiotensin II?

A

Kidney’s: Na retention and water retention
Brain: release corticotropin and adiuretin, thirst
Adrenals: Aldosterone production increased
Blood Vessels: Vasoconstriction and increased BP

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20
Q

What arteriole does ANG II vasoconstrict?

A

Efferent

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21
Q

What do prostaglandin E2 and I2 do?

A

Cause vasodilation especially at the afferent arteriole to increase renal perfusion
Promotes secretion of renin

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22
Q

When are prostaglandins produced (E2 and I2)

A

In response to decreased blood flow

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23
Q

Where is adosterone secreted from?

A

the adrenal cortex in response to ANG II

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24
Q

What does aldosterone stimulate?

A

Tubule reabsorption of sodium
Indirectly increases K excretion, and H+

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24
Q

Where is ADH secreted from?

A

Posterior pituitary in response to increased Na blood levels/ low blood volume

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25
Q

What does ADH do?

A

promotes water reabsorption by increasing permeability of collecting ducts.

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26
Q

Where is ANP stored?

A

Right atrium of the heart

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27
Q

When is ANP released?

A

In response to increased stretch of the heart muscle; indicative of fluid overload
Is elevated in HF

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28
Q

What does ANP do?

A

Opposes RAAS by causing vasodilation and increased renal excretion of sodium
(Opposite of aldosterone)

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29
Q

What does erythropoeitin do?

A

Stimulates production of RBCs

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30
Q

What % of erythropoeitin is produced by the kidney’s?

A

90%

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31
Q

What area of the kidney produces erythopoetin?

A

Peritubular interstitial cells

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32
Q

What does a lack or deficiency of erythropoeitin lead to in CKD?

A

Anemia

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33
Q

What enzyme in kidney turns calcidiol to calcitriol?

A

1-alpha-hydroxylase

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34
Q

What upregulates /dowregulates to production of calcidiol to calcitriol?

A

Up PTH, low Phosphate
Down: Calcitriol

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35
Q

What is gluconeogenisis?

A

Creation of glucose from AA’s
Most occurs in liver but, some occurs in cortex of kidneys

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36
Q

Why do we check renal function? (3)

A

Monitoring and recognizing CKD
- effects of drugs on slowing progression
- predict time to onset of ESRD
- Evaluating riskof complications
Adjust doses of meds excreted by the kidneys
Monitoring nephrotoxic medications

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37
Q

What protein do we use to measure GFR?

A

Creatinine

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38
Q

What happens to SCr when GFR is reduced?

A

Increases

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39
Q

What is the equation used for classifying the severity of kidney disease?

A

CKD-EPI

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40
Q

What equation is used for making renal dose adjustments?

A

Cockcroft-Gault

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41
Q

T or F, the CKD-EPI equation is used to estimate kidney function in a pt receiving dialysis.

A

False

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42
Q

What are some limitations of the equations used?

A

Factors affecting Cr generation –> body size, race, muscle mass, diet
Factors affecting tubular secretion of Cr
Factors affecting extra renal elimination of Cr

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43
Q

What changes were made to the eGFR calculations in 2021?

A

Race was removed from equation

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44
Q

What is the difference between indexed/normalized and non-indexed eGFR?

A

Indexed: BSA factored in (mL/min/1.73m^2)
Non-indexed: adjusted according to the patients BSA (mL/min)

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45
Q

When do we caution using non-indexed eGFR calculations?

A

In morbidly obese b/c can lead to ODs

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46
Q

Why does the measurement of BUN underestimate GFR?

A

Reabsorbed by kidneys

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47
Q

What happens to BUN in renal impairment?

A

Increases

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48
Q

What other factors can affect BUN?

A

Dietary protein
GI bleeding
Hydration status (high in dehydration)

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49
Q

What does persistent increase in protein in the urine indicate?

A

Marker for kidney damage

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50
Q

Is proteinuria good?

A

NO –> more protein = Glomerular damage = renal impairment

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51
Q

SHould there be any albumin in the urine?

A

Yes, small amounts is normal

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52
Q

What is the ACR?

A

Albumin : creatinine ratio

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53
Q

Describe Normoalbuminuria

A

A1: <3mg/mmol normal or mildly increased

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54
Q

Describe Microalbuminuria

A

A2: 3-30mg/mmol moderately increased

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55
Q

Describe macroalbuminuria

A

A3: >30mg/mmol severely increased

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56
Q

What are some potential causes of transient albuminuria?

A

Recent major exercise
UTI
Febrile illness
Decompensated CHF
Menstruation
Acute sever elevation of BG
Acute severe elevation of BP

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57
Q

What does presence of eosinophils in the urine indicate?

A

Interstitial nephritis

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58
Q

What is the definition of AKI?

A

A sudden decline in renal function (hours-days) as evidence by changes in SCr, BUN, and urinalysis

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59
Q

T or F. CKD-EPI is used to estimate kidney function in a pt suspected of experiencing an AKI.

A

False

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60
Q

What conditions can AKI be defined as? (3)

A

Increase in SCr by > 0.3mg/dL within 48hrs
Increase in SCr >1.5 x baseline presumed to have occured in last 7 days
Urine volume <0.5mL/kg/h for 6h

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61
Q

Define ANuric

A

less than 50mL/day urine output

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62
Q

DEfine Oliguric

A

Less than 500mL/day urine output

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63
Q

Define non-oliguric

A

greater than 500mL/day urine output

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64
Q

R in RIFLE?

A

Risk: SCr increase 1.5x, GFR decrease >25%, <0.5mL/kg/hfor >=6h urine output

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65
Q

I in RIFLE?

A

Injury: SCr increase 2x, GFR decrease >50%, <0.5mL/kg/hfor >=12h urine output

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66
Q

F in RIFLE?

