Week 4: chronic kidney disease and ESRD

Question 1

Define chronic kidney disease

Answer 1

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

Question 2

epidemiology of CKD

Answer 2

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

Question 3

Risk factors for CKD progression

Answer 3

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

Question 4

complications of CKD

Answer 4

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

Question 5

Principles of renal replacement therapy

Answer 5

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

Question 6

Stages of CKD

Answer 6

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

Question 7

cardiovascular complications

Answer 7

• 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)

Question 8

CKD Mineral Bone disorder

Answer 8

• 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

Question 9

Management of secondary hyperparathyroidism

Answer 9

• 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

Question 10

Anemia of CKD

Answer 10

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