Skip to main content

NSAIDs and Analgesics

NSAIDs and analgesics play eight major roles in urology: (1) acute renal colic — the most evidence-based application, where NSAIDs are first-line over opioids; (2) perioperative pain management in urologic surgery; (3) ureteral stent symptoms; (4) medical expulsive therapy (MET) for ureteral stones; (5) chronic prostatitis / chronic pelvic pain syndrome (CP/CPPS); (6) interstitial cystitis / bladder pain syndrome (IC/BPS); (7) bladder cancer chemoprevention (investigational); and (8) urinary tract analgesia (phenazopyridine). NSAIDs carry significant nephrotoxicity risk that is amplified in urologic patients (obstructive uropathy, solitary kidney, CKD, RAAS-inhibitor use), and the opioid-stewardship movement has fundamentally reshaped analgesic prescribing in the field.[1][2][3][4]

For the analgesia comparator classes — broadly framed as nonnarcotic methods of pain management[9] — see Gabapentinoids, SNRIs, and Tricyclic antidepressants.

Mechanism — Why NSAIDs Work in the LUT​

NSAIDs inhibit COX → reduced prostaglandin synthesis. The class effects are urologic at four levels:[2]

  1. Renal pelvis and ureter — prostaglandins drive ureteral spasm, mucosal inflammation, and renal vasodilation around an obstructing stone. NSAIDs blunt all three, lowering urine output and intra-pelvic pressure — a fundamentally different mechanism from opioids, which only mask central pain
  2. Ureteral smooth muscle — reduced peristaltic spasm; potential MET adjunct effect[5]
  3. Bladder and prostate — COX-2 is upregulated in inflamed prostate and urothelium; NSAIDs reduce prostatic inflammation in CP/CPPS and modulate bladder afferent signaling in IC/BPS[6]
  4. Bladder cancer biology — COX-2 is overexpressed in transitional cell carcinoma; COX-2 inhibition induces apoptosis, blocks EMT, and reduces tumor growth in preclinical models[7][8]

Urologic Applications at a Glance​

ApplicationPreferred agent(s)EvidencePosition
Acute renal colicDiclofenac IM, ibuprofen IV, ketorolac IVCochrane + multiple meta-analyses[1][2][10]EAU/AUA first-line; CDC prefers over opioids[19]
Post-ureteroscopy painKetorolac PO/IVSKOPE RCT[11]Expert consensus: 0 opioid tablets acceptable[4]
Ureteral stent symptomsNSAIDs as adjunctSystematic reviews[15]Recommended with α-blockers ± antimuscarinics
Medical expulsive therapyCelecoxib (adjunct to α-blocker)RCT[12]Not in guidelines as primary MET
CP/CPPSIbuprofen, diclofenac, celecoxib (short-term)Cochrane and network meta[6][23][24]Statistically significant but below MCID
IC/BPSNSAIDs (general principles)AUA Clinical Principle[3][25]Pain-management framework only
Bladder cancer chemopreventionCelecoxibPhase III negative trials[13][14]Not recommended (CV risk; negative)
Perioperative urologic surgeryKetorolac, ibuprofen, celecoxib + acetaminophenMeta-analyses; ERAS[21][22]Core of multimodal opioid-sparing pathways

Acute Renal Colic — the primary urologic application​

The most evidence-based use of NSAIDs in urology, supported by multiple Cochrane reviews and large meta-analyses.

Headline evidence​

  • Cochrane 2025 (29 RCTs, n = 3,593): NSAIDs reduce renal-colic pain at 30 min vs placebo (MD −3.84 cm on 10 cm VAS; 95% CI −6.41 to −1.27). IV ketorolac may be less effective than IV ibuprofen; IV and IM routes have similar effects; IV may beat rectal[2]
  • Pathan 2018 meta (36 RCTs, n = 4,887): NSAIDs marginally outperform opioids at 30 min (MD −5.58); fewer rescue treatments (NNT 11) and lower vomiting (NNT 5) vs opioids; fewer rescue treatments than paracetamol (RR 0.56; p < 0.05)[1]
  • Gu 2019 network meta (65 RCTs, n = 8,633): by route — IM diclofenac has the most evidence (recommended without CV risk); IV ibuprofen and IV ketorolac may be superior to IM diclofenac; combination therapy (NSAID + opioid) is more effective but with more AEs and is reserved for failure of NSAID monotherapy[10]
  • Pathan 2016 Lancet RCT (n = 1,645): IM diclofenac superior to IV morphine for renal-colic pain; both diclofenac and IV paracetamol superior to morphine with fewer AEs[18]
  • CDC Guideline 2022: opioids are not recommended as first-line therapy for kidney-stone pain[19]

