335.4 ð ç« æ«éèš Summary
335.4.1 ð äžå¥è©±çžœçµ
CKD = eGFR < 60 OR kidney damage (albuminuria, hematuria, abnormal imaging, biopsy) ⥠3 monthsïŒå°ç£ ~ 12% æäººçè¡çïŒtop causesïŒDM (DKD) > HTN > GN (IgA, FSGS, lupus) > PKD > tubulointerstitial > vascular > hereditary (Alport, Fabry, sickle cell)ïŒKDIGO 2012 + 2024 stagingïŒ(1) G stage by eGFR G1 ⥠90, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 < 15 or RRTïŒ(2) A stage by UACR A1 < 30, A2 30-300, A3 > 300 mg/gïŒcomplications 6 倧ïŒ(1) cardiovascular (top death cause, CHD risk equivalent)ïŒ(2) anemia (low EPO + iron deficiency + inflammation/hepcidin) â treatment: iron + ESAs + HIF-PHIs roxadustat/vadadustat/daprodustat (NEW, FDA 2023)ïŒ(3) CKD-MBD (hyperphosphatemia + â calcitriol + 2° hyperPTH + â FGF-23 + vascular calcification) â treatment: phosphate binders (non-Ca preferred) + active vit D + cinacalcet/etelcalcetide + parathyroidectomyïŒ(4) fluid + electrolyte (hyperK + acidosis â sodium bicarbonate target HCO3 22-26)ïŒ(5) uremia (encephalopathy, neuropathy, pruritus, bleeding, pericarditis)ïŒ(6) endocrine + nutrition (PEW, insulin resistance, hypothyroidism, infertility)ïŒtarget therapies 2024ïŒSGLT2i (CREDENCE/DAPA-CKD/EMPA-KIDNEY) + finerenone (FIDELIO/FIGARO) + GLP-1 RA (FLOW 2024 semaglutide) + ACE/ARB + statin â DKD nephroprotection paradigmã
335.4.2 ð æ²»ç粟èŠ
- CKD progression slowingïŒACE/ARB (first-line if proteinuria) + SGLT2i (CREDENCE/DAPA-CKD/EMPA-KIDNEY) + finerenone (FIDELIO/FIGARO) + GLP-1 RA (FLOW 2024) + BP < 130/80 + statin
- anemia of CKDïŒiron first â ESAs (target Hgb 10-11.5, CHOIR/TREAT caution higher) â HIF-PHIs (roxadustat, vadadustat, daprodustat) NEW oral option
- CKD-MBDïŒphosphate binders (non-Ca preferred: sevelamer, lanthanum, ferric citrate, sucroferric oxyhydroxide) + active vit D (calcitriol, paricalcitol) + cinacalcet (calcimimetic) + etelcalcetide (parenteral) + parathyroidectomy refractory
- acidosisïŒsodium bicarbonate to target HCO3 22-26
- hyperkalemiaïŒdietary restriction + K binders (patiromer, sodium zirconium cyclosilicate) + adjust ACE/ARB if needed
- CV riskïŒstatin (primary prevention if eGFR < 60 + albuminuria), AC for AF (CHAâDSâ-VASc-based but balance bleeding)
- bleeding (uremic)ïŒDDAVP, cryoprecipitate
- late CKD (G4-G5)ïŒrefer to nephrology, prepare RRT (AV fistula 6-12 mo, PD catheter 4-6 wk), transplant evaluation, conservative care option
335.4.3 ð¯ ç§é«åž«çèåæé
- CKD definitionïŒeGFR < 60 OR kidney damage (albuminuria, hematuria, abnormal imaging, biopsy, transplant) ⥠3 months â duration æ¯ key
- KDIGO G + A stagingïŒG1-G5 by eGFR + A1-A3 by UACRïŒcombined predicts CKD progression + CV events
- CKD top death cause = cardiovascularïŒCHD risk equivalentïŒâ statin for primary prevention if eGFR < 60 + albuminuria
- DKD (diabetic kidney disease) treatment paradigm 2024ïŒACE/ARB + SGLT2i + finerenone + GLP-1 RA â all 4 pillars éœæ nephro/cardio-protective evidence
- landmark trialsïŒCREDENCE (canagliflozin DKD)ãDAPA-CKD (dapagliflozin DKD + non-DM CKD)ãEMPA-KIDNEY (empagliflozin)ãFIDELIO-DKD + FIGARO-DKD (finerenone)ãFLOW (semaglutide CKD 2024)
- HIF-PHIs (NEW 2023 FDA)ïŒroxadustat (Evrenzo), vadadustat (Vafseo), daprodustat (Jesduvroq) â oral HIF-PH inhibitors â endogenous EPO + â hepcidin â effective for renal anemia; alternative to injectable ESAs
- CHOIR (2006) + TREAT (2009) lessonsïŒdonât normalize HgbïŒtarget 10-11.5 g/dLïŒhigher target â â CV events
- CKD-MBD ç çççïŒhyperphosphatemia â 2° hyperPTH â â FGF-23 â â calcitriol â bone disease + vascular calcificationïŒFGF-23 æ¯ earliest biomarker
- phosphate binder selectionïŒnon-Ca-based (sevelamer, lanthanum, ferric citrate, sucroferric oxyhydroxide) preferred é¿å Ca load + vascular calcificationïŒCa-based (Ca carbonate, Ca acetate) acceptable in early stages
- CKD acidosis treatment with sodium bicarbonateïŒtarget HCO3 22-26ïŒevidence (UBI trial) of slowing CKD progression + preventing bone disease + muscle wasting