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The NU 636 Unit 7 drug comparison paper, in full
Atorvastatin Versus Rosuvastatin for a 68-Year-Old Man With Stage 4 Chronic Kidney Disease: Breaking the Tie
Student Name
Department of Nursing, Herzing University
NU 636: Advanced Pharmacology
Instructor Name
March 11, 2026
Atorvastatin Versus Rosuvastatin for a 68-Year-Old Man With Stage 4 Chronic Kidney Disease: Breaking the Tie
The Agents and the Axes
Atorvastatin and rosuvastatin are the two statins most often prescribed when a patient needs a substantial reduction in low-density lipoprotein cholesterol (LDL-C). Both are available as inexpensive generics, both are taken once daily, and both can deliver high-intensity therapy. This paper compares them on six axes: LDL-C lowering, outcome evidence, handling by the kidney, interaction pathways, population-specific exposure, and practical factors of cost and convenience.
These axes were chosen because each one can change which agent a particular patient should receive. Axes on which the two agents are effectively identical, such as the class mechanism of HMG-CoA reductase inhibition, the rare risk of liver enzyme elevation, and the small increase in new-onset diabetes, are set aside because they cannot break a tie. The comparison runs axis by axis, and within each axis atorvastatin is discussed first and rosuvastatin second.
Axis One: LDL-C Lowering
Atorvastatin lowers LDL-C by roughly 30% to 50% across its dose range of 10 to 80 mg, with 40 to 80 mg qualifying as high intensity. Rosuvastatin is more potent per milligram: in the STELLAR trial, rosuvastatin 10 to 40 mg lowered LDL-C by 46% to 55%, compared with 37% to 51% for atorvastatin 10 to 80 mg (Jones et al., 2003). At their maximum doses the difference is several percentage points in favor of rosuvastatin. Verdict: rosuvastatin wins on potency, but the margin matters only when a patient needs the very largest reduction.
Axis Two: Outcome Evidence
Atorvastatin reduced coronary events in patients with hypertension and average cholesterol in the lipid-lowering arm of ASCOT, which was stopped early because of benefit (Sever et al., 2003). Rosuvastatin reduced major cardiovascular events in people with normal LDL-C and elevated high-sensitivity C-reactive protein in JUPITER, also stopped early (Ridker et al., 2008). Both agents have large randomized outcome trials behind them, and neither trial directly compared the two drugs. Verdict: a tie. Neither agent has a stronger class of evidence for general cardiovascular prevention.
Axis Three: Handling by the Kidney
Atorvastatin is cleared mainly by the liver, and less than 2% appears in the urine, so no dose adjustment is required for any level of kidney function. Rosuvastatin is partly cleared by the kidney; in severe kidney impairment not requiring dialysis, its labeling calls for a starting dose of 5 mg and a maximum of 10 mg, because exposure rises substantially as clearance falls. Verdict: atorvastatin wins clearly when kidney function is severely reduced, because it can be used across its full dose range without adjustment.
Axis Four: Interaction Pathways
Atorvastatin is metabolized by cytochrome P450 3A4, so strong inhibitors of that enzyme, including clarithromycin, itraconazole, and some antiretroviral regimens, raise its levels and the risk of myopathy. Rosuvastatin undergoes little cytochrome metabolism, which removes most of those interactions, but it depends on hepatic uptake transporters, so drugs such as cyclosporine and gemfibrozil raise its levels. Verdict: rosuvastatin wins for a patient taking a strong 3A4 inhibitor; atorvastatin wins for a patient on cyclosporine or requiring a fibrate.
Axis Five: Population-Specific Exposure
Plasma exposure to rosuvastatin is about twice as high in people of East Asian ancestry as in White people living in the same environment, a difference not explained by diet or body size (Lee et al., 2005). Its labeling therefore recommends a lower starting dose for Asian patients. No comparable ancestry-related adjustment applies to atorvastatin. Verdict: atorvastatin is simpler to dose in patients of Asian ancestry, though rosuvastatin remains usable at a lower dose.
