NU652 Unit 2 Failed Therapy Analysis, Kidney Injury Example

Reviewed by Elspeth Marlowe, MSN, RN AGACNP Acute Care Diagnosis and Management II Purdue University Global Free custom sample in 24 to 48h

This NU652 Unit 2 sample is a failed therapy analysis of a 68-year-old woman whose creatinine rose from 2.4 to 3.1 after two liters of fluid for presumed prerenal injury. It was prepared for Purdue Global NU 652, AGACNP Acute Care Diagnosis and Management II, in the MSN acute care nurse practitioner program. The paper asks whether the fluid was not enough or the diagnosis was wrong, and writes down what each answer predicts before looking at her findings. She was euvolemic, with a fractional excretion of sodium of 2.1 percent, white cell casts and sterile pyuria. The revised diagnosis is drug-induced acute interstitial nephritis from omeprazole or ciprofloxacin, with nephrology, biopsy and steroid discussion to follow.

CourseNU652 AGACNP Acute Care Diagnosis and Management II
UnitUnit 2
Paper typeFailed therapy analysis
LengthAbout 1,090 words, 6 pages double-spaced
FormatAPA 7 student paper
SchoolPurdue University Global
ProgramMSN
UpdatedSeptember 2026

Free sample paper for NU652 Unit 2

1

Not Enough Fluid, or the Wrong Diagnosis? A Failed Therapy Analysis of Kidney Injury That Worsened After Volume Replacement in a 68-Year-Old Woman

[Student Name]

Purdue University Global

NU652: AGACNP Acute Care Diagnosis and Management II

Unit 2 Failed Therapy Analysis

[Instructor Name]

[Date]

The patient is composite; values, volumes and days are bracketed.

What this part is doingThe question is framed as a fork in the first section, and every later section serves one branch or the other.
2

The Question

Mrs. [K.] was admitted with acute kidney injury after [seven] days of watery diarrhea. Her creatinine was [2.4] mg/dL; four months earlier, in clinic, it had been [0.9]. The admitting diagnosis was prerenal injury from volume loss, and she received [2,000] mL of lactated Ringer's over the first [24] hours. On day [three] her creatinine was [3.1]. The team's first instinct was to give more fluid.

Before doing so, this analysis asks which of two explanations fits: the treatment was right but not enough, or the diagnosis was wrong from the start. Each explanation predicts different findings, and the predictions are written down before the findings are examined, so the analysis cannot be shaped to fit its conclusion.

What Each Explanation Predicts

If the problem is inadequate volume replacement, the findings should include:

1. Signs of persisting volume depletion: dry mucous membranes, orthostatic changes, low urine output.

2. A low fractional excretion of sodium, typically below 1 percent, as the kidneys conserve sodium.

3. A bland urine sediment without cells or casts.

4. A creatinine that begins to turn once volume is restored.

If prerenal injury was the wrong diagnosis, the findings should include:

1. Normal or restored volume status, with no improvement.

2. A higher fractional excretion of sodium, since the tubules are no longer conserving it.

3. An active sediment that points to the kidney itself: cells, casts or protein.

4. A creatinine that continues to rise despite adequate volume.

What She Showed

Volume status is examined first, because more fluid is the reflex response. By day [three] her mucous membranes were moist, her jugular venous pressure was visible at [4] cm, she had no orthostatic drop and her weight was [1.5] kg above admission. The diarrhea had slowed to [one or two] loose stools a day. She was euvolemic, and her creatinine rose after the deficit was replaced.

Her fractional excretion of sodium was [2.1] percent, with no diuretic given. That is not the value of a kidney holding on to sodium. Her urine showed [12] to [15] white cells per high-power field and white cell casts, with [1+] protein and no bacteria; the urine culture was negative. Her peripheral eosinophil count was [620] per microliter, mildly raised.

Every prediction of the second branch was met, and none of the first; more fluid would have treated a problem she no longer had.

