Chronic Kidney Dz Flashcards
CKD: definition
Irreversible damage to parenchyma
Wide spectrum of primary diseases & different pathophysiological processes
Characteristic progressive decline: glomerulosclerosis, tubulointerstitial fibrosis
AKI v CKD
AKI: days-weeks
CKD: 6months-years
AKI: inability to regulate volume & most solutes
CKD: compensated
AKI: GFR=0
CKD: GFR = diminished but finite
AKI: potentially reversible
CKD: irreversible
Estimation of GFR: how to calculate this
1.86*Pcreatinine*age
*0.7242 for women
* 1.21 for African Americans
Pathogenesis of CKD
Primary process: dz that directly damage the kidney
Secondary process: non-dz events which inflict further damage in all primary kidney dz
Either way– loss of >50% renal mass –>
hemodynamic adaptation, glomerular htn, single nephron hyperfiltration + activation of RAAS, proteinurea + systemic htn
–> increased inflammation & oxidative stress, decrease in NO
–> damage to all parts of the kidney resulting in glomerulosclerosis & interstitial fibrosis
What is hyperfiltration?
Its a consequence of dying nephrons
The surviving nephrons compensate, so you don’t have a decline in overall GFR until >50% of the functioning nephrons are lost
How do you diagnose CKD?
Differentiate whether’ it’s acute or chronic: trend of creatinine, look for manifestations of chronic dz (anemia, hyperparathyroidism, well compensated?), imaging (to find renal vascular dz, post renal obstruction, and renal failure- tubulointerstitial fibrosis- echogenic by ultrasound, renal parenchymal volume loss, enlarged kidneys, obstruction, cystic dz)
Urinalysis: microscopic exam, quantify protein the urine with a spot sample
Renal ultrasound
Small kidneys can usually mean….
end stage renal dz
Large kidneys can mean…..
diabetic nephropathy
polycystic kidney dz
anything with deposits: amyloid, myeloma, cast nephropathy, interstitial nephritis, HIV-associated nephropathy
What are the consequences of CKD?
anemia
bone mineral dz (phos retention+decreased vitD–> 2ndary hyperparathyroidism –> renal osteodystrophy)
hypertension
cardiovascular dz: leading cause of death in ckd!
uremia
acidosis & electrolyte abnormalties
volume overload
Whats the mechanism of anemia in CKD?
Erhytheropoietin deficiency: cells in cortex sense hypoxia and seceret epo normally…this stops working
Inflammatory cytokines promote destruction of immature erythroblasts & release of hepcidin, which blocks iron absorption in the intestine and promotes iron release from macrophages
What’s the pathogensis of CVD in CKD?
CKD –> htn, ECV expansion, anemia
–>
LV hypertrophy
+ traditional and other sik fractors associated with CKD and uremia i.e. diabetes, htn, hyperlipidemia –> accelerated atherosclerosis & vascular calcification –> coronary ischemia –>
–> Cardiac fibrosis and remodeling, cardiomyopathy
–> CHF, myocardial infarction, sudden death
How do you get uremia in CKD? what are the manifestations? treatment?
Uremia = due to accumulation of organic waste products that are normally cleared by the kidney
Urea is quantitatively the most important solute excreted by the kidney but not thought to contribute substantially to uremic sx
Sx include: fatigue, anorexia, nausea, decreased mental acuity, pruritis
Treatment: dialysis or kidney transplant
How do you treat CKD?
Treat any primary cause
Proteinurea with RAAS inhibitors
Hypertension control
Glucose control in diabetics
Monitoring and treating the extra-renal manifestations of CKD
Dose ajust medications based on GFR
Avoid nephrotoxins: NSAIDS, IV contrast
Dietary modifications
Proteinurea in CKD: how do you test? whats the significance?
Screen with urine dipstick, then quantify with 24 h collection, spot microalbumin, or spot sample of urine protein and creatinine
Microalbuminurea = 30-300 mg/g
Albuminuria >300 mg/g
Independent of eGFR, proteinurea is associated with increased all cause mortality, CV events and mortality, progression of CKD, and ESRD