Preferred agents and dosing​

AgentDoseNotes
Diclofenac75 mg IMMost studied; EAU-recommended[1]
Ketorolac30 mg IVGeneric, widely available; effective for most patients[2]
Ibuprofen800 mg IVMay be more effective than IV ketorolac[2]
Paracetamol1 g IVEffective alternative when NSAIDs are contraindicated; comparable 30-min pain reduction but more rescue analgesia needed[1][18][20]

Perioperative Pain Management​

NSAIDs are the foundation of opioid-sparing multimodal analgesia in urologic surgery.

Opioid-sparing magnitude (systematic review of 32 studies)[21]​

  • Diclofenac reduces opioid consumption 17–50%
  • Ketorolac 9–66%
  • Ibuprofen 22–46%
  • Ketoprofen 34–66%

Lower nausea, vomiting, sedation, and pruritus vs placebo; no surgery-related bleeding signals across the trials.

SKOPE RCT — ketorolac vs oxycodone post-URS[11]​

The first double-blinded RCT post-ureteroscopy: ketorolac 10 mg PO non-inferior to oxycodone 5 mg PO for pain. No differences in pain scores, medication use, or AEs. Ketorolac patients reported significantly fewer days confined to bed (1.3 vs 2.3; p = 0.02). Strong evidence against routine opioid use after URS.

Opioid-stewardship results in urology​

NOPIOIDS protocol (Mian 2023)[17]​

Eliminating routine discharge opioids after radical cystectomy, radical / partial nephrectomy, and radical prostatectomy:

  • Discharge opioid prescription rate: 80.9% (control) → 57.9% (lead-in) → 2.2% (NOPIOIDS)
  • Median tablets prescribed: 14 → 4 → 0 (p < 0.001)
  • No increase in pain, unplanned healthcare utilization, or complications — feasible and safe

ORIOLES — post-prostatectomy[22][46]​

In 205 RP patients with 100% follow-up, median prescribed 225 mg OMEQ but median used 22.5 mg OMEQ — 77% of prescribed opioids unused; 84% required ≤ 112.5 mg OMEQ; only 9% appropriately disposed of leftover medication. Prescribing more was independently associated with greater use.

AUA Expert Panel Consensus — procedure-specific maximums[4]​

ProcedureMax recommended (5 mg oxy equivalents)
Cystoscopy, stent removal, vasectomy0
Hydrocele repair5
Ureteroscopy, circumcision10
Robotic prostatectomy, PCNL, robotic partial nephrectomy15

Minimum recommended for every procedure: 0 tablets. NSAIDs and acetaminophen sit at the core of every documented opioid-sparing pathway.[4][16]

Ureteral Stent–Related Symptoms​

NSAIDs are part of multimodal stent-symptom pharmacotherapy.[15]

  • Alpha-blockers carry the strongest monotherapy evidence
  • NSAIDs target the inflammatory and pain components
  • Antimuscarinics target the urinary symptom components
  • A Bayesian network meta-analysis ranked anticholinergic + pregabalin highest for the pain domain and α-blocker + anticholinergic highest for urinary symptoms (see Gabapentinoids)[15]

Medical Expulsive Therapy​

NSAIDs play a secondary role in MET, primarily as adjuncts to α-blockers.

