Week 4: chronic kidney disease and ESRD Flashcards Preview

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Flashcards in Week 4: chronic kidney disease and ESRD Deck (10):
1

Define chronic kidney disease

1. decrement in GFR <60ml/min/1.73m2 for greater than 3 months
and/or
2. evidence of renal damage
-abnormal anthology
-abnormal urine microscopy
-abnormalities on renal imaging

2

epidemiology of CKD

-prevalence: 11% of people in US have CKD
-500,000 will develop ESRD
-biggest cause is Diabetic Kidney disease
-2nd cause is HTN

3

Risk factors for CKD progression

1. proteinuria
2. hypertension
Goal is for <130/80 in presence of proteinuria. Bp is not as important without proteinuria
-inhibiting RAS if there are no contraindications

4

complications of CKD

1. metabolic derangements, impaired excretion of :
-Na, K, phosphate, H+, uric acid,
-impaired urinary dilution and concentration
2. cardiovascular complications
3. CKD mineral bone disorder
4. anemia
5. platelet dysfunction

5

Principles of renal replacement therapy

1. dialysis is a means of solute clearance and volume removal
2. primary mechanism of solute removal is diffusion
3. primary mechanism of fluid removal is hydrostatic pressure

6

Stages of CKD

STAGES
1. kidney damage with GFR >90
2. Kidney damage with GFR 60-89
3. moderate: GRF 30-59
4. severe: GFR 15-29
5. kidney failure/ESRD: GFR<15
Anyone with GFR less than 60 has CDK no matter the kidney pathology

7

cardiovascular complications

-ischemic heart disease: accelerated atherosclerosis: traditional factors (HTN, DM, hyperlipid), non traditional risk factors (inflammation, increased oxidative stress)
-heart failure: chronic volume overload, vascular calcification
-arrhythmias: cardiac remodleling, metabolic derangements (hyperkalemia)

8

CKD Mineral Bone disorder

-with decreasing GFR, PTH levels rise due to decreased levels of activated Vit D, hyperphophatemia and hypocalcemia
-high phosphorus stimulates PTH
-phophorus also complexes with Ca-->decreases Ca levels-->doesn't bind to CaSR and releases inhibition on PTH release
-P also stimulates FGF 23 (normally inhibits PTH) but in hyperparathyroidism, this function is not effective
-normally, PTH increases in response to low Ca. It increases bone turnover, reabsorption of calcium, activates Vit D
-hyperparathyroidism leads to high bone turnover, increased osteoclast activity causing irregular woven collagen matrix that is weak

9

Management of secondary hyperparathyroidism

-restrict phosphate in diet
-phosphate binders with meals
-screen for 25-OH vitamin D deficiency
-correct hypocalcemia
-treat with activated Vit D compounds (calcitriol, paricalcitol)
-treat with calcimimetics: looks like Ca and binds to CaSR receptor

10

Anemia of CKD

-EPO is synthesized by type 1 renal interstitial fibroblasts
-EPO deficiency--> normochromic normocytic anemia
-more frequent when GFR <30