CKD Flashcards
CKD
broad range of disease severity and significant heterogeneity in risk of profession to end-stage renal disease, morbidity, mortality
CKD definded
based on 3 or more months of either kidney damage (albuminuria, kidney biopsy finding, imaging abmn) or GFR ,60
CKD- epidemiology
low GFR increases risk of systemic complications-CV disease, HTN, mineral/bone disorders, anemia- mortality and progression to end stage renal disease.
Dominant Risk factors for CKD
DM and HTN
Testing, risk stratification, treatment plan
differ based on eGFR and UACR
Detection of CKD- Recommendation
Test for CKD among high risk populations with DM and HTN
early detection
allows for complication management before symptoms occur and slows loss of kidney function over time
Detection by PCP
likely to avoid NSAIDs, use ACE/ARB when indicated and receive proper nephro care
Estimated Glomerular Filtration rate
most accurate assessment of kidney function, inaccurate in setting of AKI
Urine studies- Elevated albuminuria or protenunuria
Albuminuria- critical to evaluate prognosis
Albumin-CR- Ratio- more sensitive and specific marker of CKD than spot urine protein/creatinine ratio
CKD progression and complications- treatment aims to
delay progressive loss of kidney function, prevent/manage complications
Interventions fo Delay CKD Progression
manage HTN, Statin Use, Control DM, Correct Metabolic acidosis
Manage HTN
BP target is <130/80, sodium controlled diet, <2000mg of NA per day
Use of RAAS bloackers (ACE/ARB) for albuminuria and HTN
use in CKD with/out DM + A2/A3 levels of albuminuria, hyperkalemia ensues then look into ways to lower K, D/C RAAS blocker only of other methods to lower K fail. NEVER use ace and ARB in combo
Thiazides- stage G1-3b, loop diuretics second line with stage 4- BID
Statin Control
statin based therapies reduce vascular even in CKD
Control DM-
target A1c 7%, Higher target with limited life expectancy, reduces progression of albuminuria and loss of kidney function over time
CKD Anemia
measure hgb annually, start in G3a CKD- erythropoietin production decrease with low GFR
CKD+ mineral/bone disorder
secondary hyperparthyroidsm, hypocalcemia, hyperphosphatemia, decreased Vitd, vascular calcification- Begins in stage G3b- Measure at least once for baseline levels- Ca, phosphorus, intact parathyroid hormone, total 25-hydroxy VitD
Correct Metabolic acidosis
tx with oral alkali- achieve normal serum bicarb- slows kidney disease progression, Bicarb <22 prescribe sodium bicarb (650 TID), alternative- Sodium Citrate 30ml daily, if these fail- refer to nephro
Patient safety in CKD
Meds and metabolites are excreted by kidneys- dose adjustments on eGFR need to occur to reduce complications
D/c or briefly hold
RAAS blockers, NSAIDs, diuretics, metformin- r/t lactic acidosis- A patient safety approach to CKD considers the level of eGFR in prescription practice
NSAIDs
inhibit vasodilatory prostaglandins- esp with dehydration and HF- acute kidney injury; long term use increase rate of progression of CKD; Inquire about use of these OTC meds-educate potiental harm and SE- allergic interstitial nephritis, ^K, HTN, edema. Avoid with GFR less than 30. Limit these meds with GFR <60
EXTREME caution with CKD+ RAAS And/or diuretic therapy
Metformin:
Discontinue use with GFR <30, use with caugiton for pt with GFR <30-45, not reccomended with pt with Cr men >1.5 woman >1.4 r/t to risk of lactic acidosis
iodinated Contrast
major risk of nephropathy in CKD, prevention strategies include- Minimize dose, volume expansion with IV isotonic saline/bicarb, consider holding med that increase risk fo AKI, IV fluids 1ml/kg start 1 hour prior to procedure cont for 3-6hr post, measure kidney function 48-96h after