Axis Six: Cost and Convenience
Both agents are generic and inexpensive on most insurance plans, both are taken once daily at any time of day, and both are well tolerated by most patients. Adherence is the practical issue that matters more than either drug: a statin that is prescribed but not taken prevents nothing, so the choice should favor whichever agent the patient's plan covers with the lowest copay and whichever he is least likely to stop. Verdict: a tie.
The Patient Who Breaks the Tie
Mr. J., a composite 68-year-old man, has chronic kidney disease stage 4 with an estimated glomerular filtration rate of 24 mL/min/1.73 m2, type 2 diabetes, and hypertension. He is not on dialysis. His LDL-C is 142 mg/dL. He takes insulin glargine, amlodipine, furosemide, and sodium bicarbonate, none of which is a strong 3A4 inhibitor or transporter inhibitor. He is of Filipino ancestry. For adults 50 years and older with an eGFR below 60 who are not on dialysis, statin therapy is recommended to reduce cardiovascular risk, and the kidney guideline suggests using doses that were proven in trials in this population rather than pushing to maximum intensity (Wanner & Tonelli, 2014).
For Mr. J., three axes carry the decision. His kidney function makes atorvastatin's lack of renal adjustment decisive. His ancestry adds a second reason to be cautious with rosuvastatin exposure. And the interaction axis does not favor rosuvastatin, because he takes no 3A4 inhibitors. The potency advantage of rosuvastatin is irrelevant, because his target does not require the largest possible reduction and the capped 10 mg dose of rosuvastatin would remove much of that advantage anyway.
Recommendation and What Would Reverse It
Recommendation: atorvastatin 20 mg by mouth once daily, with a lipid panel and creatine kinase only if muscle symptoms arise, and a repeat lipid panel in 6 to 12 weeks to confirm response and adherence.
What would reverse the answer: if Mr. J. needed a long course of a strong 3A4 inhibitor, such as a boosted antiretroviral regimen, rosuvastatin at a reduced dose would become the safer choice. If his kidney function were stable above 30 mL/min/1.73 m2 and he needed a very large LDL-C reduction after an acute coronary event, rosuvastatin's greater potency would matter more. If he began dialysis, the question would change altogether, because statins have not shown benefit when started in patients already on dialysis.
What the losing agent still does better: rosuvastatin delivers more LDL-C reduction per milligram and avoids the long list of 3A4 interactions that shadows atorvastatin in patients with many medications.
References
Jones, P. H., Davidson, M. H., Stein, E. A., Bays, H. E., McKenney, J. M., Miller, E., Cain, V. A., & Blasetto, J. W. (2003). Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR trial). American Journal of Cardiology, 92(2), 152-160. https://doi.org/10.1016/S0002-9149(03)00530-7
Lee, E., Ryan, S., Birmingham, B., Zalikowski, J., March, R., Ambrose, H., Moore, R., Lee, C., Chen, Y., & Schneck, D. (2005). Rosuvastatin pharmacokinetics and pharmacogenetics in white and Asian subjects residing in the same environment. Clinical Pharmacology & Therapeutics, 78(4), 330-341. https://doi.org/10.1016/j.clpt.2005.06.013
Ridker, P. M., Danielson, E., Fonseca, F. A. H., Genest, J., Gotto, A. M., Jr., Kastelein, J. J. P., Koenig, W., Libby, P., Lorenzatti, A. J., MacFadyen, J. G., Nordestgaard, B. G., Shepherd, J., Willerson, J. T., & Glynn, R. J. (2008). Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. New England Journal of Medicine, 359(21), 2195-2207. https://doi.org/10.1056/NEJMoa0807646
Sever, P. S., Dahlof, B., Poulter, N. R., Wedel, H., Beevers, G., Caulfield, M., Collins, R., Kjeldsen, S. E., Kristinsson, A., McInnes, G. T., Mehlsen, J., Nieminen, M., O'Brien, E., & Ostergren, J. (2003). Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA): A multicentre randomised controlled trial. The Lancet, 361(9364), 1149-1158. https://doi.org/10.1016/S0140-6736(03)12948-0
Wanner, C., & Tonelli, M. (2014). KDIGO clinical practice guideline for lipid management in CKD: Summary of recommendation statements and clinical approach to the patient. Kidney International, 85(6), 1303-1309. https://doi.org/10.1038/ki.2014.31
What a finished NU 636 Unit 7 drug comparison paper looks like
The finished paper is balanced and pointed. Both agents arrive in the first lines beside the axes they will be judged on, usually efficacy evidence, adverse effect profile, interaction burden, monitoring demand, dosing convenience and access. Neither agent gets more room than the other, and neither gets a stronger class of evidence, which is the detail that separates a comparison from a favorite with a rival attached. The body runs axis by axis rather than agent by agent, so each axis holds both drugs in the same block. A described patient appears partway through and does the deciding, because axes alone produce a tie. The closing states which agent that patient should receive, and then names the change in circumstances that would flip the recommendation.
