Lecture 6 - Chronic Kidney Disease Flashcards
what is the gold standard for early detection of kidney disease?
GFR
what is normal GFR level?
3.5 - 4.5
what kidney functions are impaired in CKD?
- excretory functions - nitrogenous wastes, P, K, meds, etc
- regulatory functions - fluids, electrolytes, acid-base, minerals, BP
- synthetic/endocrine function - Vit D, EPO, angiotensin-renin system
10 clinical problems seen in CKD
- azotemia
- dehydration
- UTI
- metabolic acidosis
- anemia
- hypertension
- electrolyte disorders
- hyperparathyroidism
- drug interactions
- uremia side effects: GI disturbances, neuromuscular dz, etc.
what is the most important treatment for azotemia?
decreasing the protein in the diet!!
what are 3 basic treatments for azotemia?
- decreasing protein in diet
- provide good quality diet - alter protein-calorie malnutrition
- treat inappetence by controlling nausig and vomiting
role of azodyl in tx CKD
it is an enteral dialysis used to help resolve azotemia
why are CKD patients more likely to get UTIs?
because they can’t concentrate their urine anymore making it easier for bacteria to grow
why do CKD patients get metabolic acidosis? what should serum bicarb be?
bc they are losing bicarb in the urine.
want to maintain serum bicarb > 20mEq/L
what causes anemia in CKD patients? how is it tx?
caused by EPO deficiency (EPO is produced by peritubular capillary endothelial cells and fibroblasts)
tx by: blood transfusions, recombinant human EPO and dabopoetin
when do CKD patients get hypertension?
in advanced IRIS stages
- the more progresive the CKD, the worse the hypertension and hte more uremic crises you get
consequences of hypertension in CKD patients in kidney
the higher the BP, the more likely to get proteinuria
- decreases GFR
- glomeruloscloersis
- tubular ischemia
effects of hypertension in CKD patients in teh brain and eye
- hypertensive encephalopathy
- stroke
eye:
effects of hypertension on CV in CKD patients
LV hypertrophy
cardiomegaly
murmurs
effects of hypertension in CKD patients on glomerular autoregulation. how is it tx?
- causes hydrodynamic endothelial damage
- increases protein permeability
- induces inflammatino
tx
- ACE-inhibitors: enalapril and benazapril
Amlodopine
Ca-channel blocker
- dilates AFFERENT vessels
- decreases total vascular resistance ie it lowers systemic BP
- works fast
- PROBLEM: it blocks renal autoregulation. this means in dogs you must first give an ACE-inhibitor to protect the glomerulus because it causes urinary PG excretion (~ vasodilation) to decrease.
Enalapril, Benazepril
- ACE-inhibitor
- vasodilates EFFERENT vessels
- mild anti-hypertensive, start with this then go to amlodopine
- ** anti-proteinuric **
mineral disorders seen in CKD patients
hypoK
hyperP
why does hyperparathyroidism develop in CKD patients? describe the pathogenesis
in an effort to “maintain normalcy” of serum P and Ca as CKD progresses.
pathogenesis: decrease calcitriol production which decreases Ca and increases P retention
what are the clinical consequences and Tx of hyperparathyroidism?
clinical consequences:
- renal osteodystrophy, bone pain
- PTH toxicity - increases cytosolic Ca
- dystrophic calcification
tx
- restrict P in diet
- intestinal P binder (never give > 180 mg/kg/day).
Al-based = hydroxide (most potent), carbonate
Ca-based = acetate, carbonate, citrate
Non-Al, non-Ca = sevelamer, lanthanum
you can slow progression of CKD by:
- diet - lower protein and P
- control BP with Ace-I and Ca-channel blocker
- proteinuria - diet and Ace-I
- N-3 poly-unsaturated fatty acids
what are the effects of Ace-I?
- decreases proteinuria
- decreases glomerular capillary pressure - which slows fibrosis of glomeruli
- decreases systemic BP
two types of CKD are?
- glomerular diseases –> loss of permaselectivity
- proteinuric kidney disease
- protein loss increased with hypertension - interstitial disease –> loss of permeability
- azotemic kidney disease = decreased GFR
