NURS 6521 Week 3 Cardiovascular Drug Therapy Plan Example

Choosing an Antihypertensive Class for a 62-Year-Old Woman With Albuminuric Chronic Kidney Disease and a History of ACE Inhibitor Cough

Student Name

College of Nursing, Walden University

NURS 6521: Advanced Pharmacology

Instructor Name

Month Day, Year

Choosing an Antihypertensive Class for a 62-Year-Old Woman With Albuminuric Chronic Kidney Disease and a History of ACE Inhibitor Cough

Patient Summary

Mrs. D.O. is a composite patient invented for this plan. She is a 62-year-old African American woman, a retired postal clerk, with hypertension for 14 years, type 2 diabetes for nine years, and chronic kidney disease stage G3a with an estimated glomerular filtration rate of 54 mL/min/1.73 m2, stable over two years. Her urine albumin-to-creatinine ratio has risen from 90 mg/g to 380 mg/g over the same period. Potassium is 4.6 mmol/L. Her average home blood pressure over two weeks is 148/92 on amlodipine 5 mg daily. She also takes metformin and atorvastatin. Lisinopril was stopped three years ago after she developed a persistent dry cough that resolved within a month of discontinuation. She uses naproxen several times a week for knee pain and salts her food at the table.

Options Compared

Three classes are realistic next steps. The comparison below lists, for each, its mechanism, its effect on the kidney, and its main risk for this patient.

Angiotensin II receptor blocker (ARB), for example losartan. Mechanism: blocks the angiotensin II type 1 receptor, reducing vasoconstriction, aldosterone release, and sodium retention. Kidney effect: relaxes the efferent arteriole preferentially, lowering intraglomerular pressure and reducing albumin leakage. Main risk here: hyperkalemia and an early rise in creatinine, both monitored.

Thiazide or thiazide-like diuretic, for example chlorthalidone. Mechanism: inhibits the sodium-chloride cotransporter in the distal convoluted tubule, reducing sodium reabsorption and plasma volume. Kidney effect: lowers systemic pressure but has no specific effect on glomerular pressure or albuminuria. Main risk here: hyponatremia, hypokalemia, and increases in glucose and uric acid.

Dihydropyridine calcium channel blocker, dose increase of amlodipine. Mechanism: blocks L-type calcium channels in vascular smooth muscle, dilating arterioles. Kidney effect: dilates the afferent arteriole, which can transmit more systemic pressure into the glomerulus and does not reduce albuminuria on its own. Main risk here: ankle edema, which increases with dose.

The Choice

The plan adds an ARB, losartan 25 mg daily, increased to 50 mg and then as tolerated toward 100 mg, while continuing amlodipine. The choice answers two documented findings rather than a general preference.

First, her albuminuria. Blocking angiotensin II at its receptor relaxes the efferent arteriole, which lowers the pressure inside the glomerulus and reduces the protein that leaks through the damaged filtration barrier. Lower intraglomerular pressure slows progression of albuminuric kidney disease independent of the fall in systemic blood pressure. The KDIGO guideline recommends starting a renin-angiotensin system inhibitor, an ACE inhibitor or an ARB, for patients with high blood pressure, chronic kidney disease, and moderately to severely increased albuminuria, and titrating it to the highest approved dose that is tolerated (Cheung et al., 2021).

Second, her earlier cough. ACE inhibitors block the enzyme that converts angiotensin I to angiotensin II, and the same enzyme breaks down bradykinin. Accumulated bradykinin and related peptides in the airway are the leading explanation for the dry cough ACE inhibitors cause. ARBs act at the receptor instead and leave bradykinin breakdown intact, so cough is much less common, and switching to an ARB is the standard response when an ACE inhibitor causes it (Rosenthal & Burchum, 2021). Restarting lisinopril would likely bring the cough back.

Why not the others first? A thiazide would lower her blood pressure but would not address the albuminuria, and it adds metabolic risks in a woman with diabetes; it remains a reasonable third agent if pressure stays above target. Increasing amlodipine would also lower pressure, but by dilating the afferent arteriole it can raise glomerular pressure unless an agent acting on the efferent side is present, and her risk of edema rises with the dose. Combining an ACE inhibitor with an ARB is not an option, since dual blockade increases hyperkalemia and acute kidney injury without improving outcomes (Cheung et al., 2021).

