Antihypertensive Medications in Kidney Disease Flashcards
Case 1. Patient is a 58 year old male with slowly progressively chronic kidney disease due to adult polycystic kidney disease.
Blood pressure is 157/94 mmHg despite full dose lisinopril (80mg PO daily) and chlorthalidone (25mg PO daily). Serum creatinine is 3.4 mg/dL and estimated glomerular filtration rate (GFR) is less than 30 ml/min.
What adjustment needs to be made in his antihypertensive regimen?
You want to control any degree of HTN with CKD
Note that at GFRs that low, thiazides are not going to be effective (below 30 usually), so switching to a loop diuretic may help
What is chlorthalidone?
thiazide diuretic
What kind of things would urinalysis show in this patient?
minimal proteinuria- probably normal urinalysis
What would be the effect of ARBs/ACEIs on potassium?
they would promote hyperkalemia (via lack of aldosterone)
Would this patient have salt-sensitive HTN?
Yes, in CKD salt restrictions should always be part of consouling
Why would dosage of loop diuretics need to be higher to promote diuresis in someone with kidney dysfunction (Like CKD) vs a person with normal kidney function
It is mostly the fact that in someone with CKD you cannot get enough of the drug to the site of action because of dysfunction
Case 2. 48-year-old female with type 2 diabetes mellitus has annual albumin /creatinine ratio (ACR) screening performed and it demonstrates the presence of microalbuminuria (40 mg/gm). Repeat testing confirms microalbuminuria. Blood pressure is 130/80 mmHg. Serum creatinine is 1.0 mg/dL What treatment would you recommend?
Initiate an ACEI or ARB (as long as non-pregnant!!!)
Why are ACEIs/ARBs so good when protein is getting into the urine?
They decrease intraglomerular filtration pressure by inhibitng efferent constriction and thus decrease protein loss
Case 3. 48-year-old female with type 2 diabetes mellitus has annual albumin/creatinine ratio screening performed and it demonstrates the presence of macroalbuminuria (ACR - 800mg/gm creatinine). Repeat testing confirms macroalbuminuria. Blood pressure is 140/90 mmHg. Serum creatinine is 1.0 mg/dL. What treatment would you recommend?
Regardless of the degree of proteinuria, go with ACEIs or ARBs in hopes of halting the progression
What do you need to monitor when giving an ACEI/ARB?
definitely BP but Pcr as well to make sure GFR isn’t dropping too low
Case 4. 62-year-old male with type 2 diabetes mellitus with chronic non-nephrotic range proteinuria. Physical exam demonstrates the presence of edema. Serum creatinine is 2.6 mg/dL and serum potassium is 5.0 mEq per liter. Blood pressure is 150/90. His primary care physician increased his lisinopril from 20 mg to 40 mg daily. At two week follow up blood pressure has improved 136/80, serum creatinine is 2.9 mg/dL and potassium is 5.9 mEq per liter. Plasma bicarbonate is 17 mEq per liter. How do you account for these laboratory changes and what adjustments need to be made in his treatment plan?
GFR decreases so Pcr increases
Pk increases because aldosterone is inhibited
H+ also increases (needs K+ in the urine to secrete) so HCO3- decreases (think about how the intercalated cells in the CD work)
Add a loop diuretic
Case 5. 46-year-old male with dilated cardiomyopathy, chronic congestive heart failure with chronic edema requiring diuretic therapy. He is now receiving high-dose furosemide orally but is still edematous. Other medications include carvedilol and lisinopril. Serum creatinine is 1.0 mg/dL. What steps should be done at this point to better manage his fluid overload?
If ejection fraction is less than 35%, consider adding an aldosterone inhibitor but this probably wont help a ton with the edema
assuming Na intake is good, limit water intake
consider a synergistic effect- add a thiazide
How to assess his diet?
Do a 24 hr urine collection (can only do here because weight is constant)
100mEq is good
higher is bad
What adjustments can and should be made in his diuretic therapy?
Is your dose enough? GFR is probably good here so dose should be good
make sure frequency is enough
How long does furosemide work?
aka Lasix (lasts 6 hours)
What is a major problem with long term loop diuretic use?
tolerance
How does the body develop tolerance to loop diuretics?
the segments distal to the thick ALH will hypertrophy and promote increased Na+ reabsorption
Case 6. 54-year-old African-American male with very difficult to control hypertension. Lifestyle changes have not been successful in reducing blood pressure. He is receiving maximum dose of angiotensin receptor blocker (losartan) and blood pressure remains 160/104 mm Hg. Serum creatinine is 1.0 mg/dL.
How would you assess dietary sodium intake? What medication adjustments should be made at this point?
ACE I and ARB alone are often less effective as monotherapy for blood pressure lowering in African Americans, due to higher prevalence of low renin hypertension (have lower renin dependent HTN)
add a thiazide
Case 7. 58-year-old male with coronary artery disease with intermittent angina pectoris and chronic kidney disease, serum creatinine 2.4 mg/dL, blood pressure 140/90 mmHg and heart rate 72 bpm.
He is prescribed the BB atenolol 25 mg daily (low dosage). During follow-up he feels tired and heart rate is 40 bpm? How do explain this change in vital signs?
While most beta blockers are hepatically metabolized, atenolol is highly dependent on renal elimination (roughly 50% renal and 50% feces) and here it is not being excreted well
nadolol (highly) and bisoprolol (partial) are also kidney dependent
Case 8. 34-year-old African-American female with biopsy-proven focal segmental glomerulosclerosis with nephrotic syndrome with marked lower extremity edema. Serum creatinine 0.9 mg/dL.
Treatment includes full dosage lisinopril and furosemide 80 mg once daily. What adjustments need to be made in diuretic management?
Once daily is not enough (only lasts 6 hours)
block Enac-triamterene/amiloride
What would be the effect of the addition of spironolactone?
effective
T or F. Loop diuretics need functioning kidneys to work
T. They must be delivered to the site of action, so the worse the GFR the more needed
Similarly, loop diuretics can be bound to proteins so heavy proteinuria will result in more of the drug being excreted without functioning properly AND the diuretics and thiazides must be secreted by the PT and use albumin as a transporter so the more loss of albumin= less efficacy
Purely nephrotic patients have normal plasma volumes. Why?
because there is avid salt and water retention that is restricted to the ECF. So you lose some to the interstitium but you gain extra to normalize the plasma volume at the expense of edema
Case 9. 62-year-old Caucasian male with ischemic cardiomyopathy and chronic kidney disease, serum creatinine 2.4 mg/dL.
He is receiving carvedilol and lisinopril therapy. Blood pressure is 130/80 mmHg and heart rate is 50 bpm.
His primary care physician adds low-dose spironolactone to his treatment regimen. What potential complications may occur?
Risk of hyperkalemia substantially higher with elevated SCr (>1.6 mg/dl) and also other drugs causing hyperkalemia (aka: ACEIs, ARB, NSAIDs)
start at a low dose and FOLLOW UP quickly to look at K+ levels