A

Failure: SCr increase 3x, GFR decrease >75% or SCr >= 354umol/L with acute increase >=44umol/L
Anuria for >=12h

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67
Q

L in RIFLE?

A

Loss of function for > 4 weeks

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68
Q

E in RIFLE?

A

ESRD: loss of function for > 3 months

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69
Q

AKIN Stage 1 criteria?

A

SCr increase >=27umol/L or 1.5-2x, Urine output of <0.5mL/kg/h for >=6 hours

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70
Q

AKIN Stage 2 criteria?

A

SCr increase >2-3x, Urine output of <0.5mL/kg/h for >=12 hours

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71
Q

AKIN Stage 3 criteria?

A

SCr increase > 3x or SCR .= 354umol/L with acute increase of >=44umol/L, Urine output of <0.3mL/kg/h for >=24 hours or Anuria for >12 hours

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72
Q

After developing AKI how long may it take to see an increase in SCr?

A

up to 4 days

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73
Q

What is criteria all based on? What do you need to know?

A

SCr, need to know pts baseline.

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74
Q

What are the clinical presentations of AKI?

A

Most are asymptomatic
can present with:
- dehydration
- Malaise, anorexia, N&V, pruitis
- Severe abdominal or flank pain
- Decreased force of urine stream
Cola-coloured urne
- Excessive foaming in urineSudden wt gain
- edema

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75
Q

What are some risk facors for AKI?

A

Anything tha decreased blood flow to kidneys
Pre-existing renal dysfunction
Drugs (20% of cases)

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76
Q

What are the characteristics of Pre-renal AKI?

A

Most common AKI (60%)
Hypo-perfusion –> not enough blood flow to kidneys
Kidneys are healthy
Can be decreased perfusion b/c:
- intravascular volume depletion (hemorrhage, dehydration, burns, diuretic therapy)
- decreased effective circulating volume (HF, cirrhosis)
- Hypotension
- decreased glomerular flitration pressure (ACEi/ARBS, NSAIDs)

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77
Q

What are the characteristics of Intrinsic AKI?

A

25-35% of cases
Results from direct damage to the kidney
- ischemia, toxins, or disease

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78
Q

What are the 4 main types of intrinsic AKI?

A
  1. acute tubular necrosis: endogenous(myoglobin) or exogenous(toxins, ischemia)
  2. Acute interstitial nephritis: idiopathic hypersensitivity immune reaction to drugs (NSAIDs, penicillin) infection
  3. Acute glomerulonephritis: post strep, antigen-antibody complexes
  4. Vascular kidney injury: renal artery stenosis, HTN
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79
Q

What are the characteristics of Post-renal AKI?

A

<5% of cases
Obstruction to urinary flow anywhere in the urinary tract
Causes:
- nephrolithiasis (kidney stones)
- prostate enlargement
- Cervical cancer tumors
- Drugs that crystallize

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80
Q

What do you use to diagnose AKI?

A

History
Lab data:
- SCr
- Urinary Na [ ] (decrease with pre-renal AKI, Increase with tubular damge)
- urinalysis
- SOmetimes : ultrasound(renal), kidney biopsy

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81
Q

What are the treatment goals of AKI?

A

Prevent further renal injury
Minimize extra-renal complications
Facilitate recovery of renal function back to baseline

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82
Q

Treatment for Pre-REnal failure?

A

Hydration with IV fluids
d/c diuretics of hypovelimic
BP support with vasopressors (dopamine, norepinephrine, vasopressin)
Fluid removal in volume overload states w/ diuretics
Stop drugs that impair kidney function/ urine flow

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83
Q

Treatment for Intrinsic renal failure?

A

D/c offending agent
Manage underlying autoimmune disease

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84
Q

Treatment for Post-renal failure?

A

Catheter to restore urine flow
identify and remove obstruction
adequate hydration when giving drugs with potential to crystalize

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85
Q

What are the number for mild-moderate K elevation? Severe?

A

5.1-7 mmol/L
>7mmol/L

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86
Q

What can occur with sever hyperkalemia?

A

ECG changes –> Heart block, netricular tachycardia, death

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87
Q

Treatment for mild hyperkalemia?

A

Kayexalate (sodium polystyrene sulfonate) 15-60 g po BID-QID until K normalizes
Furosemide IV admin to increase urinary excretion –> need functioning kidneys

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88
Q

How does sodium polystyrene sulfonate work?

A

Exchanges Na for K which then gets eliminated bound to polystyrene sulfonate
Has a delayed effect –> not great for severe cases

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89
Q

Treatment for Severe hyperkalemia?

A

Calcium gloconate
TO drive K out of celss :
- Raid acting/ regular insulin +/- glucose depending on BG
- Sodium bicarbonate IV infusion (if metabolic acidosis present)
- Salbutamol via nebulizer (if pulmonary congestion)
Kayexalate to eliminate excess K from body
Dialysis if refractory

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90
Q

What does Calcium gluconate do?

A

Stabilizes myocardium –> protects myocardium, has no effect on K levels just used to avoid arryhmias
Effect is in a matter of minutes

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91
Q

Treatment for fluid overload?

A

Diuretics –> Furosemide +/- metolazone

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92
Q

Treatment for metabolic acidosis?

A

Sodium bicarbonate IV

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93
Q

When do you use dialysis for AKI?

A

AEIOU
Acidosis
Electrolyte abnormalities
toxic Ingestions
fluid Overload
Uremia

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94
Q

What is the leading cause of CKD ?

A

Diabetes (38%)

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95
Q

How many canadians live with CKD?

A

~4 million; 1/10

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96
Q

What % of pts living with CKD are managed in primary care

A

95%

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97
Q

What is CKD?

A

Progressive loss of function occuring over several months-years

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98
Q

What happens to the kidney architecture in CKD?