How a NU 636 Unit 7 example is structured
The example is organized around the axes rather than the agents, which is the structural choice that makes comparison possible. It opens by naming both drugs and the axes, then spends a short section defending why these axes and not others, a move most versions omit. Each body block takes one axis and treats both agents inside it, in the same order every time, with evidence of comparable weight on each side. Once the axes are exhausted, the paper introduces the patient whose characteristics break the tie, and works through which axes matter most for that person and why. The recommendation follows, stated plainly. A reversal section then names what would change the answer, whether a different renal function, a coverage restriction, a pregnancy or an added interacting medication. The conclusion states what the losing agent still does better.
Axes chosen before the comparison starts
The paper justifies why efficacy, safety, interactions, monitoring and access are the deciding dimensions, which turns an arbitrary list into a defensible method.
Both agents evidenced equally
Comparable sources are gathered for each drug, since an uneven reference list makes the conclusion look decided before the comparison began.
The patient who breaks the tie
A described person is introduced to decide between two defensible options, because axes alone will rarely separate agents inside the same class.
A recommendation actually stated
The paper commits to one agent for that patient rather than closing on a sentence about both drugs having strengths and weaknesses.
The reversal condition named
One change in kidney function, coverage, pregnancy status or concurrent medication is identified as what would flip the recommendation the other way.
Cost and access treated as clinical
Affordability and supply are argued as factors affecting whether the patient takes the drug at all, not as an administrative footnote.
Where marks go in NU 636 Unit 7
The dominant failure is two profiles printed in sequence. If the halves could be separated and each would still read as a complete piece, no comparison occurred, and the criterion has nothing to reward. Unmatched axes cause the same damage more quietly, where one drug is judged on trial evidence and the other on convenience. Lopsided sourcing is visible immediately. Comparing agents from different classes makes the exercise meaningless, since the choice was never between them. The most common ending problem is a conclusion that both agents are effective and the choice depends on the patient, offered without describing a patient. Ignoring cost, access and adherence treats prescribing as though it stops when the prescription is written.
Get a NU 636 Unit 7 example written to your instructions
Send the Unit 7 instructions and the rubric from your NU 636 classroom, plus the two agents you have been asked to compare and any patient details supplied. We write a custom example against those criteria, with matched axes and a recommendation that commits, and return it in 24 to 48 hours. The first custom sample is free.
NU 636 Unit 7 questions, answered
How do I pick which two agents to compare?
Take two that a prescriber would realistically weigh against each other for the same indication, which usually means the same class or two classes used interchangeably. If one is obviously first line and the other is rarely used, the comparison writes itself and demonstrates nothing. The best pairs are the ones where practitioners genuinely disagree and the evidence supports both.
Is cost a legitimate axis in a graduate paper?
Yes, and treating it as clinical rather than administrative usually strengthens the work. A drug the patient cannot afford or cannot obtain is a drug that will not be taken, which affects outcomes as directly as any pharmacological property. Argue it that way, with a source where one exists, rather than asserting that one agent is cheaper without evidence for the claim.
Does the paper have to reach a winner?
For a described patient, yes. A comparison that ends by saying the decision depends on individual factors, without ever applying those factors to a person, has stopped one step short of the reasoning being graded. Describe the patient, apply the axes, commit to an agent, then name what would reverse the decision. That last part is where strong versions separate.