E. Alexopoulos et al., RELATIONSHIP BETWEEN INTERSTITIAL INFILTRATES AND STEROID RESPONSIVENESS OF PROTEINURIA IN MEMBRANOUS NEPHROPATHY, Nephrology, dialysis, transplantation, 9(6), 1994, pp. 623-629
Mononuclear inflammatory cells were retrospectively analysed using mon
oclonal antibodies in the interstitium and glomeruli of 16 renal biops
y specimens from patients with nephrotic syndrome due to idiopathic me
mbranous nephropathy (IMN). The aim of the study was to determine the
composition of the infiltrate and to assess the ability to predict the
response of proteinuria to corticosteroids. All patients had received
prednisolone as a sole treatment. Nine patients had shown a complete
or partial remission of proteinuria (group A) and seven did not respon
d at all (group B). Both groups were matched for age and degree of pro
teinuria; also both groups had normal renal function at the time of bi
opsy. Very few intraglomerular leukocytes, mostly monocytes/macrophage
s (MM) were found. The majority of interstitial cells were T lymphocyt
es and MM. CD4+ve T helper/inducer cells predominated among the inters
titial T cell population and B cells were a minor component. No signif
icant differences were found between the two groups regarding the type
s of the intraglomerular cells. However, interstitial T-cells, CD4+ve
T helper/inducer cells, CD8+ve T cytotoxic/suppressor cells and MM wer
e significantly higher in group A than in group B. Also HLA-DR express
ing interstitial cells were much in excess in group A. In addition pat
ients with complete remission of proteinuria had higher numbers of int
erstitial cells compared to those with partial response. There was no
correlation between the numbers of types of intraglomerular and inters
titial cells and the degree of proteinuria at presentation. Also no as
sociation was found between intraglomerular or interstitial cell popul
ation and subsequent relapse of proteinuria. In conclusion, interstiti
al but not intraglomerular mononuclear cells seem to determine the ini
tial response of proteinuria to corticosteroids in patients with IMN.