A

Normal kidney tissue gets replaced wirth fibrotic tissue

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99
Q

What are the 2 main causes of CKD?

A

Diabetes
Hypertension

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100
Q

At what GFR is CKD defined at?

A

<= 60 mL/min/1.73m^2 for 3 months+
with or without kidney damage

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101
Q

Can you be diagnosed with CKD without a decrease in GFR?

A

Yes;
kidney damage for 3+ months as evidenced by pathological abnormalities in blood or urine, or as seen by renal imaging

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102
Q

What ratio of of ACR is a marker for kidney damage (KDIGO)

A

> =3 mg/mmol

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103
Q

What are the riks of reduced GFR due to age alone?

A

Higher risk of AKI
Medication accumulation with reduction of GFR
REduced reserves in the event other comorbitites develop over time

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104
Q

GFR categories/stages of CKD?

A

G1: >= 90 (normal/ high GFR)
G2: 60-89 (mildly decreased)
G3a: 45-59 (mild/moderately decreased)
G3b: 30-44 (moderate-severely decreased)
G4: 15-29 (Severely decreased
G5: <15 (kidney failure: dialysis or transplant)

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105
Q

Albuminuria categories/ staging for CKD?
AER (mg/24hrs), ACR (mg/mmol)

A

A1: <30 , <3 (normal to mildly increased)
A2: 30-300, 3-30 (moderately increased)
A3: >300, >30 (severely increased)

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106
Q

What equation do you use to determine GFR estimate?

A

CKD-EPI

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107
Q

How do you stage CKD based on KDIGO?

A

Using both GFR and Albuminuria

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108
Q

What would someones staging be if they had a GFR of 55 and an ACR of 25? What would be there risk scale?

A

G3aA2 High risk

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109
Q

What would the staging be if someone had a GFR of 66 and an ACR of 32? What would be there risk scale?

A

G2A3
High risk

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110
Q

What are the clincial presentations of CKD how do they change with stage increase?

A

Symptoms are generally minimal in stage 1 and 2 and increase in incidences with stages 3 and 4
Low energy
Fatigue
Confusion
Edema
SOB
Pruitis
Foaming, tea-coloured, blood, or cloudy urine

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111
Q

What eGFR is usually managed with primary care?
Managed in consultation with a nephrologist?

A

30-59 (stage 3a/3b)
<30 (stage 4/5)

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112
Q

What are the goals of treatment for CKD?

A

Delay progression
CV risk reduction
Treat complications
Renal replacement therapies

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113
Q

Which CKD etiology’s tend progress more quickly ?

A

Diabetic nephropathy
glomerular diseases
polysyctic kidney disease
kidney disease in transplant recipients

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114
Q

Which CKD etiology’s tend progress more slowly?

A

Hypertensive kidney disease
tubulointerstitial diseases

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115
Q

What are non-modifiable factors of CKD progression?

A

African american race
Male gender
advanced age
Family history

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116
Q

What are modifiable factors of CKD progression?

A

uncontrolled HTN
Poor BG control
Proteinuria
Smoking
Obesity

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117
Q

What interventions can you use to delay the progression of CKD?

A

BP control
RAAS blockade
BG control in diabetes pts
Smoking cessation
Avoidance of nephrotoxic drugs

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118
Q

Does HTN cause or is caused by CKD?

A

Can be both

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119
Q

GFR decrease in untreated HTN /year? with BP <130/80?

A

~ 12mL/min/yr
~1-2mL/min/yr

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120
Q

BP target for pts w/ high BP and CKD (not dialysis pts)?

A

<120

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121
Q

Target BP for kidney transplant pts?

A

<130/80

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122
Q

What criteria were excluded from the SPRINT trial? (definetly know this she loves her studies)

A

Diabetes

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123
Q

What is a statement about BP in the 2020 HTN Canada guidelines say about strict BP control?

A

BP targets should be individualized at discretion of physician, considering all pt factors. Recommended to talk about potential benefits and adverse events related to lower systolic BP.

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124
Q

What are the clincial indications for SBP of <120? (AARF)

A

Age >75
Atherosclerotic plaque (CV disease)
Renal (CKD, porteinuria <1g/d, GFR 20-59mL/min)
Framingham risk score of >15%

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125
Q

What are some cautions and CI’s for SBP <120?

A

Limited or no evidence:
HF (LVEF <35%)
Recent MI (past 3 months)
Indication for a beta-blocker but not on one
Institutionalized elderly individuals
Inconclusive evidence:
Diabetes
Previous stroke
eGFR <20mL/min/1.73m^2 (includes dialysis and transplant)
CI’s:
Pt unwilling or unable to adhere to multiple meds
standing SBP<110
Inability to measure SBP accurately
Known secondary causes of HTN

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126
Q

What is a key takeaway from the SPRINT trial in relation to CKD progression?

A

Did not slow CKD progression (possibly slightly worsening, no impact on ESRD though)

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127
Q

List characteritics of a sutiable pt for SBP <120

A

Age> 50
w/o a high degree of comorbities
achieve BP w/o requiring a bunch of different meds
No issues with SE’s

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128
Q

List characteristics of a non-suitable pt for SBP <120

A

Age> 90, or living in nursing home
Requirment of >3 meds to get to target
At risk of falls from postural hypotenison
DBP of <60
SBP of 120-129
Severe HTN (>=180)
Those who fell the benefits are not worth the risks, cost, effort

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129
Q

What is the nutrition lifestyle recommendation from HTN Canada 2020? Others?

A

Salt restriction: reduce Na intake towards 2000mg/d (rather than 5000)
Exercise (30-60min moderate intensity for 4-7 days a week)
Wt reduction (BMI of 18.5-25 recommended)
Limit alcohol consumption (1-2 drinks/day)

130
Q

KDIGO first-line options for HTN?