  • Lv & Tang 2014 (RCT, n = 105): naftopidil + celecoxib 200 mg achieved the highest distal-stone expulsion (94.3%) vs naftopidil alone (82.9%) or celecoxib alone (60.6%) (p < 0.05)[12]
  • NSAIDs are listed among MET drug classes alongside α-blockers and CCBs, but α-blockers remain the primary agent.[5]

CP/CPPS​

NSAIDs are recommended for short-term use but produce statistically significant benefit that is below the clinical-importance threshold.[6][23][24]

  • Cochrane 2019 (7 RCTs, n = 372 men): anti-inflammatories vs placebo — NIH-CPSI MD −2.5 (95% CI −3.74 to −1.26), below the 6-point MCID[23]
  • Network meta-analysis 2022 (5 RCTs, n = 191): NIH-CPSI MD −1.7 (p = 0.03) — again below MCID[24]
  • AUA / 2025 JAMA review: acetaminophen or short-term NSAIDs (e.g., ibuprofen 400 mg QID × 4–6 weeks) may be considered; opioids should be avoided[6]
  • Reasonable as part of multimodal therapy; limit to short courses to minimize nephrotoxicity and GI risk.

IC/BPS​

The 2022 AUA IC/BPS Guideline addresses pain pharmacology as a Clinical Principle: pain management for IC/BPS should mirror other chronic-pain conditions; non-opioid agents should be used preferentially; pain management alone is not sufficient — multimodal therapy is essential.[3][25]

There are no IC/BPS-specific NSAID trials; use rests on general chronic-pain principles.

Phenazopyridine — the urinary-tract analgesic​

The only FDA-approved urinary-tract-specific analgesic, indicated for symptomatic relief of pain, burning, urgency, frequency, and discomfort from lower-tract irritation due to infection, trauma, surgery, endoscopic procedures, or catheter passage.[26][28]

Mechanism​

Excreted in urine where it exerts a topical analgesic effect on the urothelial mucosa. Recent work identifies TRPM8 channel inhibition as the likely molecular target — phenazopyridine inhibits TRPM8 rapidly and reversibly at urinary-relevant concentrations (IC₅₀ 2–10 μM), and TRPM8 is upregulated in painful bladder disorders.[27]

Dosing and key precautions[26]​

  • 200 mg TID after meals
  • Limit to 2 days when used with antibacterials for UTI — no benefit beyond that
  • Contraindicated in renal insufficiency (66% renally excreted unchanged)
  • Causes orange-red urine discoloration (counsel about staining of clothing and contact lenses)
  • May interfere with urinalysis-based diagnostics
  • Not for chronic use

Practical role: bridge analgesia during the interval before antibacterial control of a UTI, after endoscopic procedures, or after catheter placement — reducing or eliminating the need for systemic analgesics.

Celecoxib and Bladder Cancer Chemoprevention​

Strong preclinical rationale; clinical trials are negative, and CV risk precludes routine use.

Preclinical (strong)[7][8][29][30][31]​

  • Celecoxib reduced bladder-cancer incidence 65–95% in rat models when given preventively
  • Mechanisms include COX-2-dependent and -independent pathways: apoptosis, anti-EMT (miR-145 / TGFBR2 / Smad3), anti-inflammatory, anti-proliferative, antioxidant
  • Preventive but not curative efficacy — curative dosing may aggravate tumor malignancy

Clinical (negative)​

TrialDesignResult
BOXIT (Kelly 2019)Phase III RCT, n = 472, intermediate / high-risk NMIBCNo reduction in recurrence at 3 yr (68% vs 64%; HR 0.82, p = 0.2). Subgroup signal in pT1 (HR 0.53, p = 0.04). CV serious AEs higher with celecoxib (5.2% vs 1.7%, p = 0.07)[13]
Sabichi 2011RCT, n = 146, high-risk NMIBCDid not significantly prolong time-to-recurrence at 12 mo (88% vs 78%; HR 0.69, p = 0.17); marginal signal for metachronous recurrence (HR 0.56, p = 0.075)[14]

Bottom line: celecoxib is not recommended for bladder-cancer chemoprevention.

NSAIDs and Erectile / Gonadal Function​

The relationship between NSAIDs and ED is controversial and likely confounded by indication.

