1/25 Chronic Kidney Disease - Lefavour Flashcards
chronic kidney disease
definition
- sustained and irreversible decrease in GFR
- usually progressive once creatinine greater than 3 or GFR <25ml/min
- characterized by:
- excretory failure: accumulation of nitrogenous wastes
- regulatory failure: abnormal conservation or excretion of fluids and electrolytes
- biosynthetic failure: inadequate production of ammonia, vitD, epo
measures of renal fx
GFR
clearance
creatinine
BUN
Cystatin C
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- disprop incr in volume depletion, GI bleed, corticosteroid use, high protein diet, obstruction, catabolic state, outdated tetracycline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
definition of CKD
3 or more months of:
- markers of kidney damage (1 or more)
- decreased GFR
stages of CKD and corresponding GFR
proteinuria in CKD
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
MEMORIZE
normal lab values for:
- BUN
- creatinine
- Ca
- phosphorous
- Na
- Cl
- K
- CO2
major causes of CKD
- glomerulonephropathies
- tubulointerstitial
- hereditary
- obstructive
- vascular
acute kidney injury vs chronid kidney disease
remnant kidney model (rat)
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
progression of renal disease
(proposed mechs)
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
CKD progression prevention strategies
bp control
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
CKD progression prevention strategies
specific agents for HTN
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
CKD progression prevention strategies
protein restriction
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)
CKD progression prevention strategies
diabetes control
early intensive tx for diabetes, glucose control → helps prevent microvascular complications that would result in CKD
AKI and CKD outcome
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
complications in CKD
sodium in CKD
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
urine dilution/concentration in CKD
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
potassium in CKD
- 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
tx of hyperkalemia
- stabilize cardiac conduction: Ca gluconate → stabilize cardiac membrane (won’t lower serum K)
- move K into cells: glucose/insulin, bicarb, nebulized albuterol
- remove K from body
- diuretics (if adequate renal fx)
- medication (cation ion exchange resins)
- hemodialysis
acid/base in CKD
- 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
CKD mineral/bone disorder
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
vitamin D metabolism
role of kidney
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
FGF23
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
types of MBD
x3
-
osteitis fibrosa cystica
- most common
- hyperparathyroidism → PTH stimulates osteoclasts
- high turnover type bone reabs, subperiosteal lesions
-
adynamic
- low turnover
- spontaneously low PTH production or iatrogenic suppression
-
osteomalacia
- lack of bone mineralization
- hypovitD
hyperparathyroidism tx principles
- correct hypoCa
- dietary PO4 control
- assess PTH
- treat and control secondary hyperparathyroidism
- parathyroidectomy (rarely needed)
anemia in CKD
- 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
cardiovascular complications
- HTN (80-90 in esrd) → LVH
- CHF, edema due to salt/water retention
- pericarditis → absolute indication to initate dialysis
uremia
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
CKD tx
- 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
nutrition/metabolic effects of ESRD
modalities for ESRD tx
kidney transplatation
eval
exclusions
evaluate when GFR 20-25
- cardiovasc
- vasc
- other
exclusions:
- active infection
- malignancy
- medical (?)
- unmanageable patients