A

ACEi/ARB
diuretics
long-acting CCBs

131
Q

What is first-line treatment for HTN if a pt has proteinuria?

A

ACEi/ARBs (reduces proteinuria more than any other antihypertensive drug)

132
Q

How do ACEi/ARBs reduce BP?

A

reduce BP and glomerular capillary pressure by selectively vasodilating the efferent arteriole
(Inhibit RAAS system as well)

133
Q

What stage of albuminuria are ACEi/ARBs first-line therapy for kideny diseases?

A

Diabetes: ACR of >3mg/mmol –> A2
Non-daibetic: ACR >30mg/mmol –> A3

134
Q

What are CI’s of ACEi/ARB therapy?
When is are they cautions?

A

CI:
Angioedema
Bilateral renal artery stenosis
Pregnancy
Caution:
Intravascular fluid depeletion
GFR of <30mL/min
Hypotension (<110/70)
hyperkalemia (>5.5mmol/L)

135
Q

What monitoring parameters are there for ACEi/ARBs?
TImeline for mnitoring

A

2-4weeks following intiation or dose increase
SCr
K+
BP
Urinary albumin: Creatinine ratio(ACR)

136
Q

What increase of SCr from baseline may warrant a d/c of an ACEi/ARB

A

> 30% increase

137
Q

How do you dose ACEi/ARBS for renal protection?

A

Start low, monitor and reach maximum tolerated dose
Dose-dependant reduction in albuminuria lowering.
Need to watch out for SCr increase of >30%, Hyperkalemia

138
Q

Do you combine ACEi/ARBS in CKD?

A

Not any more but used to.
Superior effect of reducing proteinuria and BP but worsened renal outcomes (nephrotoxic drugs)

139
Q

What did the ALTITUDE trial show with direct renin inhibitors? (Aliskiren)

A

More frequent AE’s such as:
- non-fatal stroke
- renal complications
- hyperkalemia
- hypotension

140
Q

What were the findings of the cochrane review 2014 (MRAs)

A

Mainly in combo with ACE/ARB:
reduced proteinuria 30-40%
improved BP
Rossible slowing of CKD progression
No CV/ESRD outcomes
dobuled risk of hyperkalemia
5-fold risk pf gynecomastia

141
Q

What are the steroidal MRA’s? are the selective or non-selective?

A

Spironolactone, eplerenone
Non-selective

142
Q

What drug is the non-steroidal MRA is it selective or non-selective?

A

Finerenone
Selective

143
Q

What are the main differences between the steroidal and non-steroidal MRA’s?

A

Non-steriodal have mich higher specificity for MR vs glucocorticoide/androgen receptors, and reduce albuminuria while having less SE’s
–> Much less likely to exerpeince gynocomastia than steroidal b/c no androgen affect.

144
Q

What was the eligibility for KDIGO CKD in diabetes 2022 trial for non-steroidal MRA use?

A

K+ <4.8
eGFR >=25
ACR of >=3

145
Q

What are the KDIGO HTN 2021 guideines for MRA use?

A

Possible use in refractory HTN (uncontrolled on 3 other drugs including a diuretic) with a GFR of > 45mL/min

146
Q

What is the most important monitoring parameter for MRA’s?

A

K+

147
Q

What are some of the main limitations of Finerenone?

A

Coverage
Less evidence available in pts also taking SGLT2i
Not to be used in combo with steroidal MRA’s in pts with HF(not to replace them in HF treatment either)

148
Q

Which diuretic do you start with in CKD?

A

Thiazide diuretic

149
Q

What is a major contributing factor to HTN in CKD?

A

Fluid retention

150
Q

What were the issues with the CLICK trial?

A

short term study (12 weeks long)
No hard endpoints

151
Q

What medication is preferred over thiazides in combo with ACEi/ARBs in pts with daibetes?

A

DHP-CCBs (amlodipine)

152
Q

What is a potential problem with using DHP-CCB in CKD?

A

Fluid retention/ edema

153
Q

Where do you see fluid retention/edema with DHP-CCBs?

A

Seen in ankles due to leakage b/c it vasodilates the periphery

154
Q

What are non-DHP-CCBs shown to do in CKD?

A

Decrease proteinuria but not as good as ACEi/ARBs
No evidence of slowing CKD

155
Q

What issues are there with Non-DHP-CCBs?

A

Constipation and bradycardia
LOTS of DI’s Cyp3A4

156
Q

Which Non-DHP-CCBs are used?

A

Diltiazem and Verapamil

157
Q

Which alpha-2 agonist is used in CKD? Why?

A

Clonidine
Good adjunctive therapy for HTN as it has no DI’s with commonly used BP meds

158
Q

When do we caution the use of clonidine?

A

Elderly b/c CNS SE’s

159
Q

Why must you tapper off of clonidine?

A

b/c can have rebound HTN if stopped abruptly

160
Q

Beta blockers used in CKD?

A

For HTN, need to monitor HR and BP and if GFR below 30 need to watch out for accumulation

161
Q

When would you consider using an alpha-1-blocker in CKD?

A

If pt also has prostatic hypertrophy

162
Q

What are the alpha-1-blockers?

A

Terazosin, Prazosin

163
Q

SE’s of alpha-1-blockers?

A

Dizziness, orthostatic hypotension

164
Q

What is the direcrt vasodilator used?

A

Hydralazine

165
Q

When is hydralazine used? what is its limiting feature?

A

Adjunct therapy, limited by its SE’s of headache, fluid retention

166
Q

What is the proteinuria linked to?

A

progression of CKD
High risk of progressing to kidney failure
Indicator of subclinical CVD

167
Q

Which stage of albuminuria predicts loss of kidney function

A

A2; Microalbuminuria

168
Q

What is normal proteinuria numbers? Mild (A2)? Moderate(A3)? Nephrotic range?

