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.