StudyDirection
Gleason 2011 (n = 80,966)Regular NSAID use associated with ED (aOR 1.38)[32]
Shiri 2006 (n = 1,126)NSAID use raised ED risk (IDR 2.0)[33]
Senbel preclinicalIndomethacin reduced rat erectile responses; diclofenac less; celecoxib unaffected[34]
Patel PCPT (n = 4,726)After controlling for indication, NSAID use not associated with ED — apparent association attributable to confounding[35]
Halpern NHANES (n = 3,749)Regular NSAID use not associated with testosterone, AMH, or compensated hypogonadism[36]
Li 2018 systematic reviewMixed; methodologically heterogeneous[37]

Practical message: current evidence does not support counseling patients that NSAIDs cause ED, although non-selective COX inhibitors (especially indomethacin) may have direct effects on erectile physiology in preclinical models.

Nephrotoxicity — the critical urologic concern​

NSAID nephrotoxicity is amplified in urologic patients.[38][39][40][41]

Mechanisms​

  1. Hemodynamic AKI (most common, usually reversible) — NSAIDs blunt prostaglandin-mediated compensatory vasodilation in low-perfusion states → reduced GFR
  2. Acute interstitial nephritis (rare, idiosyncratic) — any NSAID
  3. Renal papillary necrosis — chronic use
  4. Electrolyte disturbance — sodium / water retention, hyperkalemia, hyponatremia
  5. CKD — regular use may raise CKD incidence; relationship with progression less clear

Risk factors that matter for the urologist​

  • Pre-existing CKD (CrCl < 60)
  • Volume depletion / dehydration
  • Concurrent RAAS inhibitors and diuretics (the "triple whammy")
  • Advanced age (> 65)
  • Solitary kidney — common after nephrectomy
  • Bilateral or high-grade obstruction
  • Heart failure, cirrhosis

Practical implications​

  • Renal colic — NSAIDs remain first-line in patients with adequate renal function; check baseline function and avoid in significant CKD, dehydration, or bilateral obstruction[1][41]
  • Solitary-kidney patients — favor acetaminophen as primary analgesic
  • Stone formers on thiazides — combination raises nephrotoxicity risk
  • Lowest effective dose for the shortest possible time is the universal rule[39][40]

Acetaminophen / Paracetamol in Urology​

A first-line analgesic when NSAIDs are contraindicated.

  • Renal colic — IV paracetamol 1 g comparable to NSAIDs at 30 min; both superior to morphine in the Pathan Lancet trial with fewer AEs[1][18][20]
  • Perioperative — core component of multimodal analgesia in ERAS protocols; reduces opioid consumption when paired with NSAIDs; recommended as the first agent administered postoperatively[42]
  • Renal safety — generally safe at recommended doses (≤ 4 g/day); little evidence that chronic paracetamol monotherapy causes CKD or analgesic nephropathy; a suitable first-line choice in CKD with dose individualization in advanced renal failure[43][44][45]
  • CP/CPPS — recommended alongside short-term NSAIDs; opioids should be avoided[6]

Opioid Stewardship in Urology — Key Principles​

  • Opioids are not first-line for kidney-stone pain[19]
  • When opioids are warranted, prescribe immediate-release at the lowest effective dose for the shortest expected duration[19]
  • Maximize NSAIDs and acetaminophen; explore non-pharmacologic options
  • Most urologic procedures can be discharged with 0–10 opioid tablets per the AUA expert panel[4]
  • NOPIOIDS-style protocols demonstrate that even major urologic cancer surgery can be discharged with zero routine opioid prescriptions without compromising pain control or safety[17]
  • 77% of opioids prescribed after RP are unused — calibrate prescribing accordingly using initiatives like ORIOLES[22][46]

Clinical Positioning​

  • Renal colic → NSAID first-line in patients with adequate renal function (IM diclofenac, IV ibuprofen, IV ketorolac); IV paracetamol is the alternative when NSAIDs are contraindicated; opioids reserved for true NSAID failure[1][2][10][19]
  • Post-URS, post-cystectomy, post-RP — multimodal NSAID + acetaminophen is the standard; SKOPE and NOPIOIDS show 0–minimal opioid prescribing is feasible[11][17]
  • Stent symptoms — NSAIDs as adjunct to α-blockers ± antimuscarinics; pregabalin is the pain-domain combination winner in network meta-analysis[15]
  • MET — α-blocker is the workhorse; celecoxib adjunct may add expulsion benefit in distal stones[12]
  • CP/CPPS — short-term NSAIDs are reasonable but the effect is below MCID; avoid opioids[6]
  • IC/BPS — NSAIDs as part of general non-opioid pain management; multimodal therapy required[3]
  • Phenazopyridine is the only urinary-tract-specific analgesic; 2-day limit with antibacterials, contraindicated in renal insufficiency[26]
  • Bladder cancer chemoprevention — celecoxib is not recommended despite preclinical signal[13][14]
  • Nephrotoxicity is the dominant safety concern in urologic patients — assess renal function, avoid in volume depletion / triple-whammy combinations / solitary kidney / bilateral obstruction, use the lowest effective dose for the shortest possible time[38][39][40][41]
  • Don't counsel patients that NSAIDs cause ED — the apparent association is confounded by indication[35][37]