A

Normal: 40-80 mg/d protein in urine
Mild: 150-500mg/d protein in urine
Moderate: >500mg/d protein in urine
Nephrotic range: >3000mg protein or >2200mg of albumin excreted in the urine in a day

169
Q

What is nephrotic syndrome associated with? (signs)

A

hyperlipidemia
Hypoalbuminemia
generalized edema
thromboembolic risk
Foamy urine

170
Q

What is the most significant cause of kideny diseases associated with proteinuria?

A

Diabetic nephropathy

171
Q

Why would you use an ACEi/ARB in CKD patients without HTN?

A

REduce glomerular capillary pressure and volume
Dialate efferent vessel (therefore decrease pressure)
Help reduce proteinuria

172
Q

Are SGLT2i’s used in CKD for pts w/o diabetes?

A

Yes; 2022 guidelines indicate SGLT2i’s for CKD to reduce progression to ESRD, and reduce mortality due to kidney disease, CV reduction of nonfatal MI’s, and reduction of hospitalizations for HF

173
Q

what % of T2DM pts have CKD?

A

40%

174
Q

What shoud you screen T2DM pts for to rule in/out CKD?

A

Random urine ACR and SCr should be checked annually

175
Q

When should you begin screening for CKD in T1DM and T2DM?

A

5 years after diagnosis in T1DM
At time of diagnosis of T2DM
Screen annually after

176
Q

How does the progression of nephropathy occur?

A

THe drop/yr of GFR increases as kidney disease gets worse; worsening of progression i.e. GFR will drop by more mL/min/yr as worsening continues.

177
Q

Why is BG control important in CKD?

A

Prevents and delays progression of daibetic nephropathy

178
Q

When would an HbA1C measurment be less accurate in regards to CKD?

A

Pts with advanced CKD (stages G4-G5 especially with dialysis)

179
Q

At what GFR is metformin said to be avoided in? Can it be used in dialysis?

A

at GFR of <30mL/min but may be seen in stable pts at 500mg/day
Can be used in dialysis with altered dosing

180
Q

When is SGLT2i a first-line agent?

A

pts w/ CKD, T2DM, and a GFR of >20mL/min

181
Q

At what percent of a decrease in GFR would SGLT2i be d/c?

A

Greater than 30% reduction of GFR

182
Q

What is the main barrier for GLP-1 agonists?

A

Cost

183
Q

When would a GLP-1 agonist be used?

A

If A1C target not reached w/ SGLT2i + metformin then it is added

184
Q

How does smoking increase the progression of CKD?

A

Increases BP and HR
Decreases renal blood flow (via constriction)
Vasular injury

185
Q

Ex’s of nephrotoxic drugs?

A

NSAIDs
Lithium
aminoglycosides
amphotericin B
calcineurin inhibitors
cisplatin

186
Q

What is the “triple whammy” of nephrotoxic drugs?

A

ACEi/ARB + NSAIDs + diuretics

187
Q

SADMANS?

A

Sulfonylureas
ACEi
Diuretics/ direct renin inhibitors
Metformin
ARB
NSAID
SGLT2i

188
Q

What is the leading cause of death in CKD?

A

CVD

189
Q

Is CKD a statin indicated condition?

A

Yes if;
>=50yrs old, GFR <60mL/min/1.73m^2 or
ACR > 3mg/mmol

190
Q

Treatment guidelines for dyslipidemia in CKD (KDIGO)?

A

> 50 with GFR of <60 and not on dialysis –> Tx with low-dose statin or statin/ezetimibe combo
=50 with CKD and GFR of >=60 –> tx w/ statin
18-49 with CKD tx w/ statin if CV risk is >10%
If on dialysis do not intiate therapy but if already on, continue
Kidney transplant: Tx w/ statin in some cases

191
Q

When would low dose ASA be used in CKD?

A

For secondary prevention (post-MI /CV event)

192
Q

When do you intiate REnal Replacement therapy in CKD?`

A

No set GFR; based on clincial status of pts
Based on signs and symptoms such as:
- serositis
- inability to control volume satus or BP
- malnutrition refractroy to dietary intervetntion
- cognitive impairment

193
Q

What is the most common renal replacement therapy?

A

Hemodialysis

194
Q

How does hemodialysis work?

A

Pt blood is passed through an external filter to remove wastes and fluid
Conducted 3x a week usually
Takes about 3-5hrs/ visit

195
Q

What does hemodialysis require?

A

a chromic vascular access that can withstand high bloodflow rates
Ex: Arteriovenous fistula, insertion of a synthetic AV graft, catheter in neck
Require systemic anticoagulation during procedure to avoid clotting

196
Q

What are hemodialysis pts more prone to during procedure?

A

Hypotension b/c of massive fluid shifts

197
Q

Complications of hemodialysis?

A

fatigue, hypotension, hypertension, cramps, N/V
Infection, Clotting, bleeding

198
Q

What is a special consideration needed for hemodialysis? what needs to be done?

A

water soluble vitamins are removed during treatment
Must take Replavite 1 tablet once daily and avoid multivitamins

199
Q

What is in replavite?

A

B1: 1.5mg
B2: 1.7mg
B3: 20mg
B6: 10mg
Folic acid: 1mg
B12: 6mcg
Biotin: 300mcg
Vit C: 100mg

200
Q

How does peritoneal dialysis work?

A

relies on pts own peritoneal membrane to act as filter
2-3L of dialysate is isntilled in the peritoneal cavity through an indwelling catheter,
wastes and fluid diffuse accross the peritoneal membranes down the concetration gradient, dialysate is drained and replaced with fresh solution

201
Q

How do Continuous ambulatroy peritoneal dialysis and Automated peritoneal dialysis differ?