What this part is doingLaboratory data carry the weight of the argument, set against predictions written before them.
3

The Revised Diagnosis

Sterile pyuria with white cell casts, a fractional excretion above 2 percent and a rising creatinine in a euvolemic patient point to acute interstitial nephritis. The next question is cause, and the medication list answers it. She had taken omeprazole daily for [six] years, and [eight] days before admission an urgent care clinic had prescribed ciprofloxacin for presumed infectious diarrhea. Both are well-recognized causes. In a series of 133 patients with biopsy-proven interstitial nephritis, drugs caused 70 percent of cases, and omeprazole and ciprofloxacin were among the three most common single drugs (Muriithi et al., 2014). Drug-induced interstitial nephritis often lacks the classic triad of fever, rash and eosinophilia, and its onset can follow a new drug by days or a long-standing one by months (Perazella & Markowitz, 2010).

The diarrhea itself probably did cause some prerenal injury at first, which is why the initial diagnosis was reasonable. The error was not the first label but keeping it after the patient stopped behaving as it predicted.

Why the First Label Held On

Three things kept the prerenal label in place for two days. The first was that it fit the story told at admission: a week of diarrhea and a rising creatinine is the textbook pairing, and the diagnosis was made before any urine was examined. The second was that the plan it produced, fluid, was easy to continue. When a treatment is simple and low in risk, a poor response tends to be read as a need for more of the same rather than a signal that the diagnosis is wrong. The third was timing. The urinalysis was sent on admission, but the microscopy was not reviewed until day [three], when the creatinine had already risen, so the one test that could have changed the label sat unread.

None of these is a failure of knowledge. Everyone on the team knew that white cell casts point to the interstitium and that a fractional excretion above 2 percent argues against a prerenal state. What was missing was a moment on day [two] when someone asked what the diagnosis predicted and whether the patient was keeping to it. The prediction table above is that moment, written down.

Revised Management

1. Stop ciprofloxacin; it had already been completed, so the record now lists it as a probable cause.

2. Stop omeprazole and replace it with an H2 blocker if acid suppression is still needed.

3. Stop further fluid boluses; maintenance intake by mouth.

4. Nephrology consultation on day [three] for kidney biopsy, which confirms the diagnosis and guides steroid use.

5. Discuss corticosteroids with nephrology. Their benefit is debated, but in the same case series, delays in stopping the culprit drug and in starting steroids were associated with worse recovery of kidney function (Muriithi et al., 2014).

6. Daily creatinine, electrolytes and urine output; avoid nephrotoxins, including contrast and nonsteroidal anti-inflammatory drugs.

Why the First Plan Failed

The KDIGO guideline calls for prompt evaluation of the cause of acute kidney injury, with particular attention to causes that can be reversed (Khwaja, 2012), and that evaluation does not end once a first label has been written. This case shows why. The first plan did not fail because the fluid was too little. It failed because the diagnosis stopped fitting, and the only way to see that was to write down what the diagnosis predicted and check each prediction against the patient.

What this part is doingThe lesson is framed as a method, predictions before findings, which can be reused on the next patient whose therapy seems to fail.
4

Follow-Up

Mrs. [K.] underwent biopsy on day [four], which showed interstitial inflammation with eosinophils. Prednisone was started. Her creatinine peaked at [3.4] on day [five] and was [1.6] at discharge on day [nine]. Omeprazole and all fluoroquinolones are now listed as drug reactions in her record, and her primary care provider has been asked to review whether she needs acid suppression at all.

5

References

Khwaja, A. (2012). KDIGO clinical practice guidelines for acute kidney injury. Nephron Clinical Practice, 120(4), c179-c184. https://doi.org/10.1159/000339789

Muriithi, A. K., Leung, N., Valeri, A. M., Cornell, L. D., Sethi, S., Fidler, M. E., & Nasr, S. H. (2014). Biopsy-proven acute interstitial nephritis, 1993-2011: A case series. American Journal of Kidney Diseases, 64(4), 558-566. https://doi.org/10.1053/j.ajkd.2014.04.027

Perazella, M. A., & Markowitz, G. S. (2010). Drug-induced acute interstitial nephritis. Nature Reviews Nephrology, 6(8), 461-470. https://doi.org/10.1038/nrneph.2010.71

The Purdue Global NU652 Unit 2 instructions

The Unit 2 assignment gives you a patient whose initial treatment did not produce the expected response and asks you to analyze why. You state the original diagnosis and plan, identify the possible explanations for failure, weigh the evidence for each, reach a conclusion and revise the management. Most prompts distinguish between a correct diagnosis treated inadequately and an incorrect diagnosis, and expect you to test both. Laboratory and examination findings should carry the argument, with sources for how each finding is interpreted. Four to five pages is typical. The analysis should also say why the first label persisted, since that is how the same error is avoided next time.

