1/25 Chronic Kidney Disease - Lefavour Flashcards
(33 cards)
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- disprop incr in volume depletion, GI bleed, corticosteroid use, high protein diet, obstruction, catabolic state, outdated tetracycline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