Patient Factors

Age

At 62 she is not at the age where orthostatic hypotension typically limits therapy, but reduced renal reserve means the rise in creatinine that often follows ARB initiation must be interpreted with care. A rise of up to about 30 percent in the first weeks reflects the intended fall in glomerular pressure and is not a reason to stop; a larger rise suggests volume depletion or renal artery stenosis and is investigated.

Genetics

Losartan is a prodrug in part: CYP2C9 converts it to an active carboxylic acid metabolite responsible for much of its effect. People who carry reduced-function CYP2C9 variants form less of the active metabolite and may respond less (Rosenthal & Burchum, 2021). If her blood pressure responds poorly at an adequate dose, that is one reason to consider an ARB that does not depend on this conversion rather than concluding that the class has failed. Her kidney disease may also have a genetic contribution: APOL1 risk variants, found more often in people of recent African ancestry, are associated with faster progression of nondiabetic kidney disease, which adds to the case for kidney-protective therapy.

Ethnicity

Some hypertension guidance has recommended drug classes by race. The 2014 panel report recommended a thiazide or calcium channel blocker as initial therapy for Black patients without chronic kidney disease, based on trial evidence of greater blood pressure response to those classes (James et al., 2014). That same report made an exception for chronic kidney disease, recommending an ACE inhibitor or ARB for all patients with it regardless of race. This plan leans on measured findings, her albuminuria and her creatinine trend, rather than on race, because the kidney finding is what the drug is chosen to treat, and a race-based rule would steer her toward a class that does not address it.

Behavior

Two behaviors reduce the effectiveness of the plan and increase its risks. High dietary sodium blunts the antihypertensive and antiproteinuric effect of renin-angiotensin blockade, so salt reduction is part of the therapy rather than general advice. Regular naproxen use raises blood pressure, reduces renal prostaglandins that maintain afferent arteriolar flow, and, combined with an ARB, increases the risk of acute kidney injury and hyperkalemia. Topical diclofenac or acetaminophen is recommended for her knee pain instead.

Education and Follow-Up

Mrs. O. is told that the new pill protects her kidneys as well as lowering her blood pressure, and that it is chosen because it works differently from the pill that made her cough. She is asked to stop naproxen and to avoid salt substitutes, which usually contain potassium. She is told to hold the medicine and call if she has vomiting or diarrhea that stops her from drinking, since dehydration while taking it can harm the kidneys. She continues home blood pressure readings twice a day and brings the log to her next visit. Basic metabolic panel is rechecked in two weeks to reassess potassium and creatinine, and again after each dose increase. At three months, the plan reassesses blood pressure against a target below 130/80, the threshold most current guidance uses for adults with chronic kidney disease (Carey et al., 2022), the urine albumin-to-creatinine ratio, and whether a third agent is needed.

References

Carey, R. M., Moran, A. E., & Whelton, P. K. (2022). Treatment of hypertension: A review. JAMA, 328(18), 1849-1861. https://doi.org/10.1001/jama.2022.19590

Cheung, A. K., Chang, T. I., Cushman, W. C., Furth, S. L., Hou, F. F., Ix, J. H., Knoll, G. A., Muntner, P., Pecoits-Filho, R., Sarnak, M. J., Tobe, S. W., Tomson, C. R. V., & Mann, J. F. E. (2021). KDIGO 2021 clinical practice guideline for the management of blood pressure in chronic kidney disease. Kidney International, 99(3S), S1-S87. https://doi.org/10.1016/j.kint.2020.11.003

James, P. A., Oparil, S., Carter, B. L., Cushman, W. C., Dennison-Himmelfarb, C., Handler, J., Lackland, D. T., LeFevre, M. L., MacKenzie, T. D., Ogedegbe, O., Smith, S. C., Jr., Svetkey, L. P., Taler, S. J., Townsend, R. R., Wright, J. T., Jr., Narva, A. S., & Ortiz, E. (2014). 2014 evidence-based guideline for the management of high blood pressure in adults: Report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA, 311(5), 507-520. https://doi.org/10.1001/jama.2013.284427

Rosenthal, L. D., & Burchum, J. R. (2021). Lehne's pharmacotherapeutics for advanced practice nurses and physician assistants (2nd ed.). Elsevier.