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M2 Renal > 1/25 Chronic Kidney Disease - Lefavour > Flashcards

1/25 Chronic Kidney Disease - Lefavour Flashcards

1
Q

chronic kidney disease

definition

A
  • sustained and irreversible decrease in GFR
  • usually progressive once creatinine greater than 3 or GFR <25ml/min
  • characterized by:
    1. excretory failure: accumulation of nitrogenous wastes
    2. regulatory failure: abnormal conservation or excretion of fluids and electrolytes
    3. biosynthetic failure: inadequate production of ammonia, vitD, epo
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2
Q

measures of renal fx

GFR

clearance

creatinine

BUN

Cystatin C

A

GFR

  • unit of measure to determine kidney fx → can use to estimate severity and progression of renal disease
  • measures amt of plasma filtered across glom caps

clearance

  • indirect measurement of substance feely filterable (not bound to proteins, neither reabs nor secreted)
  • gold standard: inulin clearance

creatinine: muscle breakdown pdt produced at relatively constant rate

  • freely filtered by glom then neither significantly secreted nor reabs
  • gives you a ROUGH ESTIMATE of kidney fx
  • limitations
    • serum Cr is a poor estimate of GFR
    • 24h Cr clearance hard to measure/less accurate in adv renal failure

BUN

  • usually 10:1 prop to Cr
  • disprop incr in volume depletion, GI bleed, corticosteroid use, high protein diet, obstruction, catabolic state, outdated tetracycline
  • disprop decr in low protein diet, liver disease, malnutrition, SIADH

cystatin C

  • Cys protease produced by all cells → completely filtered by glom
  • might be used in formula in combo with Cr
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3
Q

definition of CKD

A

3 or more months of:

  • markers of kidney damage (1 or more)
  • decreased GFR
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4
Q

stages of CKD and corresponding GFR

A
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5
Q

proteinuria in CKD

A

marker of kidney damage when persistently elevated

  • due to incr glomerular permeability to macromolecules

incr urinary albumin excretion (UAE) is a sensitive marker for CKD due to: DM, GN, HTN

edit to pic: second row is A2

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6
Q

MEMORIZE

normal lab values for:

  • BUN
  • creatinine
  • Ca
  • phosphorous
  • Na
  • Cl
  • K
  • CO2
A
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7
Q

major causes of CKD

A
  • glomerulonephropathies
  • tubulointerstitial
  • hereditary
  • obstructive
  • vascular
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8
Q

acute kidney injury vs chronid kidney disease

A
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9
Q

remnant kidney model (rat)

A

5/6 nephrectomy (remove 1 kidney, 2/3 of other kidney)

see:

  • glomerular hypertrophy
  • FSGS: focal segmental glom sclerosis
  • marked incr in single nephron GFR (due to marked reduction in glom arteriolar resistance: aff > eff) →
    • incr intraglom pressure
    • marked incr in plasma flow

hyperfiltration and hypertrophy of remaining nephrons is mediated by cytokines, vasoactive hormones, gfs →

  • impaired GFR
  • scarring
  • progressive deterioration
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10
Q

progression of renal disease

(proposed mechs)

A

incompletely understood!

  • direct endothelial cell damage
  • detachment of glom epithelial cells from wall stress and incr diameter → proteinuria
  • production of cytokines and matrix from strain on mesangial cells → tubulointerstitial infl and fibrosis
    • feedback loop: further nephron dropout → ESRD
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11
Q

CKD progression prevention strategies

bp control

A

blood pressure control

  • reduce to < 140/80, <130/80 if significant proteinuria
  • helps decr rate of progression in diabetic/non CKD
  • ACE inhibitors (ARB in DM2) have benefit beyond bp lowering → more effective with low salt diet, diuretics
    • imp to check BMP for creat, K 7-14d after ACEI/ARB/dose increase
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12
Q

CKD progression prevention strategies

specific agents for HTN

A

AII inhibition

  • ACE inhibitors or ARBs inhibit angiotensin II → slows deterioration by
    • decr intraglom HTN
    • decr proteinuria (through changing glom barrier size selectivity)
  • may also effect growth factors, fibrosis

benefit most with pt w significant proteinuria

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13
Q

CKD progression prevention strategies

protein restriction

A

GFR under30-60: lower protein intake to .6-.8 g/kg/d

  • need to be of high biologic value
  • can help reduce other complications from high protein intake (acidosis, hyperP, HTN, edema, uremic sx)
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14
Q

CKD progression prevention strategies

diabetes control

A

early intensive tx for diabetes, glucose control → helps prevent microvascular complications that would result in CKD

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15
Q

AKI and CKD outcome

A

AKI is a major risk factor for long term kidney fx loss

  • 15-20% of AKI cases will progress to adv CKD
  • progression of CKD often characterized by repeated episodes of non-dialysis-requiring AKI
  • any AKI assoc with excess mortality
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16
Q

complications in CKD

A
17
Q

sodium in CKD

A

normally filter approx 25k mEq → excrete approx 100-150 mEq

  • FeNa < 1%

decrease in GFR means the kidney needs to excrete a progressively larger fraction of filtered load to stay in balance!