See Also​

References​

1. Pathan SA, Mitra B, Cameron PA. "A systematic review and meta-analysis comparing the efficacy of nonsteroidal anti-inflammatory drugs, opioids, and paracetamol in the treatment of acute renal colic." Eur Urol. 2018;73(4):583–595. doi:10.1016/j.eururo.2017.11.001

2. Afshar K, Gill J, Mostafa H, Noparast M. "Nonsteroidal anti-inflammatory drugs (NSAIDs) for acute renal colic." Cochrane Database Syst Rev. 2025;3:CD006027. doi:10.1002/14651858.CD006027.pub3

3. Clemens JQ, Erickson DR, Varela NP, Lai HH. "Diagnosis and treatment of interstitial cystitis/bladder pain syndrome." J Urol. 2022;208(1):34–42. doi:10.1097/JU.0000000000002756

4. Koo K, Faisal F, Gupta N, et al. "Recommendations for opioid prescribing after endourological and minimally invasive urological surgery: an expert panel consensus." J Urol. 2020;203(1):151–158. doi:10.1097/JU.0000000000000514

5. Lim I, Sellers DJ, Chess-Williams R. "Current and emerging pharmacological targets for medical expulsive therapy." Basic Clin Pharmacol Toxicol. 2022;130(Suppl 1):16–22. doi:10.1111/bcpt.13613

6. Borgert BJ, Wallen EM, Pham MN. "Prostatitis." JAMA. 2025;334(11):1003–1013. doi:10.1001/jama.2025.11499

7. Grubbs CJ, Lubet RA, Koki AT, et al. "Celecoxib inhibits N-butyl-N-(4-hydroxybutyl)-nitrosamine-induced urinary bladder cancers in male B6D2F1 mice and female Fischer-344 rats." Cancer Res. 2000;60(20):5599–5602.

8. Liu X, Wu Y, Zhou Z, et al. "Celecoxib inhibits the epithelial-to-mesenchymal transition in bladder cancer via the miRNA-145/TGFBR2/Smad3 axis." Int J Mol Med. 2019;44(2):683–693. doi:10.3892/ijmm.2019.4241

9. Finnerup NB. "Nonnarcotic methods of pain management." N Engl J Med. 2019;380(25):2440–2448. doi:10.1056/NEJMra1807061

10. Gu HY, Luo J, Wu JY, et al. "Increasing nonsteroidal anti-inflammatory drugs and reducing opioids or paracetamol in the management of acute renal colic: based on three-stage study design of network meta-analysis of randomized controlled trials." Front Pharmacol. 2019;10:96. doi:10.3389/fphar.2019.00096

11. Fedrigon D, Faris A, Kachroo N, et al. "SKOPE — Study of Ketorolac vs Opioid for Pain after Endoscopy: a double-blinded randomized control trial in patients undergoing ureteroscopy." J Urol. 2021;206(2):373–381. doi:10.1097/JU.0000000000001772

12. Lv JL, Tang QL. "Comparative evaluation of efficacy of use of naftopidil and/or celecoxib for medical treatment of distal ureteral stones." Urolithiasis. 2014;42(6):541–547. doi:10.1007/s00240-014-0708-6

13. Kelly JD, Tan WS, Porta N, et al. "BOXIT — a randomised phase III placebo-controlled trial evaluating the addition of celecoxib to standard treatment of transitional cell carcinoma of the bladder (CRUK/07/004)." Eur Urol. 2019;75(4):593–601. doi:10.1016/j.eururo.2018.09.020

