Prevention, Diagnosis and Treatment of Acute Tubulointerstitial Nephritis

A special issue of Medicina (ISSN 1648-9144). This special issue belongs to the section "Urology & Nephrology".

Deadline for manuscript submissions: closed (20 September 2023) | Viewed by 2462

Special Issue Editor


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Guest Editor
Azienda Ospedaliero - Universitaria di Parma, Parma, Italy
Interests: nephrology; renal pathology; kidney transplantation; glomerular diseases

Special Issue Information

Dear Colleagues,

Tubulointerstitial nephritis defines a wide spectrum of acute and chronic inflammatory diseases affecting renal tubules and the interstitium. Inflammation can be the consequence of autoimmune or infectious diseases, but hypersensitivity phenomena involving exposure to drugs are among the most frequent causes. Moreover, novel antitumoral medications acting through immune system modulation may induce tubulointerstitial nephritis. The diagnosis is frequently suspected based on clinical history and presentation, but renal biopsies may reveal specific morphological features and drive the clinical decision. Prognosis is extremely variable as the clinical approach can differ radically based on the etiology, and should include, when possible, removal of the causal agent, requiring immunomodulatory or anti-infectious medications in specific cases.

The aims of this Special Issue include collecting current knowledge about the pathogenesis, diagnosis and treatment of tubulointerstitial nephritis, and providing kidney clinicians and pathologists with novel tools to understand and face this heterogeneous and insidious disease.

This Special Issue will collect original research and review papers on the “epidemiology and clinical outcomes of tubulointerstitial nephritis”, as well as “novel physiopathological insights and novel forms of tubulointerstitial nephritis”, “clinical and histological features” and “therapeutic approaches: pharmacological and non-pharmacological therapies”.

Dr. Marco Delsante
Guest Editor

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Keywords

  • tubulointerstitial nephritis
  • interstitial inflammation
  • tubulitis
  • drug-induced kidney disease
  • renal pathology
  • acute kidney injury
  • immunosuppressive therapy

Published Papers (1 paper)

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Research

14 pages, 1314 KiB  
Article
Protective Effect of Neutral Electrolyzed Saline on Gentamicin-Induced Nephrotoxicity: Evaluation of Histopathologic Parameters in a Murine Model
by Nomely S. Aurelien-Cabezas, Brenda A. Paz-Michel, Ivan Jacinto-Cortes, Osiris G. Delgado-Enciso, Daniel A. Montes-Galindo, Ariana Cabrera-Licona, Sergio A. Zaizar-Fregoso, Juan Paz-Garcia, Gabriel Ceja-Espiritu, Valery Melnikov, Jose Guzman-Esquivel, Iram P. Rodriguez-Sanchez, Margarita L. Martinez-Fierro and Ivan Delgado-Enciso
Medicina 2023, 59(2), 397; https://doi.org/10.3390/medicina59020397 - 17 Feb 2023
Cited by 2 | Viewed by 2136
Abstract
Background and Objectives: Gentamicin (GM) is a nephrotoxic aminoglycoside. Neutral electrolyzed saline (SES) is a compound with anti-inflammatory, antioxidant, and immunomodulatory properties. The objective of the present study was to evaluate whether kidney damage by GM can be prevented and/or reversed through [...] Read more.
Background and Objectives: Gentamicin (GM) is a nephrotoxic aminoglycoside. Neutral electrolyzed saline (SES) is a compound with anti-inflammatory, antioxidant, and immunomodulatory properties. The objective of the present study was to evaluate whether kidney damage by GM can be prevented and/or reversed through the administration of SES. Materials and Methods: The study was carried out as a prospective, single-blind, five-arm, parallel-group, randomized, preclinical trial. The nephrotoxicity model was established in male BALB/c mice by administering GM at a dose of 100 mg/kg/day intraperitoneally for 30 days, concomitantly administering (+) SES or placebo (physiologic saline solution), and then administering SES for another 30 days after the initial 30 days of GM plus SES or placebo. At the end of the test, the mice were euthanized, and renal tissues were evaluated histopathologically. Results: The GM + placebo group showed significant tubular injury, interstitial fibrosis, and increased interstitial infiltrate of inflammatory cells compared with the group without GM. Tubular injury and interstitial fibrosis were lower in the groups that received concomitant GM + SES compared with the GM + placebo group. SES administration for 30 days after the GM administration periods (GM + placebo and GM + SES for 30 days) did not reduce nephrotoxicity. Conclusions: Intraperitoneal administration of SES prevents gentamicin-induced histologic nephrotoxicity when administered concomitantly, but it cannot reverse the damage when administered later. Full article
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