CKD Flashcards

1
Q

definition of CKD

A

GFR<60 for at least 3 months
+/- kidney damage

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2
Q

what stage of CKD do symptoms begin to present? and what are the most common early symptoms?

A

they are beginning in G3a/b but they may go unnoticed: tired, nocturia, mild anemia
Stage G4:
nocturia, fatigue, cold intolerance, abnormal taste, anorexia, increased Phos, decreased Ca, increased K, metabolic acidosis, worsening anemia, inability to adjust to changes in Na intake

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3
Q

protein recommendations for CKD 3-5 without DM?

A

restrict protein intake to 0.55-0.6 g/kg/day. can supplement with amino acid analogs

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4
Q

protein recommendations for CKD 3-5 WITH DM?

A

restrict protein intake to 0.6-0.8 g/kg/day

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5
Q

protein recommendations for CKD on dialysis?

A

(with or without DM)
restrict protein intake to 1-1.2 g/kg/day

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6
Q

what are some pharm agents recommended to decrease proteinuria?

A

RAAS inhibitors
SGLT2 inhibitors
nonsteroidal MRA finerenone

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7
Q

when are RAAS inhibitors (ACE/ARB) initiated/ discontinued?

A

first line for albumin category A2 (30-300)
regardless of GFR category
titrate to maximum tolerated dose and CONTINUE AT THE MAX DOSE: IF HYPERKALEMIA DEVELOPS CONTINUE THE RAAS INHIBITOR AND TREAT HYPERKALEMIA
don’t discontinue until >30% decrease in GFR, or when dialysis is initiated.
monitor SCr, K every 2-4 weeks

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8
Q

when are SGLT2 inhibitors initiated/discontinued

A

1st line for DM2 (eGFR at least 20)
if eGFR falls below 20, continue SGLT2 if it was already initiated.
discontinue when dialysis is initiated.

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9
Q

when is finerenone initiated

A

T2DM with:
-eGFR >25
-normal serum potassium
-albuminuria (>30) despite max dose of RAAS

(role in non-DM CKD unknown)

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10
Q

role of SGLT-2 inhibitors in non-DM CKD?

A

heart failure
ACR>200

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11
Q

what causes hypertension associated with CKD?

A

fluid overload and RAAS hyperactivity (adaptive responses)

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12
Q

goal BP in CKD

A

SBP<120
don’t care about diastolic

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13
Q

treatment of hypertension in CKD

A

1st line: RAAS inhibitor
if BP not at goal: anything that achieves BP goal, any antihypertensive

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14
Q

what are the adaptive responses of CKD that cause fluid imbalance by impaired sodium/water balance??

A

increase in atrial natriuretic peptide (ANP)
increased fractional excretion of sodium (FENa) of functioning nephrons (caused by ANP)
osmotic diuresis: increased solute load in functioning neurons, obligatory water losses that presents as nocturia. kidney unable to concentrate urine

net effect of all this: increased total body Na
(not meaning hypernatremia; it gets diluted out w/ water)

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15
Q

what is the clinical presentation of fluid imbalance in CKD?

A

nocturia
decrease total sodium excretion
volume overload
increased BP

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16
Q

pharmacologic therapy for fluid imbalance in CKD and what to do when there is tolerance

A

first line: loop diuretics (start low and titrate up)
as CKD progresses there will be diuretic tolerance: overall diuresis decreases with long term use. management: add on therapy for synergistic effect with thiazide diuretics (usually don’t work as a single agent when GFR<30, but as an add on they work)
higher doses required to achieve desired effect

17
Q

what causes hyperkalemia associated with CKD

A

decreased renal potassium excretion: decreased glomerular filtration, decreased potassium secretion from distal tubules

18
Q

when does hyperkalemia present in CKD

A

when GFR<20

19
Q

goal potassium in late CKD

A

4.5-5.5

20
Q

treatment of hyperkalemia in CKD

A

nonpharm: dietary restriction (cutting back on tomatoes, bananas, potatoes)
severe hyperkalemia: dialysis

pharmacologic:
Use medications that can increase potassium with CAUTION:
-ACE inhibitors
-K-sparing diuretics
-(even beta blockers can inhibit intracellular sodium potassium pump)

Increase potassium excretion with the following agents:
-loop diuretics (kill 2 birds with one stone because they are probably fluid overloaded by this point)
-potassium binders: patiromer, sodium zirconium cyclosilicate, odium piolystyrene sulfonate)
-fludrocortisone

21
Q

patiromer (Veltessa) pros/cons

A

onset: 7 hours, max by 48 hours– do do not use when there is acute hyperkalemia w/ EKG changes
drug interactions: separate from all other drugs by 3 hours
ADEs: diarrhea, constipation, nausea, abdominal discomfort, decreases Mg levels

22
Q

sodium zirconium cyclosilicate (Lokelma) pros/cons

A

decreases K within 1 hour, max effect in 48 hours (a little faster but still not best for EKG changes)
ADEs: edema
separate from other drugs by 2 hours

23
Q

sodium polystyrene sulfonate pros/cons

A

decreases K within 6 hours of dose
ADEs: serious rare GI effects like colon necrosis, bowel perforation
common ADEs: diarrhea, abdominal pain

24
Q

fludrocortisone pros/cons

A

onset: several days
ADEs: HTN, Edema
can be an add on to patients who have hypotension with dialysis since it causes HTN

25
Q

what causes acid/base imbalance in CKD?

A

decreased renal ammoniagenesis: decreased ammonium production, decreased elimination of acid

26
Q

what happens to the acid/base balance in stage 3 CKD

A

bicarb reabsorption is maintained
decreased ammonium production
decreased acid excretion
results in nonanionic gap metabolic acidosis

27
Q

what happens to the acid/base balance in stage 4 CKD

A

bicarb reabsorption maintained
worsening of decreased ammonium production
worsens acid excretion
accumulation of organic anions
creates anion gap metabolic acidosis
net effect: serum CO2 stabilizes as 12-18

28
Q

what are some of the consequences of metabolic acidosis in CKD

A

bone disease
fatigue
dec exercise tolerance
cardiac
hyperkalemia
etc

29
Q

treatment of acid/base in CKD

A

goal CO2 is >22 (avoid rapid changes in pH)
non pharm: increase bicarb in the dialysis solution
pharm: oral bicarb supplements

30
Q

what stage of CKD do electrolyte imbalances begin?

A

stage 4
increase in Phos, K
decrease in Ca