Prerenal Acute Kidney Injury After Five Days of Gastroenteritis: A Mechanism Analysis in a 71-Year-Old Man
[Author Name]
College of Nursing and Health Care Professions, Grand Canyon University
NUR-631 Advanced Physiology and Pathophysiology
Topic 3 Assignment
[Faculty Name]
August 11, 2026
Composite case written as a model document. No real patient, clinic or clinician is described.
The Case in Brief
A 71-year-old man came to an outpatient clinic on the fifth day of an illness that began with vomiting and watery diarrhea after a family meal. The vomiting stopped after 48 hours; the diarrhea continued at six to eight stools daily. He drank little other than black coffee, kept taking his usual medications, and lost 4.2 kg from a documented baseline of 86 kg. In the final 24 hours he passed urine twice, both times a small volume of dark urine. He reports fatigue, light-headedness on standing and cramping in both calves, and denies fever, flank pain, hematuria and dysuria.
His medication list matters as much as the illness. He takes lisinopril 20 mg daily for hypertension, hydrochlorothiazide 25 mg daily added 14 months ago, and naproxen 500 mg twice daily, begun three months ago for knee osteoarthritis and continued through the illness because the cramping hurt. He has had no antibiotic, no contrast agent and no new prescription since. Baseline serum creatinine from routine laboratory work six months earlier was 1.0 mg/dL, with an estimated glomerular filtration rate above 60 mL/min/1.73 m2. He has no diagnosed kidney disease, no diabetes and no history of heart failure.
Examination on arrival: blood pressure 96/58 mmHg supine, falling to 78/50 mmHg after two minutes standing, with heart rate rising from 98 to 122 beats per minute. Respirations 22 and slightly deep. Temperature 36.9 degrees Celsius. Mucous membranes are dry, the axillae are without moisture, skin turgor over the sternum is reduced, and jugular venous pulsation is not visible with the head of the table flat. Heart sounds are regular without murmur. The abdomen is soft with hyperactive bowel sounds. There is no peripheral edema, no rash and no asterixis.
Laboratory values drawn that morning: sodium 141 mEq/L, potassium 5.4 mEq/L, chloride 110 mEq/L, bicarbonate 17 mEq/L, blood urea nitrogen 62 mg/dL, creatinine 3.2 mg/dL, with a calculated anion gap of 14. Urinalysis shows specific gravity 1.028, no protein, no blood, and a bland sediment with occasional hyaline casts. Urine sodium is 12 mEq/L and the fractional excretion of sodium is 0.4 percent. Venous pH is 7.30. The electrocardiogram shows sinus tachycardia with peaked T waves. A creatinine at three times baseline with urine output under 0.5 mL/kg/h for more than 12 hours places the episode at the most severe stage in the KDIGO staging system (KDIGO Acute Kidney Injury Work Group, 2012).
The Physiology That Normally Prevents This
The kidneys receive roughly a fifth of cardiac output, and filtration depends not on total blood flow alone but on hydrostatic pressure inside the glomerular capillary, which is set by the relative tone of the afferent and efferent arterioles. Autoregulation holds filtration nearly constant across mean arterial pressures of about 80 to 180 mmHg through two mechanisms. The myogenic response contracts the afferent arteriole when its wall is stretched by rising pressure. Tubuloglomerular feedback runs the other way: the macula densa senses sodium chloride delivery to the distal tubule and signals the afferent arteriole to constrict when delivery climbs (Hall & Hall, 2021).
Below that autoregulatory floor, two hormonal arms take over, and they are the arms this case turns on. Locally produced prostaglandins, chiefly prostaglandin E2 and prostacyclin, dilate the afferent arteriole and keep filtrate entering the glomerulus as perfusion pressure falls. Angiotensin II, generated as renin rises, preferentially constricts the efferent arteriole and holds pressure inside the capillary tuft instead of letting it drain away. One arm opens the inlet, the other narrows the outlet. In a person with normal volume neither arm is doing much work, which is why the drugs that block them are usually silent.
Volume loss triggers a wider defense. Arterial and cardiopulmonary baroreceptors sense the fall in stretch and raise sympathetic outflow, which lifts heart rate and contractility and constricts systemic vessels. Renin release from juxtaglomerular cells rises through three signals: reduced afferent arteriolar stretch, reduced sodium chloride at the macula densa, and direct beta-1 sympathetic stimulation. Aldosterone follows angiotensin II and drives sodium reabsorption in the collecting duct in exchange for potassium and hydrogen ions. Antidiuretic hormone is released non-osmotically once volume falls by roughly 8 to 10 percent, adding water reabsorption through aquaporin channels.
Those responses leave fingerprints in the urine, and reading them is how a clinician separates a kidney that is under-perfused from a kidney that is damaged. Avid sodium reabsorption drops urine sodium and pushes the fractional excretion of sodium below 1 percent. Antidiuretic hormone concentrates the urine, raising specific gravity and osmolality. Slow tubular flow gives urea longer to be reabsorbed with water, so blood urea nitrogen climbs out of proportion to creatinine. A tubule that is working hard but still intact sheds no cells, so the sediment stays bland (Norris, 2019).