14. Sabichi AL, Lee JJ, Grossman HB, et al. "A randomized controlled trial of celecoxib to prevent recurrence of nonmuscle-invasive bladder cancer." Cancer Prev Res (Phila). 2011;4(10):1580–1589. doi:10.1158/1940-6207.CAPR-11-0036

15. Koprowski C, Kim C, Modi PK, Elsamra SE. "Ureteral stent-associated pain: a review." J Endourol. 2016;30(7):744–753. doi:10.1089/end.2016.0129

16. Cabo JJS, Miller NL. "Nonopioid pain management pathways for stone disease." J Endourol. 2024;38(2):108–120. doi:10.1089/end.2023.0266

17. Mian BM, Singh Z, Carnes K, et al. "Implementation and assessment of no opioid prescription strategy at discharge after major urologic cancer surgery." JAMA Surg. 2023;158(4):378–385. doi:10.1001/jamasurg.2022.7652

18. Pathan SA, Mitra B, Straney LD, et al. "Delivering safe and effective analgesia for management of renal colic in the emergency department: a double-blind, multigroup, randomised controlled trial." Lancet. 2016;387(10032):1999–2007. doi:10.1016/S0140-6736(16)00652-8

19. Dowell D, Ragan KR, Jones CM, Baldwin GT, Chou R. "CDC clinical practice guideline for prescribing opioids for pain — United States, 2022." MMWR Recomm Rep. 2022;71(3):1–95. doi:10.15585/mmwr.rr7103a1

20. Al-Terki A, Hussain J, El-Nahas AR, et al. "Parecoxib vs paracetamol for treatment of acute renal colic due to ureteric calculi: a randomized controlled trial." Urology. 2021;149:76–80. doi:10.1016/j.urology.2020.12.017

21. Martinez L, Ekman E, Nakhla N. "Perioperative opioid-sparing strategies: utility of conventional NSAIDs in adults." Clin Ther. 2019;41(12):2612–2628. doi:10.1016/j.clinthera.2019.10.002

22. Patel HD, Srivastava A, Patel ND, et al. "A prospective cohort study of postdischarge opioid practices after radical prostatectomy: the ORIOLES initiative." Eur Urol. 2019;75(2):215–218. doi:10.1016/j.eururo.2018.10.013

23. Franco JV, Turk T, Jung JH, et al. "Pharmacological interventions for treating chronic prostatitis/chronic pelvic pain syndrome." Cochrane Database Syst Rev. 2019;10:CD012552. doi:10.1002/14651858.CD012552.pub2

24. Qin Z, Zhang C, Guo J, et al. "Oral pharmacological treatments for chronic prostatitis/chronic pelvic pain syndrome: a systematic review and network meta-analysis of randomised controlled trials." EClinicalMedicine. 2022;48:101457. doi:10.1016/j.eclinm.2022.101457

25. Imamura M, Scott NW, Wallace SA, et al. "Interventions for treating people with symptoms of bladder pain syndrome: a network meta-analysis." Cochrane Database Syst Rev. 2020;7:CD013325. doi:10.1002/14651858.CD013325.pub2

26. US Food and Drug Administration. Phenazopyridine Hydrochloride — prescribing information. Updated 2025-09-05.

27. Luyts N, Daniluk J, Freitas ACN, et al. "Inhibition of TRPM8 by the urinary tract analgesic drug phenazopyridine." Eur J Pharmacol. 2023;942:175512. doi:10.1016/j.ejphar.2023.175512

28. US Food and Drug Administration. Phenazopyridine Hydrochloride — prescribing information. Updated 2022-05-31.

29. Parada B, Sereno J, Reis F, et al. "Anti-inflammatory, anti-proliferative and antioxidant profiles of selective cyclooxygenase-2 inhibition as chemoprevention for rat bladder carcinogenesis." Cancer Biol Ther. 2009;8(17):1615–1622. doi:10.4161/cbt.8.17.9199

30. Dhawan D, Jeffreys AB, Zheng R, Stewart JC, Knapp DW. "Cyclooxygenase-2 dependent and independent antitumor effects induced by celecoxib in urinary bladder cancer cells." Mol Cancer Ther. 2008;7(4):897–904. doi:10.1158/1535-7163.MCT-07-0313