A

CAPD: manual exchange usually 4-5x per day taking 30-45 min
APD: uses machine while you sleep, takes 8-10hrs, may also require fluid in abdomen during the day

202
Q

What is the most common complication with peritoneal dialysis?

A

peritonitis (inflammaton and infection of peritoneal lining)
Treated w/ local or systemic antibiotics

203
Q

When is continuous renal repalcement therapy recommended?

A

FOr hemodynamically unstable pts requirng renal repalcement therapy for an AKI

204
Q

Treatment of Sodium and water imbalance as a CKD complication?

A

Sodium and water restriction (<2g salt, 1-2L fluid per day)
Furosemide +/- metolazone
Stage 5: dialysis

205
Q

Why is metolazone synergistic with furosemide?

A

Has natriuetic action at distal tubule

206
Q

What do you need to monitor for diuretic treatment of sodium and water imbalance treatment in CKD?

A

Electrolytes; all but especially K
Monitor 1-2 weeks then every 3-6 months when stable
dehydration

207
Q

Characteristics of Metabolic acidosis?

A

Dercrease pH in blood, decreased bicarb (<22mmol/L)

208
Q

What does metabolic acidosis lead too?

A

Retention of H+ as less ammonia is produced by kidneys

209
Q

Treatment for metabolic acidosis?

A

Sodium bicarbonate 325-500mg po BID-TID
Baking soda dissolved in water

210
Q

Concern of treatment of metabolic acidosis?

A

Sodium loading possible

211
Q

How can most CKD pts with mild hyperkalemia be managed?

A

dietary restriction of K

212
Q

What is the definition of CKD-MBD?

A

Systemic disorder of mineral and bone metabolism due to CKD manifested by one or more of:
Abnormalities of Ca, Phosphorus, PTH, or Vit D metabolism (minerals)
Abnormalities in bone turnover, mineralization, volume, linear growth, or strength (bone metabolism)
Vascular or other soft tissue calcification

213
Q

What are the outcomes of CKD-MBD?

A

Bone pain, Fractures, CVD, death

214
Q

How is CKD-MBD diagnosed?

A

Biochemical abnormalities (Ca, Phos, PTK, ALP) to help predict underlying bone turnover
Bone abnormalities: bone biopsy, bone mineral density
Vascular calcification: echocardiogram to identify valvular calcification

215
Q

What stage of CKD does canadian society of nephrology say to monitor Ca, PO4, PTH?

A

G4-G5

216
Q

When should hypocalcemia be corrected?

A

In Severe or symptomatic hypocalcemia but, do not over correct b/c hypercalcemia associated with higher mortality and risk of CV events in CKD pts

217
Q

What is ionized Calcium?

A

“active” calcium

218
Q

What is Total calcium?

A

free + bound calcium to albumin

219
Q

What is corrected calcium?

A

Calcium adjusted for albumin levels

220
Q

When should PTH increases be treated?

A

When progressively rising or persistently high (target in CKD G5D is 2-9x upper limit of normal)
High PTH may be appropriate in response to worsening kidney function (modest elevations)

221
Q

What are the 3 types of renal osteodystrophy

A

Hyperparathyroid bone disease
Adynamic bone disease
Osteomalacia

222
Q

What is FGF-23 and what does it do?

A

fibroblast growth factor 23
promotes PO4 excretion in the kidneys, stimulates PTH to increase PO4 renal excretion, and supresses formation of calcitriol to decrease PO4 absorption from GI tract.

223
Q

How does PTH affect Ca?

A

increases Ca reabsorption and PO4 excretion in kidneys, increases Ca mobilization from bone

224
Q

How does advanced CKD impact FGF-23 and PTH?

A

Kidneys fail to respond to FGF-23 and PTH

225
Q

What does persistent calcium reabsorption from the bone lead too?

A

high bone turnover leading to osteitis fibrosis cystica

226
Q

What is calciphylaxis?

A

the calcification and occlusion of small blood vessels
Leads to ulceration, gangrene, secondary infection (sepsis), and is associated with high mortality rate.

227
Q

How do you treat Hyperparathyroid bone disease?

A

DEcrease phosphate:
Restrict dietary phosphate + a phosphate binder such as: Ca products, aluminum or magnesium binders, severlamer, lanthanum, sucroferric oxyhydroxide
Intensify dialysis schedule

+
Supress PTH:
Vit D: Calcitriol, alfacalcidol, ergo or cholecalciferol
Calcimimetics: Cinacalet
Parathyroidectomy

228
Q

What does aggressive PO4 restriction require the need of?

A

A dietician

229
Q

How do phosphate binders work?

A

Bind to dietary PO4 in the GI tract and eliminate it n the feces

230
Q

How must phosphate binders be taken?

A

At the beginning of a meal, taken multiple times per day (with all meals and snacks)

231
Q

Do patients on PO4 binders still need to be on a dietary restriction of PO4?

A

Yes

232
Q

What is the first line phosphate binder? Dosing? AE’s?

A

Calcium carbonate
500mg TID w/ meals
constipation, stomach cramps
Hypercalcemia –> especially if coadminstered w/ calcitriol

233
Q

Why are Aluminum and Magnesium phosphate binders not first line?

A

Not recommended for chronic use b/c risk of accumulation and toxicity

234
Q

What is the main problem with using Sevelamer HCl (renagel/renvela)

A

Expensive
EDS only for ESRD where Ca and Al binders are inappropriate/ not tolerated

235
Q

What is the main difference of Lanthanum (fosrenol) compared to Sevelamer?

A

Lanthanum is chewable

236
Q

What is the newest calcium free binder how does it work?

A

Sucroferric oxyhydoxide (velphoro)
Iron based but, negligible contribution to iron intake
EDS for ESRD

237
Q

When should Vit D therapy not be used routinely?

