Non-steroidal anti-inflammatory drugs-associated acute interstitial nephritis with granular tubular basement membrane deposits

Dixit, Mehul; Nguyen, Cuong C.; Carson, Thomas H.; Guedes, Ben; Dixit, Naznin; Bell, Jane M.; Wang, Yihan

doi:10.1007/s00467-007-0585-0

Cited by 20 publications

(23 citation statements)

References 15 publications

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“…However, no specific infection could be identified in our patient. Although tubulointerstitial immune-complex nephritis is a very rare form of TIN, such nephritis can be caused by treatments such as nonsteroidal anti-inflammatory drugs [9], by autoimmune diseases such as lupus erythematosus [10], or IgG4-related diseases [11]. However, our patient received no long-term drug treatment apart from IVIG, and had no collagen disease or IgG4-related disease according to repeated laboratory examinations.…”

Section: Discussionmentioning

confidence: 95%

Tubulointerstitial nephritis complicating IVIG therapy for X-linked agammaglobulinemia

et al. 2014

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BackgroundPatients with X-linked agammaglobulinemia (XLA) develop immune-complex induced diseases such as nephropathy only rarely, presumably because their immunoglobulin (Ig) G concentration is low. We encountered a patient with XLA who developed tubulointerstitial nephritis during treatment with intravenous immunoglobulin (IVIG).Case presentationA 20-year-old man was diagnosed with XLA 3 months after birth and subsequently received periodic γ-globulin replacement therapy. Renal dysfunction developed at 19 years of age in association with high urinary β2-microglobulin (MG) concentrations. A renal biopsy specimen showed dense CD3-positive lymphocytic infiltration in the tubulointerstitium and tubular atrophy, while no IgG4-bearing cell infiltration was found. Fibrosclerosis and crescent formation were evident in some glomeruli. Fluorescent antibody staining demonstrated deposition of IgG and complement component C3 in tubular basement membranes. After pulse steroid therapy was initiated, urinary β2-MG and serum creatinine concentrations improved.ConclusionNeither drug reactions nor collagen disease were likely causes of tubular interstitial disorder in this patient. Although BK virus was ruled out, IgG in the γ-globulin preparation might have reacted with a pathogen present in the patient to form low-molecular-weight immune complexes that were deposited in the tubular basement membrane.

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Section: Discussionmentioning

confidence: 95%

Tubulointerstitial nephritis complicating IVIG therapy for X-linked agammaglobulinemia

et al. 2014

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“…Permanently high resistance to antibiotics with increasing resistance rates of E. coli to ampicillin and TMP/SMX were shown in studies from the UK, Austria, Spain and Brasil [9,11,12,19 23]. Because of that, some authors concluded that ampicillin, trimetoprim, and TMP/SMX were insufficient for the monotherapy of UTI, as recommended by Wolff et al (2007) [9,24].…”

Section: Discussionmentioning

confidence: 99%

Changes in bacterial resistance patterns in children with urinary tract infections on antimicrobial prophylaxis at University Hospital in Split

et al. 2011

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SummaryBackgroundWe assessed prevalence and resistance of uropathogens on antimicrobial agents (AA) from urine cultures (UC) in children hospitalized with urinary tract infections (UTI) at University Hospital in Split.Material/MethodsDuring the 7-year period, children hospitalized only once with UTI alone were compared to those repeatedly hospitalized, and who received long-term antimicrobial prophylaxis (LTAP), as well as those with associated anomalies of the urinary system (US).ResultsE. coli was the most frequent isolate (67.7%) with resistance to ampicillin by 69.5%, amoxicillin/clavulonic acid by 3.5%, cephalexin by 6.6%, trimethoprim/sulfamethoxazole (TMP-SMX) by 27.5%, and nitrofurantoin by 0.4%. For other uropathogens, AA resistance rates were the following: 64.3%, 5.8%, 10.5%, 21.3%, and 7.9%. The high or increasing resistance to TMP-SMX is characterized by all uropathogens. Patients with anomalies of US showed a lower prevalence of E. coli and Enterococcus sp., but a higher prevalence of Pseudomonas sp., ESBL-producing E. coli and Klebsiella sp. than those without US anomalies. Repeatedly hospitalized patients showed a lower prevalence of E. coli, but a higher prevalence of Pseudomonas sp. and Klebsiella sp. than patients hospitalized only once. Both groups displayed significantly less resistance of Enterococcus sp. In patients receiving LTAP before hospitalization, E. coli was significantly more resistant to ampicillin, amoxicillin/clavulonic acid and TMP/SMX than in those without LTAP.ConclusionsBased on our results, we recommend excluding ampicillin altogether, and reconsideration of further use of TMP-SMX, as well as use of nitrofurantoin, cephalexin and amoxicillin/clavulonic acid for LTAP in our region.

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“…4 Drug-induced TIN with TBM immune complex deposition has been rarely documented in association with nonsteroidal anti-inflammatory drugs. 5 Polyclonal IgG and C3 TBM deposits are present without glomerular deposits. Two cases showed giant cell tubulitis with TBM deposits.…”

Section: Discussionmentioning

confidence: 99%

Immune Complex Tubulointerstitial Nephritis Due to Autoantibodies to the Proximal Tubule Brush Border

Rosales¹,

Collins²,

Carmo³

et al. 2016

Journal of the American Society of Nephrology

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Immune complex tubulointerstitial nephritis due to antibodies to brush border antigens of the proximal tubule has been demonstrated experimentally and rarely in humans. Our patient developed ESRD and early recurrence after transplantation. IgG and C3 deposits were conspicuous in the tubular basement membrane of proximal tubules, corresponding to deposits observed by electron microscopy. Rare subepithelial deposits were found in the glomeruli. The patient had no evidence of SLE and had normal complement levels. Serum samples from the patient reacted with the brush border of normal human kidney, in contrast with the negative results with 20 control serum samples. Preliminary characterization of the brush border target antigen excluded megalin, CD10, and maltase. We postulate that antibodies to brush border antigens cause direct epithelial injury, accumulate in the tubular basement membrane, and elicit an interstitial inflammatory response.

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Non-steroidal anti-inflammatory drugs-associated acute interstitial nephritis with granular tubular basement membrane deposits

Cited by 20 publications

References 15 publications

Tubulointerstitial nephritis complicating IVIG therapy for X-linked agammaglobulinemia

Tubulointerstitial nephritis complicating IVIG therapy for X-linked agammaglobulinemia

Changes in bacterial resistance patterns in children with urinary tract infections on antimicrobial prophylaxis at University Hospital in Split

Immune Complex Tubulointerstitial Nephritis Due to Autoantibodies to the Proximal Tubule Brush Border

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