chronic interstitial nephritis (analgesic nephropathy, drug-induced chronic interstitial nephritis)
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Etiology
- medications
- chronic analgesic use (daily use for years)
- patients generally do not admit to analgesic abuse
- aspirin or acetaminophen* alone does not cause analgesic nephropathy, but many NSAIDs may[1]
- sodium phosphate
- orlistat, high doses of vitamin C
- lithium
- calcineurin inhibitors (cyclosporine, tacrolimus)
- proton pump inhibitors
- H2 blockers (ranitidine, famotidine, nizatidine, cimetidine)
- allopurinol
- antiretrovirals (indinavir, abacavir, tenofovir)
- diuretics (triamterine, furosemide, thiazides)
- anticonvulsants (phenytoin, carbamazepine, phenobarbital, valproate)
- mesalamine
- antibiotics (cephalosporins, fluoroquinolones. penicillins, rifampin. sulfonamides)
- chemotherapeutic agents
- immunosuppressive agents
- chronic analgesic use (daily use for years)
- toxins
- autoimmune
- hereditary
- infections
- malignancies
- hypertensive nephrosclerosis
- obstructive uropathy
- hyperuricemia
* ref 2 indicates acetaminophen alone may cause analgesic nephropathy
Epidemiology
- 20% of cases of tubulonephritis
- 85% of patients are women
Pathology
- phenacetin & its metabolites are concentrated in the renal papillae
- these metabolites damage the papillae by lipid peroxidation
- aspirin diminishes local renal blood flow
- a total dose of 1 kg of phenacetin or 1 g/day for 3 years is necessary to cause analgesic nephropathy
- transitional cell carcinomas are more common in patients with analgesic nephropathy
- patients have accelerated atherosclerosis
- papillary necrosis (30%)
- interstitial scarring, fibrosis, renal tubular atrophy
- renal concentrating deficits
Clinical manifestations
- chronic pain problem, but may present as flank pain
- arthritis & muscular aches
- headache (80%)
- history of peptic ulcer (40%)
- hypertension (40%)
- urinary tract infections with dysuria (25%)
- history of urinary obstruction (10%)
- polyuria, nocturia due to renal concentrating deficits
- hematuria
- predisposition to volume depletion
- NSAID-induced interstitial nephritis may present as nephrotic syndrome
- premature aging
- slow decline in renal function over months-to-years
- Fanconi syndrome
- normal anion gap metabolic acidosis (RTA1 or RTA4)
Laboratory
- anemia (85%)
- urinalysis
- sterile pyuria
- hematuria
- isosthenuria (urine concentrating deficit)
- urine protein may reveal nephrotic syndrome, but generally < 1500 mg/24 hr
- serum albumin may be low with nephrotic syndrome
- basic metabolic panel
- decline in GFR
- autoantibodies to TINAG
Radiology
- renal ultrasound: small kidneys (50%)
- normal excretory urogram (10%)
- papillary calcification & papillary necrosis may be seen with:
Complications
- may progress to end-stage renal disease
Management
- discontinue offending agent
- supportive measures
More general terms
Additional terms
References
- ↑ 1.0 1.1 Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 612
- ↑ Medical Knowledge Self Assessment Program (MKSAP) 11, 18, 19. American College of Physicians, Philadelphia 1998, 2018, 2021.
- ↑ eMedicine: Nephritis, Interstitial http://www.emedicine.com/med/topic1596.htm
- ↑ Analgesic Nephropathy (Painkillers and the Kidneys) http://kidney.niddk.nih.gov/kudiseases/pubs/analgesicnephropathy/index.htm
Patient information
chronic interstitial nephritis (analgesic nephropathy) patient information