How this NU652 Unit 2 example is built

The example frames the question as a fork in its opening section. It then writes two sets of predictions, one for each branch, before any findings are shown, so the analysis cannot be bent to fit its ending. Volume status is examined first, because more fluid is the reflex answer, and the paper shows she was euvolemic. Laboratory results follow, set against the predictions. A highlighted sentence states which branch the findings met. The revised diagnosis section uses a large biopsy series to connect her two medications to the finding. A section on why the first label held on names three reasons, and the revised plan lists six steps with a follow-up outcome.

Reading the NU652 Unit 2 grading rubric

The Unit 2 rubric generally weighs identification of the failure, the quality of the differential explanations, the use of data, the revised plan and the use of evidence. Identifying the failure earns full credit when the original plan and its expected result are stated clearly. The explanations are judged on whether both inadequate treatment and misdiagnosis are considered fairly. Use of data is weighted heavily; each finding should be interpreted, not just listed. The revised plan counts when it follows from the new diagnosis and includes stopping the likely cause. Evidence should support interpretation, such as a case series on drug-induced interstitial nephritis. Reflection on why the error occurred often earns additional credit.

NU652 Unit 2 help from the desk

The most common mistake is recommending more of the same treatment without testing the diagnosis. Another is listing laboratory values without explaining what each predicts. Students often forget to review the medication list, which in this case held both likely culprits. The fractional excretion of sodium is sometimes over-read; it helps, but it is not definitive on its own, and diuretics make it unreliable. Some papers conclude with a new diagnosis but no plan to confirm it. And many analyses never explain why the first label persisted, which is the part of the paper most useful for future practice. Keep the predictions short and concrete, one line each, so the reader can check them quickly.

Get an NU652 Unit 2 example written to your instructions

A case involving a different organ and a different failed plan works just as well, since the analysis adapts to whatever the prompt supplies. Share the scenario, its data and the grading rubric for this unit. A first sample costs nothing, arrives within 24-48h and follows those instructions, testing both branches of the fork before it commits to a verdict. The paper above is an original model document written by our desk, not a submitted student paper and not an official Purdue University Global document.

More NU652 papers and MSN samples

NU652 Unit 2 questions, answered

What if the evidence points to inadequate treatment instead?

Then the analysis says so. Some composite cases are built to reward the conclusion that the plan was right but underdosed or too short. The sample follows your case wherever its findings lead, and the two-column structure works equally well in that direction, showing why the diagnosis holds and which change to the treatment the data support.

Should a failed therapy analysis recommend a kidney biopsy?

Only if the case supports it. Here the paper requests nephrology input on biopsy because stopping the drug is the main treatment and corticosteroids remain debated; clear improvement after withdrawal might make a biopsy unnecessary. The sample states the question for the consultant rather than ordering the procedure, which fits the scope an advanced practice paper in this unit usually expects.

How much pathophysiology belongs in the paper?

Enough to justify each prediction and no more. A sentence on why prerenal injury conserves sodium supports the fractional excretion row; a page on nephron physiology does not. Instructors typically reward reasoning from data here, so the sample keeps mechanism brief and ties every sentence of it to a finding in the table.

Where can I find a free NU652 Unit 2 sample paper?

The complete NU652 Unit 2 failed therapy analysis is on this page, with the predictions for each branch, her findings, the revised diagnosis and the new plan. For a different therapy that seems to have failed, a free analysis can be drafted from your case.

What points to interstitial nephritis in the NU652 Unit 2 sample?

Sterile pyuria with white cell casts, a fractional excretion of sodium above 2 percent without diuretics, mild eosinophilia and a creatinine that kept rising after volume was restored, together with two drugs that commonly cause it.