09/08/2009 Chronic Kidney Failure #1 Kuma

Front 1

2 main causes of chronic kidney failure

Back 1

HTN
DM

Front 2

Chronic Kidney Disease (CKD) definition

Back 2

Kidney damage for ≥ 3 months with or
without a decrease in GFR

Front 3

Stage 0 CKD

Front 4

Stage 1: Pre-clinical CKD

Back 4

GFR ≥ 90 ml/min/1.73 m2 + evidence of kidney damage

Front 5

Stage 2 (Mild CKD):

Back 5

GFR= 60-89 ml/min/1.73 m2 + evidence of kidney
damage

Front 6

Stage 3 (Moderate CKD):

Back 6

GFR = 30-59 ml/min/1.73 m2

Front 7

Stage 4 (Severe CKD):

Back 7

GFR = 15-29 ml/min/1.73m2

Front 8

Stage 5 (Kidney Failure):

Back 8

GFR <15 ml/min/1.73 m2
Goal: renal replacement therapy, treat complications

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Screening for CKD

Back 9

Goal is to identify patients before stage 3

Front 10

when do you use the MDRD equation

Back 10

used for the staging of disease

Front 11

Initiation factors for CDK

Back 11

Diabetic Kidney Disease
Vascular (Hypertensive
Nephrosclerosis)
Glomerulonephritis
Tubulointerstitial
Polycystic Kidney Disease
(PKD)

Front 12

Diabetic Kidney Disease initial kidney changes

Back 12

mesangial expansion, GBM thickening --> glomerulosclerosis & arterionephrosclerosis

Front 13

Vascular (Hypertensive
Nephrosclerosis) initial kidney changes

Back 13

hyaline deposits & thickening of renal
arterioles, a process known as
nephrosclerosis

Front 14

Glomerulonephritis initial kidney changes

Back 14

variety on non-immune or immune imbalances which damage the glomeruli

Front 15

Tubulointerstitial initial kidney changes

Back 15

long-term exposure to analegesic, heavy metals or toxins

damages tubules

Front 16

Polycyctic kidney disease (PKD)

Back 16

genetic disorder characterized by the growth of numerous cysts in the kidneys

Front 17

Negative consequence of adaptation=

Back 17

progression of kidney failure

overtime the nephron dies

progession of damage

Front 18

Insult to kidney (initiation factor) leads to loss of nephrons--->

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adaptation---> increase in size and function of remaining nephrons

Front 19

Solute balance is maintained through an..

Front 20

Proteinuria causes?

Back 20

Increase in cytokines wich leads to inflammatory cell inflamation--> glomerular and tubulointerstitial fibrotic scaring-->damage and slow loss of remaining nephrons

Front 21

Steps of Adaptation

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1. loss of nephrons--> vasodialte afferent arteriole and vasoconstrict efferent arterial
2. increase GFR in remaining nephrons (due to increased glomerular pressure
3. capillary endothelial and epithelial dysfunction; basement membrane thickening; filtration barrier breakdown
(all of the above leads to proteinuria)
4. damage and slow loss of remaining nephrons

Front 22

indicator of kidney damage

Back 22

proteinuria

Front 23

Tone of the afferent arteriole is controled by...

Back 23

prostaglandin (vasodilator)

some angiotensin II activity

Front 24

Tone of the efferent arteriole is controlled by...

Back 24

Angiotensin II

Front 25

Normal kidey flow

Back 25

the afferent arteriole is dialated and the efferent is only slightly constricted

So glomerular pressure and GFR is normal

Front 26

Kidney blood flow after adaptation

Back 26

The Afferent arteriole is dialted due to prostaglandins so GFR increases

The efferent arteriole is constricted due to angiotensin II and therefore golmerular capillary pressure is increased

Front 27

Intact filtration barrier prevents...

Back 27

proteinuria

Front 28

An intact filtration barrier consist of..

