The Knee Pain That Hurt His Kidneys

This is prerenal acute kidney injury, KDIGO stage 2 (creatinine 2.8 times baseline), from the "triple whammy": an NSAID, an ACE inhibitor, and a diuretic taken together, tipped over by volume loss.

When effective circulating volume drops, the kidney maintains intraglomerular pressure two ways, and each drug removes one:

• Prostaglandins dilate the afferent arteriole. Ibuprofen inhibits cyclooxygenase, reducing prostaglandin synthesis.
• Angiotensin II constricts the efferent arteriole. Lisinopril inhibits angiotensin-converting enzyme, reducing angiotensin II formation.
• The thiazide, the vomiting, and the diarrhea reduce effective circulating volume and renal perfusion.

With both compensations blocked and volume down, GFR falls and the creatinine climbs. His BUN-to-creatinine ratio is 20, right at the line where a ratio above 20 suggests a prerenal cause. It supports the picture but does not prove it. Because he is on a thiazide, FENa is unreliable; FEUrea below 35% is the better marker of a prerenal state.

• Monitor and access: continuous cardiac monitoring and IV access. With potassium 5.6 and no peaked T waves, repeat the ECG and potassium, and treat per protocol if the potassium rises or ECG changes develop.
• Stop the ibuprofen. Hold the lisinopril and the hydrochlorothiazide.
• Restore volume: IV isotonic crystalloid per order, then reassess blood pressure, heart rate, urine output, and lung sounds.
• Rule out urinary retention. Older men are prone to bladder outlet obstruction, often from BPH. His bladder scan of 60 mL makes that unlikely.
• Rule out a GI bleed. NSAID use plus vomiting is a classic setup, and blood in the gut also raises the BUN. His history and normal hemoglobin make it unlikely; trend the hemoglobin.
• Send a urinalysis. Bland urinary sediment supports a prerenal cause over intrinsic renal injury, such as acute tubular necrosis or the interstitial nephritis NSAIDs can cause.
• Protect the kidney: strict intake and output, trend the creatinine, avoid nephrotoxins and IV contrast when possible, and renally dose all medications with pharmacy.

• Avoid NSAIDs such as ibuprofen and naproxen, including combination over-the-counter cold and sleep products that contain them. Ask his provider about acetaminophen for the knee instead.
• Sick-day rule: if he is vomiting, has diarrhea, or cannot keep fluids down, call his provider about holding his lisinopril and hydrochlorothiazide until he is eating and drinking again.
• Check his blood pressure at home while his antihypertensives are on hold, and call his provider if it is outside the range they give him.
• Restart the lisinopril and hydrochlorothiazide only when his provider says so, and get a basic metabolic panel rechecked as ordered.
• Skip salt substitutes and potassium supplements unless his provider approves them. Many salt substitutes are potassium chloride.

The ibuprofen was stopped, both antihypertensives were held, and he received IV crystalloid. His urinalysis was bland. His creatinine fell from 2.8 to 1.9 on day 2 and to 1.2 on day 3. His potassium came down to 4.6 without other treatment, and his urine output recovered.

He was discharged on acetaminophen for his knee, with both antihypertensives on hold. His primary care provider restarted them at follow-up and rechecked a basic metabolic panel.

None of his three medications was wrong on its own. Together, plus volume depletion from gastroenteritis, they caused acute kidney injury.