Acute interstitial nephritis and acute renal failure associated with cimetidine therapy

Richman, Alan V.; Narayan, Janaki L.; Hirschfield, Jan S.

doi:10.1016/0002-9343(81)90837-8

Cited by 34 publications

(4 citation statements)

References 8 publications

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“…Famotidine 80 mg (a maximal therapeutic daily dose) given 3 h before a 3-h clearance period did not change creatinine clearance (Andreev, unpublished observations) for the same reason. Occasionally cimetidine is reported to cause acute interstitial nephritis [8,27,28] …”

Section: Cimetidinementioning

confidence: 99%

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

Andreev

Koopman

Arisz

1999

Journal of Internal Medicine

163

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Abstract. Andreev E, Koopman M, Arisz L (Medical University-Sofia, Sofia, Bulgaria and University of Amsterdam, Amsterdam, The Netherlands). A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible? (Review.) J Intern Med 1999; 246: 247±252. This is a review of the available information about drugs which cause an increase in plasma creatinine concentration without decreasing glomerular filtration rate (GFR). The GFR is the main, but not the single, determinant of the plasma creatinine levels. Several drugs, such as cimetidine, trimethoprim, corticosteroids, pyrimethamine, phenacemide, salicylates and active vitamin D metabolites, have been reported to increase plasma creatinine without influencing its glomerular filtration. Cimetidine, trimethoprim, pyrimethamine and salicylates can inhibit secretion of creatinine by the proximal tubule. Corticosteroids and vitamin D metabolites probably modify the production rate and the release of creatinine. The exact mechanism of phenacemide±creatinine interaction is not fully explained. These drug-induced alterations in plasma creatinine concentration have clinical significance when GFR is estimated by using plasma creatinine.

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Section: Cimetidinementioning

confidence: 99%

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

Andreev

Koopman

Arisz

1999

Journal of Internal Medicine

163

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“…did not observe such significant association in patients with critical illness. Besides PPIs, another commonly used acid‐suppressive drugs (ASDs), histamine 2 receptor antagonist (H 2 RA), has been reported similar adverse kidney effects, such as interstitial nephritis and acute renal failure …”

Section: Introductionmentioning

confidence: 99%

“…Besides PPIs, another commonly used acid-suppressive drugs (ASDs), histamine 2 receptor antagonist (H 2 RA), has been reported similar adverse kidney effects, such as interstitial nephritis and acute renal failure. 13,14 Given the widespread use of ASDs, it is important to determine whether there is a relationship between ASDs and KD worthy of being alerted. The published systematic reviews by Yang et al 15 only examined the associations between PPI and acute KD but ignored the impacts of PPI on long-term KD.…”

Section: Introductionmentioning

confidence: 99%

Acid‐suppressive drugs and risk of kidney disease: A systematic review and meta‐analysis

Qiu

Zhou

Zhang

2018

J of Gastro and Hepatol

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“…These interactions with cimetidine are clinically significant because a decrease in drug clearance may lead to an increase in adverse effects, especially in the elderly and in those with impaired renal function. Numerous cases of acute interstitial nephritis have been reported with cimetidine therapy (Handa 1986;Kaye et al 1983;McGowan & Vermillion 1980;Richman et al 1981;Rudnick et al 1982). Renal biopsies of those cases all showed typical features of interstitial nephritis with infiltrates consisting of plasma cells, lymphocytes and eosinophils.…”

Section: Cimetidinementioning

confidence: 99%

Renal Effects of Peptic Ulcer Therapy

Burgess

Muruve

1992

Drug Safety

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Drugs used in the treatment of peptic ulcer disease may interact with the renal system in a variety of ways. Since many agents are eliminated by renal excretion, clearance of these agents may be reduced and half-life extended in the presence of renal insufficiency. The histamine H2-receptor antagonists may interfere with renal tubular excretion of creatinine and cationic drugs, resulting in elevated serum concentrations and reduced renal clearance. The prostaglandin E1 analogue misoprostol is used as a cytoprotective agent but has renal effects. The renal effects differ between systems studied. In the rat, misoprostol reduces cyclosporin-induced renal tubular toxicity, whereas in humans it has been shown to attenuate renal allograft rejection. Sucralfate is the aluminium salt of sucrose octasulfate. It permits the absorption of aluminium in amounts similar to aluminium-containing antacids, and toxicity has been demonstrated in the presence of renal insufficiency. Bismuth compounds are used increasingly to treat peptic ulcer disease, and bismuth toxicity has been described in association with renal insufficiency. Aluminium-, calcium- and magnesium-containing antacids are used as oral phosphate binders in patients with renal insufficiency in addition to their usual indications. Cation absorption and accumulation with all of these antacid preparations has been described and may lead to toxicity.

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Acute interstitial nephritis and acute renal failure associated with cimetidine therapy

Cited by 34 publications

References 8 publications

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible?

Acid‐suppressive drugs and risk of kidney disease: A systematic review and meta‐analysis

Renal Effects of Peptic Ulcer Therapy

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