Back 28

Epithelial Cells
(Podocytes):
Coated in (-) charged
glycosialoproteins-->
Charge exclusive

GBM:(-) charged glycosaminoglycans
-->Both charge & size exclusive

Front 29

Direct Glomerular injury & ↑GCP lead to?

Back 29

Damage
to Filtration Barrier--> Proteinuria

Front 30

Factors that ↑ Progression of
Kidney Disease

Back 30

Persistence of underlying initiation factor
Elevated blood pressure Microalbuminuria/proteinuria
Hyperglycemia (uncontrolled diabetes)
Dyslipidemia
Smoking
Genetics
obesity (don't know if is the obesity or the conditions associated with it)

Front 31

Susceptibility
Factors for CKD

Back 31

↑ susceptibility to
kidney damage

Front 32

Examples of Susceptibility
Factors for CKD

Back 32

Older age, family history of
CKD, reduction in kidney
mass, low birth weight, racial
or ethnic minority status, and
low income/education

Front 33

Initiation
Factors of CKD

Back 33

Directly initiate kidney
damage

Front 34

Examples of Initiation
Factors of CKD

Back 34

Diabetes, HTN, autoimmune
diseases, systemic infections,
UTIs, urinary stones, urinary
obstruction, drug toxicity, and
hereditary diseases

Front 35

Progression
Factors of CKD

Back 35

Cause worsening
kidney damage and
faster decline in kidney
function after initiation
of kidney damage

Front 36

Examples of Progression
Factors of CKD

Back 36

Albuminuria, uncontrolled
HTN, poor glycemic control in
diabetes, possibly
dyslipidemia and smoking

Front 37

Reversing/Slowing Progression of CKD

Back 37

Identification in early Stages is essential
Aggressive management of modifiable
“progression” factors

Front 38

Goal BP in CKD

Back 38

<130/80 mmHg

consider goal of < 125/75 only if >1gm/day proteinuria

Front 39

Usual preferred drugs for BP control in CKD =

Back 39

angiotensin converting enzyme inhibitors (ACE-i) or
angiotensin II receptor blockers (ARBs)

May need 2-3 drugs to get BP to goal:

Front 40

Microalbuminuria

Front 41

Macroalbuminuria

Front 42

Normal Albuminuria*

Back 42

< 30 mg/g

Front 43

Persistent Microalbuminuria

Back 43

30-300 mg/g

Front 44

Persistent Macroalbuminuria

Back 44

> 300 mg/g

Front 45

How many test for albuminuria need to be (+) to determine the patients albumin levels?

Back 45

Need 2 out of 3 tests (+) in a 3-6 month period (due to variability in test)

1st morning specimen (after waking) is ideal

Front 46

Screening for Albuminuria

Back 46

Diagnosis only made after 2 out of 3 samples (+)
during a 3-6 month time period

Front 47

factors that can falsely ↑ albuminuria):

Front 48

Patients with evidence of kidney disease,
with or without high blood pressure,
should be treated with...

Back 48

An ACE inhibitor
or an ARB to reduce albuminuria

Front 49

Goals of Therapy of Micro or Macroalbuminuria

Back 49

Titrate therapy to:

Front 50

Protective effects of ACE and ARBs

Back 50

ACE block angiotensin and ARB block the recpeptor preventing efferent arteriole vasoconstriction

ARB block the recpeptor

Front 51

In the long run ARBS and ACEs work by...

Back 51

decreasing the glomerular pressure and reduce damage

adaptation in also reverse

Front 52

Improve Glycemic Control

Back 52

Can decrease progression in both
Type-1 and Type-2 diabetes

Front 53

What is the gola for A1c?

Back 53

A1c < 7.0%

Front 54

Preventing Progression
Protein Restriction

Front 55

dyslipidemia and preventing progression of CKD

Back 55

Dyslipidemia: patients with stage 1-4 CKD
should be screened annually and treated
according to ATP III (NCEP) Guidelines

Front 56

What other factor can prevent progression of CKD?

Back 56

Smoking cessation