31. Sereno J, Parada B, Reis F, et al. "Preventive but not curative efficacy of celecoxib on bladder carcinogenesis in a rat model." Mediators Inflamm. 2010;2010:380937. doi:10.1155/2010/380937

32. Gleason JM, Slezak JM, Jung H, et al. "Regular nonsteroidal anti-inflammatory drug use and erectile dysfunction." J Urol. 2011;185(4):1388–1393. doi:10.1016/j.juro.2010.11.092

33. Shiri R, Koskimäki J, Häkkinen J, et al. "Effect of nonsteroidal anti-inflammatory drug use on the incidence of erectile dysfunction." J Urol. 2006;175(5):1812–1815. doi:10.1016/S0022-5347(05)01000-1

34. Senbel AM. "Functional inhibition of erectile process in rats by indomethacin." World J Urol. 2011;29(4):523–527. doi:10.1007/s00345-010-0600-0

35. Patel DP, Schenk JM, Darke A, et al. "Non-steroidal anti-inflammatory drug (NSAID) use is not associated with erectile dysfunction risk: results from the Prostate Cancer Prevention Trial." BJU Int. 2016;117(3):500–506. doi:10.1111/bju.13264

36. Halpern JA, Fantus RJ, Chang C, et al. "Effects of nonsteroidal anti-inflammatory drug (NSAID) use upon male gonadal function: a national, population-based study." Andrologia. 2020;52(4):e13542. doi:10.1111/and.13542

37. Li T, Wu C, Fu F, et al. "Association between use of aspirin or non-aspirin non-steroidal anti-inflammatory drugs and erectile dysfunction: a systematic review." Medicine (Baltimore). 2018;97(28):e11367. doi:10.1097/MD.0000000000011367

38. Ković SV, Vujović KS, Srebro D, Medić B, Ilic-Mostic T. "Prevention of renal complications induced by non-steroidal anti-inflammatory drugs." Curr Med Chem. 2016;23(19):1953–1964. doi:10.2174/0929867323666160210125920

39. Whelton A. "Nephrotoxicity of nonsteroidal anti-inflammatory drugs: physiologic foundations and clinical implications." Am J Med. 1999;106(5B):13S–24S. doi:10.1016/s0002-9343(99)00113-8

40. LaForge JM, Urso K, Day JM, et al. "Non-steroidal anti-inflammatory drugs: clinical implications, renal impairment risks, and AKI." Adv Ther. 2023;40(5):2082–2096. doi:10.1007/s12325-023-02481-6

41. Baker M, Perazella MA. "NSAIDs in CKD: are they safe?" Am J Kidney Dis. 2020;76(4):546–557. doi:10.1053/j.ajkd.2020.03.023

42. Coccolini F, Corradi F, Sartelli M, et al. "Postoperative pain management in non-traumatic emergency general surgery: WSES-GAIS-SIAARTI-AAST guidelines." World J Emerg Surg. 2022;17(1):50. doi:10.1186/s13017-022-00455-7

43. Alchin J, Dhar A, Siddiqui K, Christo PJ. "Why paracetamol (acetaminophen) is a suitable first choice for treating mild to moderate acute pain in adults with liver, kidney or cardiovascular disease, gastrointestinal disorders, asthma, or who are older." Curr Med Res Opin. 2022;38(5):811–825. doi:10.1080/03007995.2022.2049551

44. Abbasi M, Teakell J. "Literature review: are NSAIDs harmful and is acetaminophen well tolerated?" Curr Opin Nephrol Hypertens. 2023;32(3):284–289. doi:10.1097/MNH.0000000000000886

45. Blantz RC. "Acetaminophen: acute and chronic effects on renal function." Am J Kidney Dis. 1996;28(1 Suppl 1):S3–S6. doi:10.1016/s0272-6386(96)90561-2

46. Su ZT, Becker REN, Huang MM, et al. "Patient and in-hospital predictors of post-discharge opioid utilization: individualizing prescribing after radical prostatectomy based on the ORIOLES initiative." Urol Oncol. 2022;40(3):104.e9–104.e15. doi:10.1016/j.urolonc.2021.10.007