8-20 Chronic Kidney Disease Flashcards
What are the essentials of dx’ing chronic kidney disease (CKD)?
Decline in the GFR over months to years
Persistent proteinuria or abnormal renal morphology may be present.
Hypertension in most cases.
Symptoms and signs of uremia when nearing end-stage disease.
Bilateral small or echogenic kidneys on ultrasound in advanced disease.
What are the stages of CKD? What GFR is associated with each stage?
1 Kidney damage with normal or ↑↑ GFR ≥ 90
2 Kidney damage with mildly ↓ GFR 60–89
3 Moderately ↓ GFR 30–59
4 Severely ↓ GFR 15–29
5 End-stage renal disease (ESRD) < 15
Why does CKD lead to a progressive decline in kidney fxn, even if the cause of it is identified and treated?
Destruction of nephrons leads to compensatory hypertrophy and supranormal GFR of the remaining nephrons in order to maintain overall homeostasis
compensatory hyperfiltration leads to overwork injury in the remaining nephrons, which in turn causes progressive glomerular sclerosis and interstitial fibrosis
What is an initial treatment option for CKD?
Angiotensin receptor blockers (ARBs) and ACE inhibitors can help reduce hyperfiltration injury
helpful in slowing the progression of proteinuric CKD
Why is serum creatine not a great marker for renal damage?
serum creatinine may remain relatively normal even with significant loss of renal mass due to remaining nephron’s hyperfiltration
- relatively insensitive marker for renal damage and scarring
What are the major signs and symptoms of CKD?
initially asymptomatic
HTN
Coronary artery disease
Heart failure
pericarditis
Bone metabolism problems
anemia
hypercoagulopathy
hyperkalemia
acid-base problems
neurologic deficits
endocrine disorders
What is the most common complication of CKD? Why?
HTN
- hyperreninemic and hyperaldosteronism
- disturbed Na+ homeostasis -> needs low salt diet, diuretics
titrate meds carefully, can destroy remaining GFR and kidney fxn if kidneys are over-diuresed with diuretics, or underperfused with ACEi or ARBs
Why are people with CKD at increased risk for CAD?
Increased risk for uremia-mediated vascular calcification
- abnormal Ca++, PO4 metabolism
Decrease risk factors and pursue lifestyle changes aggressively to reduce risk
Why are people with CKD at an increased risk for HF?
increased cardiac workload:
hypertensive disease
volume overload
anemia
reduced vessel compliance
calcification of vessels, atherosclerosis
People who have CKD can develop HF with what characteristics?
left ventricular hypertrophy
diastolic, systolic dysfxn
How can you treat HF in someone with CKD?
Restrict salt
Start with thiazide diuretics, move to loop diuretics at GFR <30
Can use ACE inhibitors, or ARBs if closely monitored for hyperkalemia and kidney fxn
Digoxin toxicity increased
What symptoms of pericarditis can be detected with CKD?
Pericarditis as result of CKD is rare
Hear pericardial friction rub
pleuritic chest pain
Hemorrhagic cardiac tamponade
EKG abnormalities assoc. with K+ abnormalities
CKD is associated with bone problems. Why?
Deranged tubule fxn -> hyperphosphatemia, hypocalcemia, hypo-Vit D
Low Ca+ and high PO4 leads to unopposed PTH
PTH stimulates osteoblasts to secrete RANK-L
continuous RANK-L secretion leads to constant osteoclast breakdown
Ca++ liberated from bone, bone turns to swiss cheese equivalent
What specific bone problems/renal osteodystrophy are associated with CKD? What are the symptoms of each?
osteitis fibrica cystica
- too much PTH leads to lesions, proximal mm weakness and bone pain
adynamic bone disease
low bone turnover
osteomalacia
- lack of bone mineralization
If your patient has renal osteodystrophy, what should you look out for? How should you treat it?
- watch for fractures
Block oral absorption of PO4 with PO4 binders with meals
Titrate active vitamin D
Use meds (cinacalcet) that block PTH release
