Week 4: chronic kidney disease and ESRD Flashcards Preview

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

Define chronic kidney disease

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


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


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


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


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


Stages of CKD

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


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)


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


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


Anemia of CKD

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