The Association of Mesalamine With Kidney Disease

Adiga, Avinash; Goldfarb, David S.

doi:10.1053/j.ackd.2019.09.002

Cited by 18 publications

(23 citation statements)

References 34 publications

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“…tified PPK inhibitors, mesalamine (also known as mesalazine or 5-aminosalicylic acid), has been validated by treating different bacteria ranging from clinically isolated uropathogenic E. coli and P. aeruginosa strains to human gastrointestinal luminal samples (25). Mesalamine is a drug commonly used to treat IBD patients, and rare side effects have been reported (44)(45)(46). Mesalamine exerts its anti-inflammatory effects locally on the colorectal mucosa, and the efficacy is dependent on achieving high intraluminal concentrations (47,48).…”

Section: Fig 10mentioning

confidence: 99%

The Polyphosphate Kinase of Escherichia coli Is Required for Full Production of the Genotoxin Colibactin

Tang-Fichaux

Chagneau

Bossuet-Greif

et al. 2020

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Section: Fig 10mentioning

confidence: 99%

The Polyphosphate Kinase of Escherichia coli Is Required for Full Production of the Genotoxin Colibactin

Tang-Fichaux

Chagneau

Bossuet-Greif

et al. 2020

mSphere

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“…The exact pathogenic mechanism of AKI is not completely known. The classic form of acute TIN, as we present, is thought to be a form of generalized delayed cell-mediated hypersensitivity reaction, characterized by mixed inflammatory cell infiltrate, composed of B and T lymphocytes and macrophages, and interstitial oedema [2,[4][5][6]. In chronic stage, the extent of interstitial fibrosis and tubular atrophy will dictate irreversibility and progression to chronic kidney disease [5].…”

Section: Discussionmentioning

confidence: 99%

“…In chronic stage, the extent of interstitial fibrosis and tubular atrophy will dictate irreversibility and progression to chronic kidney disease [5]. 5-ASA toxicity likely occurs as an idiosyncratic dose-independent phenomenon, unrelated to dosage or time of drug exposure [2,[4][5][6]. Several authors suggest that undercurrent steroid therapy may mask AKI or delay presentation [4,5].…”

Section: Discussionmentioning

confidence: 99%

“…Clinical suspicion or declared 5-ASA-induced-TIN should lead to prompt discontinuation of the drug. Recovery to baseline kidney function occurs in 85% of patients if the drug is stopped within 10 months of its initiation, but in only 33% if the time to diagnosis and drug withdrawal is longer than 18 months [2,4,6]. Albeit potentially reversible, it has been calculated that about 10% of patients with 5-ASA nephrotoxicity will progress to end-stage renal disease [2,4].…”

Section: Discussionmentioning

confidence: 99%

“…Renal impairment may occur in up to 1 in each 100 patients treated but clinically significant AKI was estimated to occur only in 1 in 500 patients [2][3][4][5]. It may present as TIN or, rarely, as minimal-change nephropathy [3,6]. TIN clinical presentation is usually scanty and unspecific.…”

Section: Discussionmentioning

confidence: 99%

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Acute Kidney Injury in the Context of Inflammatory Bowel Disease - A Clinical Case

Cristóvão¹,

Rui²,

Lemos³

et al. 2021

J Clin Nephrol Ren Care

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Crohn’s disease may promote inflammation in IgA nephropathy: a case–control study of patients undergoing kidney biopsy

et al. 2022

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Intestinal immunity has been closely associated with the pathogenesis and progression of renal diseases, a relationship known as the “gut–kidney axis.” To determine the association between immunoglobulin A nephropathy (IgAN) and Crohn’s disease (CD), a clinico-pathological study was performed on patients who had IgAN with CD (CD-IgAN) and without CD (NOS-IgAN). We enrolled 29 patients diagnosed with IgAN via renal biopsy at the Tokyo Yamate Medical Center from 2009 to 2017. The patients were divided into CD-IgAN (n = 18) and NOS-IgAN (n = 11) and evaluated for clinical and pathological findings. IgA subclasses and galactose-deficient IgA1 (Gd-IgA1) were examined via immunohistochemistry using formalin-fixed paraffin-embedded sections from renal biopsy. Our results showed no significant difference in the extent of mesangial IgA subclasses or Gd-IgA1 deposition according to the presence or absence of CD. Pathologically, however, those with CD-IgAN had remarkably higher percentage of global glomerulosclerosis and extent of interstitial fibrosis and tubular atrophy (IF/TA) compared to those with NOS-IgAN. Moreover, the extent of macrophage infiltration in the glomerulus and interstitium was significantly higher in CD-IgAN than in NOS-IgAN. Clinically, the CD-IgAN group had significantly worse responsiveness to steroid treatment compared to the NOS-IgAN group. In conclusion, the similar immunological characteristics of deposited IgA molecules in the glomeruli between the CD-IgAN and NOS-IgAN groups might suggest their etiological similarity. However, a renal pathology showing advanced glomerular and tubulointerstitial sclerosis accompanying increased macrophage infiltration and highly resistant clinical features in patients with CD-IgAN suggests that some pathophysiological factors in CD, including abnormal intestinal immunity, may promote and activate the inflammatory process in IgAN via undetermined mechanisms.

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The Association of Mesalamine With Kidney Disease

Cited by 18 publications

References 34 publications

The Polyphosphate Kinase of Escherichia coli Is Required for Full Production of the Genotoxin Colibactin

The Polyphosphate Kinase of Escherichia coli Is Required for Full Production of the Genotoxin Colibactin

Acute Kidney Injury in the Context of Inflammatory Bowel Disease - A Clinical Case

Crohn’s disease may promote inflammation in IgA nephropathy: a case–control study of patients undergoing kidney biopsy

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