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CVPR: Renal > Chronic Kidney Disease > Flashcards

Flashcards in Chronic Kidney Disease Deck (17)
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1

Chronic kidney disease (CKD) definition

  • permanent reduction in GFR
  • divided into 5 stages
  • ==> end stage renal disease (ESRD) = CKD progressed to point where renal replacement therapy (dialysis, transplant) needed

2

Stages of CKD (Description, GFR, Action)

  • Stage 1 = kidney damage, normal GFR
    • GFR > 90
    • Dx & Tx
  • Stage 2 = kidney damage, mild GFR decrease
    • GFR = 60-89
    • Estimate progression
  • Stage 3 = moderate GFR decrease
    • GFR = 30-59
    • Tx complication
  • Stage 4 = severe GFR decrease
    • GFR = 15-29
    • Prepare for renal replacement
  • Stage 5 = kidney failure
    • GFR < 15 or dialysis
    • Dialysis or transplant

3

Most common causes of CKD

  • Diabetic nephropathy**
  • Hypertensive nephrosclerosis & Renal vascular disease
  • Glomerulonephritis
  • Polcystic kidney disease
  • Interstitial nephritis
  • Obstruction

4

Renal adaptation that maintain solutes despite renal insufficiency

  • Intact nephron hypothesis: fxning nephrons compensate/balance filtration & net excretion
  • Magnification phenomenon: altered solute handling to maintain balance
  • Individual solute control systems
  • Trade-off hypothesis: mechanisms that maintain individual solutes => negative effects on other systems => contribute to uremia

5

Creatine and Urea balance in CKD

  • rate of filtration is maintained @ expense of elevated plasma concentration
  • excretion rates are constant despite diminished clearance

6

Water balance in CKD

  • faction of water reabsorbed must decrease
  • progressive CKD => compromised ability to excrete water => hypoosmolality (hyponatremia)
  • fixed urine concentrating => dehydration = water deficiency (hypernatremia)

7

Sodium balance in CKD

  • fraction of sodium reabsorbed must be decreased/excreted must increase
  • increased natriuretic peptide => increased excretion
  • unable to respond to sudden changes in sodium intake or extrarenal loss

8

Potassium balance in CKD

  • increased tubular secretion of potassium helps maintain balance until severe CKD
  • then fecal excretion of potassium increases

9

Hydrogen ion balance in CKD

  • fxning nephrons produce mroe NH4+ to compensate/maintain acid balance
  • @ GFR < 20-25ml/min => retention of hydrogen ions + bicarb => non-anion gap metabolic acidosis

10

Uremia definition

  • "urine in blood"
  • clinical syndrome from retention of substances normally ecreted into urine
  • substances accumulate ==> toxicity

11

Main components in pathogenesis of uremia

  • retained metabolic products
    • e.g. urea, nitrogenous waste
  • overproduction of counter-regulatory hormones
    • overproduction of PTH in response to hypocalcemia
    • overproduction of natriuretic hormone in response to volume overload
  • underproduction of renal hormones
    • decreased EPO => anemia
    • decreased 1-hydroxylation of vitamin D => bone disease & 2o hyperparathyroidism

12

Clinical features/organ systems affected by uremia

  • Neurological Disorders:
  • Hematological Disorders
  • Cardiovascular Disorders
  • Pulmonary Disorders
  • Gastrointestinal Disorders
  • Metabolic-Endocrine Disorders
  • Bone, Calcium, Phosphorus Disorders
  • Skin Disorders:
  • Psychological Disorders
  • Fluid and Electrolyte Disorders

13

Characteristics of Anemia in CKD

  • occurs @ GFR < 25 ml/min; may occur @ mild CKD
  • EPO production/response is depressed
  • Red cell survival decreased
  • blood loss due to decreased platelet fxn
  • marrow space fibrosis <==osteitis fibrosa of 2o hyperPTHism

14

Characteristics of HTN in CKD

  • occurs @ 80-90% of CKD pts
  • expansion of ECG <== reduced sodium excretion ability
  • increased RAS
  • dysfxn of ANS: insensitive barorecptors ==> increased sympathetic tone
  • diminished vasodilaors

15

Characteristics of Mineral Bone Disease in CKD

  1. trade-off: 
    1. phosphorous retained => low Ca2+ => PTH release
    2. prolonged elevated PTH => no further response @ renal tubules => hyperphosphatemia + hypocalcemia
    3. high PTH => bone disease + osteitis fibrosa
  2. PTH regulation
    1. Ca2+ receptor: binding to receptor => downregulation of PTH
    2. 1,25 vitamin D: downregulates PTH
    3. FGF-23 downregulates 1,25 vitamin D => decreased calcium/phosphorous absorption @ gut + increased PTH activity

16

Pathophysiology of progression of CKD

  • compensatory events + loss of nephrons ==> accelerate rate of destruction
  • @ slowly progressive phase: loss of kidney fxn occurs at constant rate
  • glomerular HTN = compensatory mechanism to attempt to maintain GFR ==> glomerular destruction over time

17

Tx of CKD

  • aggressive tx of HTN w/ACE-I & ARBs
  • maintain serum phosphorous w/in normal using dietary counseling and phosphate binders
  • @ uremic syndrome: hemodialysis, peritoneal dialysis, renal transplantation