Analgesic nephropathy pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

Overview

The pathogenesis of analgesic nephropathy caused by phenacetin may be due to several reasons. Toxic metabolites of phenacetin cause capillary sclerosis in the renal medulla, which results in renal papillary necrosis, tubulointerstitial nephropathy and cortical atrophy. Renal ischemia and renal papillary necrosis may be result from the methemoglobinemia caused by phenacetin. Additionally, It has been reported that the concentration of phenacetin is higher at the papillary which is suggestive of direct damage to the renal papillary cells. Although non-phenacetin analgesics (such as NSAIDs, aspirin and acetaminophen) or their combinations have been reported in some studies as causes to analgesic nephropathy, but there is insufficient evidence that suggests these drugs cause analgesic nephropathy.

Pathophysiology

  • There is a strong association between phenacetin and analgesic nephropathy.[1]
  • The classic analgesic nephropathy is disappearing after the removal of phenacetin from the markets over 30 years ago.[2]
  • Although non-phenacetin analgesics (such as NSAIDs, aspirin and acetaminophen) or their combinations have been reported in some studies as causes to analgesic nephropathy, but there is insufficient evidence that suggests these drugs cause analgesic nephropathy.[3][4]

Phatogenesis of Analgesic Nephropathy Caused by Phenacetin

Phatogenesis of Renal Papillary Necrosis Caused by Acetaminophen

Phatogenesis of Renal Papillary Necrosis Caused by NSAIDs and Aspirin

Gross Pathology

On gross pathology, the following findings are found in analgesic nephropathy:[11]

Microscopic Pathology

On microscopic histopathological analysis, the following are seen in analgesic nephropathy:[11]

Immunofluorescent Microscopy

On immunofluorescent microscopy, the following findings are seen:[11]

  • Segmental lesions show coarse blobs of C3
  • Membranous lesions show granular deposits of IgG and C3 along glomerular capillary loops (epimembranous distribution)
  • Arteries may be normal or show nephrosclerosis

References

  1. Yaxley J (2016). "Common Analgesic Agents and Their Roles in Analgesic Nephropathy: A Commentary on the Evidence". Korean J Fam Med. 37 (6): 310–316. doi:10.4082/kjfm.2016.37.6.310. PMC 5122661. PMID 27900067.
  2. 2.0 2.1 Mihatsch MJ, Khanlari B, Brunner FP (2006). "Obituary to analgesic nephropathy--an autopsy study". Nephrol. Dial. Transplant. 21 (11): 3139–45. doi:10.1093/ndt/gfl390. PMID 16891638. Unknown parameter |month= ignored (help)
  3. Feinstein AR, Heinemann LA, Curhan GC; et al. (2000). "Relationship between nonphenacetin combined analgesics and nephropathy: a review. Ad Hoc Committee of the International Study Group on Analgesics and Nephropathy". Kidney Int. 58 (6): 2259–64. doi:10.1046/j.1523-1755.2000.00410.x. PMID 11115060. Unknown parameter |month= ignored (help)
  4. Delzell E, Shapiro S (1998). "A review of epidemiologic studies of nonnarcotic analgesics and chronic renal disease". Medicine (Baltimore). 77 (2): 102–21. doi:10.1097/00005792-199803000-00003. PMID 9556702.
  5. Mihatsch MJ, Hofer HO, Gudat F, Knüsli C, Torhorst J, Zollinger HU (1983). "Capillary sclerosis of the urinary tract and analgesic nephropathy". Clin. Nephrol. 20 (6): 285–301. PMID 6641031. Unknown parameter |month= ignored (help)
  6. Gault MH, Shahidi NT, Barber VE (1974). "Methemoglobin formation in analgesic nephropathy". Clin Pharmacol Ther. 15 (5): 521–7. doi:10.1002/cpt1974155521. PMID 4827469.
  7. 7.0 7.1 Bluemle LW, Goldberg M (1969). "Renal accumulation of salicylate and phenacetin: possible mechanisms in the nephropathy of analgesic abuse". J Clin Invest. 47 (11): 2507–14. doi:10.1172/JCI105932. PMC 297415. PMID 5813230.
  8. 8.0 8.1 Duggin GG (1996). "Combination analgesic-induced kidney disease: the Australian experience". Am. J. Kidney Dis. 28 (1 Suppl 1): S39–47. PMID 8669429. Unknown parameter |month= ignored (help)
  9. 9.0 9.1 Sabatini S (1996). "Pathophysiologic mechanisms in analgesic-induced papillary necrosis". Am J Kidney Dis. 28 (1 Suppl 1): S34–8. doi:10.1016/s0272-6386(96)90567-3. PMID 8669428.
  10. Beyer KH, Gelarden RT (1978). "Renal concentration gradients of salicylic acid and its metabolic congeners in the dog". Arch Int Pharmacodyn Ther. 231 (2): 180–95. PMID 25632.
  11. 11.0 11.1 11.2 Nanra RS (1980). "Clinical and pathological aspects of analgesic nephropathy". Br J Clin Pharmacol. 10 Suppl 2: 359S–368S. doi:10.1111/j.1365-2125.1980.tb01824.x. PMC 1430193. PMID 7002190.

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