  • ANP and other modulators of tubule transport account for incr excretion per nephron
  • conservation of Na impaired → can develop volume depletion if too severe

typical pt: 2-3L urine/day ~50mEq Na/L to remain in balance

18
Q

urine dilution/concentration in CKD

A

dilution

  • in CKD, retain water because just cant filter as much volume with a low GFR
  • incr water intake? positive water balance, hypoNa

concentration

  • in CKD, fixed urine osmolality at approx 300
  • water deprivation? → hyperNa, volum e depletion
19
Q

potassium in CKD

A
  • most K is in ICF
  • filtered K is reabs, then secreted in distal nephron
  • normally, only 5-10% excreted in stool, but see some adaptation and incr in CKD

major mediators of K excretion

  • aldosterone
  • urine flow

K restriction is imp in dietary management of pts with adv CKD

hyperkalemia develops late in course of CKD unless exhibiting type IV RTA

20
Q

tx of hyperkalemia

A
  1. stabilize cardiac conduction: Ca gluconate → stabilize cardiac membrane (won’t lower serum K)
  2. move K into cells: glucose/insulin, bicarb, nebulized albuterol
  3. remove K from body
    • diuretics (if adequate renal fx)
    • medication (cation ion exchange resins)
    • hemodialysis
21
Q

acid/base in CKD

A
  • metabolic acidosis common when GFR <25
    • decr nephron mass → decr ammonia secretion → decr excretion of acid load
    • slight decr in plasma bicarb → tubular cells incr ammonium production and H secretion
  • tx: maintain bicarb in normal range with bicarb supplements or citrate salts
22
Q

CKD mineral/bone disorder

A

systemic disorder of mineral and bone metabolism due to CKD manifested by:

  • abnormalities of Ca, P, PTH, vitDmetabolism (maybe FGF23)
  • abnormalities in bone turnover, mineralization, volume, linear growth, strength
  • vascular or other soft tissue calcification
  • often see: low serum Ca, elevated serum P, elevated iPTH
23
Q

vitamin D metabolism

role of kidney

A

kidney makes active form of vitD (1,25 OH2 vitD) aka calcitriol

  • incr Ca and PO4 absorption from gut
  • enhances bone resorption along with PTH
    • calcitriol drops before PTH increases
  • decr urinary Ca, PO4 (possible)
  • inhibition of PTH production/release
24
Q

FGF23

A

fibroblast growth factor 23

  • secreted by osteocytes
  • functions
    • promotes renal PO4 excretion
    • stimulates PTH
    • suppresses calcitriol → drops PO4 absorption from gut
  • levels increased early in CKD bc stimulated by elevated PO4
25
Q

types of MBD

x3

A
  1. osteitis fibrosa cystica
    • most common
    • hyperparathyroidism → PTH stimulates osteoclasts
    • high turnover type bone reabs, subperiosteal lesions
  2. adynamic
    • low turnover
    • spontaneously low PTH production or iatrogenic suppression
  3. osteomalacia
    1. lack of bone mineralization
    2. hypovitD
26
Q

hyperparathyroidism tx principles

A
  • correct hypoCa
  • dietary PO4 control
  • assess PTH
  • treat and control secondary hyperparathyroidism
  • parathyroidectomy (rarely needed)
27
Q

anemia in CKD

A
  • almost universal in severe CKD
  • develops when creatinine > 2-3mg
  • normocytic, normochromic

major component: decr epo production by kidney due to decr renal mass

  • epo binds to erthroid progenitors → differentiation into erythrocytes
28
Q

cardiovascular complications

A
  • HTN (80-90 in esrd) → LVH
  • CHF, edema due to salt/water retention
  • pericarditis → absolute indication to initate dialysis
29
Q

uremia

A

manifestation of severe kidney failure

accumulation of organic waste products normally cleared by kidney, impaired reg mechs, hormonal alterations

BUN and creatinine are surrogate markers for accumulation of toxins

30
Q

CKD tx

A
  • treat correctable causes
    • obstruction, drugs, ECF vol depletion, CHF, infection, vascular issues, metabolic issues
  • slow progression
  • minimize sx, maintain nutrition, fluid/electrolyte balance,
  • treat metabolic acidosis, anemia, hyperparathyroidism, HTN
  • adjust med dosages (tox)
  • prep for dialysis and transplant
31
Q

nutrition/metabolic effects of ESRD

A
32
Q

modalities for ESRD tx

A
33
Q

kidney transplatation

eval

exclusions

A

evaluate when GFR 20-25

  • cardiovasc
  • vasc
  • other

exclusions:

  • active infection
  • malignancy
  • medical (?)
  • unmanageable patients

M2 Renal (12 decks)

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