A

In patients not on dialysis

238
Q

Vit D treatment?

A

Calcitriol or Alfacalcidol
0.25-1 mcg daily

239
Q

AE’s of Vit D treatment?

A

Hypercalcemia, Hyperphosphatemia (b/c FGF-23 levels being increased)

240
Q

What calcimimetics is sometimes used in dialysis +/- Vit D therapy?

A

Cinacalcet but, very expensive and not covered
30-180mg daily

241
Q

What are the AE’s of Cinacalcet?

A

NVD,
HYPOCALCEMIA (75%) !!!!!

242
Q

What are risks of using bisphosphonates (alendronate) for CKD-MBD?

A

Can induce/exacerbate low bone turnover
Cautioned in CrCl of <35 mL/min but is rarely nephrotoxic

243
Q

What is required if using Denosumab?

A

Monitoring as risk of hypocalcemia

244
Q

How often should monitoring of Ca, PO4, and PTH levels occur for CKD-MBD?

A

at least monthly

245
Q

What is a Parathyroidectomy?

A

PArtial rewmoval of the parathyroid gland
Reserved for pts where PTH,Ca, and phosphate abnormalities are not medically correctable

246
Q

What can occur post-op parathyroidectomy?

A

Hungry bones syndrome

247
Q

What is adynamic bone disease?

A

low bone turnover disease
- lack of osteoblast/osteoclast stimulation aka no bone remodelling

248
Q

What is ABD associated with?

A

more fractures and calcification

249
Q

How does someone get ABD?

A

Oversupression of PTH; Ca and Vit D treatment (to much)

250
Q

How do you treat ABD?

A

Stopping Vit D treatment/ reduce suppression of PTH

251
Q

What is osteomalacia?

A

inadequate mineralization of Ca and PO4 aka softening of the bone

252
Q

How can osteomalacia develop?

A

Reduced production and action of calcitriol or
Aluminum deposition in the bone

253
Q

What can result from osteomalacia?

A

Fractures, myopathy, neurological deficits, dementia, seizures

254
Q

Treatment for osteomalacia?

A

Stop aluminum intake

255
Q

What occurs when vascular calcification is seen?

A

vascular smooth muscle cells change into osteoblast-like cells

256
Q

In CKD where is there an increased prevalence of clacification?

A

CV; coronary arteries, heart valves

257
Q

What anemia is seen in stage 3-5 CKD? Lab work seen?

A

Normochromic, normocytic
Hgb <130g/L in male, <120g/L in female
decrease in reticulocytes

258
Q

What does CKD anemia primarily result from?

A

a loss of erythropoeitin generation by the kidneys

259
Q

What stages is iron deficient anemia most common in?

A

stages 4-5 due to deceased GI absorption

260
Q

What happens to TSAT and ferritin in absolute iron deficiency?

A

both decrease

261
Q

What happens to TSAT and ferritin in functional iron deficiency?

A

Decrease or normal TSAT
Increased ferritin

262
Q

Signs and Symptoms of Anemia?

A

Weakness
lethargy
malaise
SOB
impaired memory/concentration
feeling cold

263
Q

Treatment for anemia?

A

Erythropoiesis stimulating agents

264
Q

What do ESA agents have an associated risk of?

A

Stroke and thromboembolic events

265
Q

Hemoglobin, TSAT, and ferritin targets for anemia treatment?

A

100-110 g/L
>20%
100mcg/L in non dialysis, >200mcg/L in Hemodialysis

266
Q

What is the order of treatment for anemia?

A

Correct bood loss
Replace vitamin and iron deficiency
ESA if needed
Dialysis to corect uremia
Blood transfusions if required

267
Q

What should you do before intiating ESA treatment?

A

Address all correctable causes first

268
Q

What is the usual suggested dose of Iron for iron deficient anemia usually?

A

100-200mg elemental daily divided BID or TID

269
Q

Which ESA has a shorter half-life?

A

Epoetin alfa (eprex)

270
Q

Which ESA is a second generation molecule with a longer half-life?

A

Darbepoetin alfa (aranesp)

271
Q

What dosage form is ESA agents?

A

Single-use pre-filled syringes
Need to be refrigerated

272
Q

Dosing for each ESA agent?

A

Eprex: 50-100 units/kg IV or subcut 2-3x weekly
Aranesp: 0.45mcg/kg weekly IV or subcut

273
Q

Dose adjustment for ESA for hemoglobin <10g/L increase after 4 weeks?

A

increase dose by ~25%

274
Q

Dosing adjust for ESA for hemoglobin >10g/L in 2 weeks?

A

decrease dose y ~25%

275
Q

Monitoring for ESA therapy?

A

Serum iron, TIBC, TSAT, and ferritin every 1-3 months
Hemoglobin every 1-2 weeks intially, then monthly

276
Q

AE’s of ESA treatment?

A

Well tolerated;
HTN (dose-dependant)
Transient flu-like symptoms
Thrombosis (VTE)
Stroke, MI, death
Pure red cell aplasia (rare)

277
Q

Main cause of “erythropoeitin resistance” ?

A

Iron deficinecy

278
Q

What dosing of ESA should you avoid?

A

> 4x intial dose

279
Q

How do HIF-PHI’s work? Dosing? AE?

A

inhibt enzyme that defrades hypoxia-inducible factor therefore improves iron mobilization into serum, increase indogenous EPO production which increases Hgb
Drug: daprodustat (jesduvroq) approved for treatmne tof anemia in dialysis
Dosing: 1-24mg po daily
AE: possible risk of malignancy

280
Q

What % of pts have HTN in stage 5 CKD?

A

~90%

281
Q

Contributing factors to HTN in CKD?

