Non-steroidal anti-inflammatory drugs and the kidneys
You’re right that non-steroidal anti-inflammatory drugs (NSAIDs) have an effect on the glomerular arterioles by inhibiting prostaglandin production. This is why they can be renotoxic; if the affereny arteriole constricts, the filtration pressure drops and this can lead to renal failure in susceptible individuals or those on interacting drugs (like angiotensin converting enzyme (ACE) inhibitors, which dilate the efferent arteriole).
Nephrolithiasis (kidney stones)
However, these arterioles are blood vessels. Kidney stones (renal calculi) form in the nephron or further down the drainage system in the ureters by the precipitation and crystallisation of calcium or oxalate salts.
NSAIDs do reduce excretion of calcium, so it was thought they might reduce the formation of calculi. However, they also reduce secretion of other protective factors (such as glucosaminoglycans, or GAG), so there is no significant overall benefit, other than analgesia.
I found this old paper from the International Journal of Clinical Pharmacology, Therapy and Toxicology that looked at the effects of the NSAID diclofenac in people with hypercalciuria (higher than normal calcium levels in the urine).
Non-steroidal anti-inflammatory drugs decrease urinary calcium excretion in male
Sprague-Dawley rats. Indomethacin decreases significantly the urinary
calcium excretion in hypercalciuric patients. These observations
encouraged the use of NSAID in the treatment of nephrolithiasis with
encouraging initial results. However, NSAID (indomethacin and
naproxen) retard both glycosaminoglycans (GAGs) synthesis and
degradation thereby causing a significant reduction in the urinary
excretion of GAGs, known to be potent inhibitors of calcium oxalate
crystallization. Therefore, the effect of another NSAID, diclofenac-Na
(50 mg t.i.d. for 4 weeks) was studied on 31 recurrent calcium oxalate
nephrolithiasis patients who were not hypercalciuric or
hyperuricosuric. The 24-h urinary excretion of creatinine, calcium and
uric acid remained unchanged at 2 weeks and 4 weeks of therapy.
However, after treatment of 2 weeks and 4 weeks, there was a
significant decrease in the 24-h urinary excretion of GAGs (from 17.04
+/- 7.39 mumol to 11.54 +/- 7.02 and 12.7 +/- 6.2 mumol, respectively), and urinary concentration of GAGs (from 10.77 +/- 7.09
mumol/l to 6.03 +/- 5.00 mumol/l and 7.35 +/- 4.81 mumol/l,
respectively). Thus diclofenac-Na (50 mg t.i.d.) did not reduce
urinary excretion of calcium but significantly lowered the urinary
excretion and concentration of GAGs in normocalciuric nephrolithiasis
patients, an observation which cautions against the use of
diclofenac-Na in prevention of nephrolithiasis in this group of
Thus, the reason NSAIDs are used is for analgesia. They do not have an overall effect to reduce e stone formation and there is no mechanism by which they facilitate the passage of the stone. This is in keeping with current practice on the management of neprolithiasis.
To help facilitate the passage of a stone, alpha adrenoceptor antagonists (like doxazosin) can be used. They relax the smooth muscle surrounding the ureters and urethra, allowing any calculi to pass more easily.
A K Hemal, H Sidhu, S K Thind, R Nath, S Vaidyanathan. Effect of diclofenac-Na on 24-hour urinary excretion of creatinine, calcium, uric acid and glycosaminoglycans in adult patients with recurrent calcium oxalate nephrolithiasis. International Journal of Clinical Pharmacology, Therapy, and Toxicology. 1989 Jan; 27 (1) : 44-6.
Conor P Moran, Aisling E Courtney. Managing acute and chronic renal stone disease. Practitioner. 2016 Feb; 260 (1790) : 17-20, 2-3.
Renee R. Koski, PharmD, CACP, FMPA and William H. Zufall, PharmD. Efficacy and Safety of Alpha-Blockers for Kidney Stones in Adults. Journal of Pharmacy Technology, 2018 Apr; 34(2): 54–61. DOI: 10.1177/8755122517750398