RECENT ASPECTS OF DRUG-INDUCED OR TOXIC I NTERSTITIAL NEPHROPATHIES

Citation
Jp. Fillastre et al., RECENT ASPECTS OF DRUG-INDUCED OR TOXIC I NTERSTITIAL NEPHROPATHIES, La Presse medicale, 26(10), 1997, pp. 477-484
Citations number
45
Categorie Soggetti
Medicine, General & Internal
Journal title
ISSN journal
07554982
Volume
26
Issue
10
Year of publication
1997
Pages
477 - 484
Database
ISI
SICI code
0755-4982(1997)26:10<477:RAODOT>2.0.ZU;2-V
Abstract
Phenotyping interstitial infiltrations:; Recent progress has led to th e distinction between type I and type II fibroblasts in the renal inte rstitium. The cellular phenotype of pathological infiltrations can be identified with monodonal antibodies. Drug-induced interstitial nephro pathies: Extrarenal manifestations (skin eruptions, fever, joint pain) often suggests the diagnosis but may be absent in which case renal hi stology is required. Causal drugs: Among the different causal agents, nonsteroid anti-inflammatory drugs cause abnormal leakage from glomeru lar capillaries favoring the development of a nephrotic syndrome assoc iated with renal failure and major cell infiltration into the intersti tial tissue. Chronic disease: Chronic interstitial nephropathy is near ly asymptomatic and may only be discovered at an advanced stage. Brief ly there are three categories which result from long-term administrati on of 5-aminosalicylate, use of Chinese herbal medicines to lose weigh t, and chronic intoxication with ochratoxin (a mycotoxin). Complex phy siopathology: Immunological mechanisms are involved although it is not always easy to distinguish between manifestations of humoral and cell ular reactions. Both could be implicated as indicated in recent experi mental animal models which throw more light on the pathological proces s in humans. Renal prognosis: Different strategies can be used to halt or limit the development of fibrosis and thus improve prognosis of to xic interstitial nephropathies: counteract cellular immunity reactions , inhibit fibroblast proliferation and activation, reduce synthesis an d stimulate degradation of the extracellular matrix, and inhibit colla gen formation.