Where the Mechanism Failed and How the Presentation Follows
Three agents disabled that defense at the same time. Naproxen inhibits cyclooxygenase, so the prostaglandins that dilate the afferent arteriole were unavailable when perfusion pressure fell. Lisinopril blocks conversion of angiotensin I to angiotensin II, so the efferent arteriole could not constrict to hold pressure inside the capillary tuft. Hydrochlorothiazide kept promoting sodium and water loss into a deficit six to eight stools a day were already widening. The danger of that combination is not additive but multiplicative: with the inlet unable to open and the outlet unable to narrow, filtration follows arterial pressure downward with nothing left to buffer it (Kellum et al., 2021).
Every finding on the first sheet now has an owner. The 4.2 kg loss is close to a 4 L deficit, because acute weight change in this setting is water. An orthostatic fall of 18 mmHg with a rise of 24 beats per minute is baroreceptor compensation that has run out of reserve. Urine sodium of 12 mEq/L and a fractional excretion of sodium of 0.4 percent are aldosterone and sympathetic tone doing exactly what they are built to do. Specific gravity of 1.028 is antidiuretic hormone at work. A urea to creatinine ratio near 19 to 1 is slow tubular flow, and the bland sediment says the tubular cells are still alive.
The acid-base and potassium picture is mixed, and saying so is more accurate than forcing it into one pattern. Stool carries bicarbonate, so five days of diarrhea produce a hyperchloremic acidosis, which is why chloride sits at 110 mEq/L. Falling filtration then adds retained sulfate and phosphate, lifting the anion gap to 14 and making the disorder part gap and part non-gap. The potassium of 5.4 mEq/L deserves attention precisely because diarrhea and a thiazide should both be pushing it down. It is high anyway: filtration has collapsed, the ACE inhibitor has cut aldosterone signaling to the collecting duct, and a hyperchloremic acidosis shifts potassium out of cells. The peaked T waves are that value showing itself on the membrane.
The mechanism also predicts what comes next in either direction. Prerenal physiology is reversible while tubular cells are alive, and restoring circulating volume returns filtration quickly. If hypoperfusion continues, the outer medulla fails first, because the thick ascending limb works at a high metabolic rate in a region that is relatively hypoxic even in health. Ischemic tubular injury would then announce itself with a different set of readings: fractional excretion of sodium above 2 percent, specific gravity drifting toward 1.010, muddy brown granular casts in the sediment, and a creatinine that no longer falls with volume repletion (Rogers, 2023).
References
Hall, J. E., & Hall, M. E. (2021). Guyton and Hall textbook of medical physiology (14th ed.). Elsevier.
Kellum, J. A., Romagnani, P., Ashuntantang, G., Ronco, C., Zarbock, A., & Anders, H. J. (2021). Acute kidney injury. Nature Reviews Disease Primers, 7, Article 52.
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. (2012). KDIGO clinical practice guideline for acute kidney injury. Kidney International Supplements, 2(1), 1-138.
Norris, T. L. (2019). Porth's pathophysiology: Concepts of altered health states (10th ed.). Wolters Kluwer.
Rogers, J. L. (2023). McCance and Huether's pathophysiology: The biologic basis for disease in adults and children (9th ed.). Elsevier.
How this NUR 631 Topic 3 example is structured
In many sections this topic asks for a case-based analysis that traces a presentation back to the mechanism behind it; your classroom's instructions and rubric decide the exact form, so read this NUR-631 Topic 3 example as a model of the genre rather than a copy of one prompt. The paper runs in three sheets, and it moves in an order a mechanism argument needs. The first sheet lays out the case with its timeline, medications, examination and laboratory values, so that every later claim has something to answer to. The second sheet describes the physiology that normally prevents this outcome, because a failure cannot be shown without first showing the working system. The third sheet names where that system was disabled and maps each sign and value onto the step that produced it.
NUR-631 Topic 3 questions, answered
What does the NUR-631 Topic 3 assignment usually ask for?
Grand Canyon University does not publish topic-by-topic deliverable names for this course, so start with your classroom's instructions and rubric. In many sections this topic asks for a case-based paper that explains a presentation through the physiology and pathophysiology behind it. The example here is written as that genre: case, normal function, then the point of failure and its consequences.
How much normal physiology should a pathophysiology case paper include?
Enough that the failure has something to fail against, and no more. This example spends one sheet on renal autoregulation, the prostaglandin and angiotensin arms, and the volume response, because each of those reappears by name in the analysis. Normal physiology that never returns later is padding, and graders read it as a summary of the textbook rather than as analysis.
Can I cite a textbook in a graduate pathophysiology paper?
Yes, for established mechanism. Core texts are the right source for autoregulation or tubular transport, while a guideline or a current review is the right source for staging, diagnostic thresholds and anything that has changed recently. Mixing the two shows a reader you know which claims need current evidence and which have been settled for decades.
Write yours, or have the desk draft it
This paper is an original model document written by our desk, not a submitted student paper and not an official Grand Canyon University document. Read it for the moves, then write your own to the instructions in your classroom. If you want one built to your exact prompt and rubric, the first custom sample is free and arrives in 24 to 48 hours.