A

Salt and water retention
RAAS activation
ESA therapy
Hyperparathyroidism
Renal vascular disease

282
Q

Why might you see unusual dosing in CKD pts on hemodialysis?

A

B/c of hypotension worry

283
Q

What is the most common structural cardiac abnormality in CKD?

A

LVH

284
Q

Risk factors of LDH in CKD?

A

HTN/ fluid retention
Anemia
Diabetes
Older age
Uremia
Abnormal Ca/ PO4 homeostasis

285
Q

Treatmnet for LVH?

A

manage HTN, anemia, Ca PO4 and PTH levels

286
Q

What is a moajor thing you need to monitor in HF CKD pts?

A

K+

287
Q

Neurological complication of CKD?

A

peripheral neuropathy
uremic encephalopathy
uremic polyneuropathy
- restless legs syndrom
- leg cramps
- numbness/tingling/parahtesias
- carpal tunnel
- myopathy

288
Q

Treatment of neruological complications of CKD?

A

Dialysis or change in dialysis prescription

289
Q

% affected by chromic pruritis in ESRD?

A

40%

290
Q

Complications of chronic pruritis?

A

ulcers, infection, QoL, sleep

291
Q

Treatment of chronic pruritis?

A

gabapentinoids
capsaicin
setraline
antihistamines
uremol lotion

292
Q

Difelikefalin dosing, AE’s, and clinical significance?

A

peripheral kappa opiod receptor agonist
IV 3x week following hemodialysis
clinical significance in decreasing itch (52% VS 31% with placebo)
AE: dizziness, somnolence, mental status change

293
Q

What is DIKD? how is it diagnosed?

A

Adverse functional or structural change to kidney after administration of drug, chemical, or biological poduct
Diagnosis:
Changes in SCr or urine output consistent of AKI
associated with nephrotoxic drug
Kidney injury due to disease ruled out

294
Q

Is DIKD reversible?

A

Yes if caught early enough, can progress to ESRD if not treated soon enough

295
Q

Presentation of DIKD?

A

Metabolic acidosis
Changes in electrolytes
proteinuria
pyuria
hematuria
rise in SCr
decreased (or increased) urine output

296
Q

Symptoms of DIKD?

A

Malaise
anorexia
N&V
Volume overload(SOB, Edema)

297
Q

Drug examples that can cause DKID?

A

NSAIDs
ACEi/ARBs
PPIs
Aminoglycosides
etc.

298
Q

Why are NSAIDs “special” when it comes to DKID?

A

Can cause it in multiple ways; hemodynamically mediated, acute interstitial nephritis pathway

299
Q

How does pre-renal (indirect nephrotoxicity) cause DKID?

A

Drug interferes with afferent or efferent arteriole, decreases GFR

300
Q

What % of CO do kidneys usually recieve?

A

25%

301
Q

WHo is at risk of pre-renal DKID?

A

HF, renal artery stenosis, volume depletion, CKD, other nephrotoxins

302
Q

How do you manage pre-renal DKID?

A

Recognize cause and address it, Starting a possible nephrotoxic drug start low and titrate slow

303
Q

What is something to watch for that can cause pre-renal DKID?

A

Concurrent diuretics, hypotensive agents

304
Q

What can caue intra-renal (direct kidney injury/damage) DKID? (3)

A

Acute tubular necrosis
Interstitial nephritis
Glomerulonephritis

305
Q

What occurs in acute tubular necrosis?

A

Ischemic or toxic cellular injury to renal tubules
Dose-dependant (usually)

306
Q

What is an important preventative measure to take w/ drugs that can cause ATN?

A

Maintain adequate hydration

307
Q

Who is at risk of ATN?

A

pts predisposed to renal injury
Pre-exisitng CKD, older, multiple nephrotoxic drugs

308
Q

Treatment of ATN?

A

D/c drug causing it
Monitor SCr, BUN, electrolytes
Hydration may be necessary

309
Q

What occurs in acute interstitial nephritis?

A

immune-mediated kidney injury associated with hypersensitivity reactions;
Idiosnycratic, inflammatory reaction

310
Q

When dose acute interstitial nephritis occur?

A

usually 7-14 days post-exposure

311
Q

What can be seen in the urine?

A

pyuria, eosinophils but, no bacteria

312
Q

When do NSAID’s usually cause acute interstitial nephritis?

A

in chronic use after 6+ months

313
Q

Risk factors of acute interstitial nephritis?

A

NONE –> “allergic reaction” so anyone can have it happen to them

314
Q

Treatment of Acute interstitial nephritis?

A

D/c drug, sometimes give corticosteroids
Monitor Scr, BUN.

315
Q

Difference between chronic and acute interstitial nephritis?

A

chronic: progressive and irreversible; kidney scaring leads to fibrosis

316
Q

What occurs in obstructive nephropathy?

A

blockage by precipitated drug cystals

317
Q

Characteristics of obstructive nephropathy?

A

dose-dependant
Associated with inadequate hydration (stimulates RAAS)
More acidic urine; new environment allowing for some drugs to be able to precipitate out

318
Q

Management of obstructive nephropathy?

A

High urine volume
Urinary alkalinization

319
Q

What equation do you use to calculate GFR for potential dose adjustment?

A

Cockroft-Gault; but do NOT use equations in isolation to determine drug dosing –> range of GFR empirical dosing is usually on drug monograph

320
Q

At what % of renal clearance does drug accumulation of clinical significance occur?

A

> =50% (In PK we learned 30% but okay)

321
Q

What is an important trend to monitor in drug dosing in AKI?

A

SCr –> increasing, decreasing, leveling off?

322
Q

Is SCr appropriate to use to estimate CrCl in patients recieving diaysis?

A

NO, lack of accuracy general assumption is 10mL/min but some patients may have residual function

PHAR 255 (14 decks)

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