Glomerulopathy, membranous

Renal toxicity induced by penicillamine is usually manifested as reversible proteinuria and hematuria, but may progress to nephrouritic syndrome with membraneous glomerulopathy. 

In the circulation of the BN rat there is a simultaneous and transient presence of antiglomerular basement membrane antibodies and circulating immune complexes [175]. Another characteristic is a striking increase in total and antigen-specific IgE level [190], which also has been found in Hooded Lister rats [ 191 ], as well as anti-single-stranded DNA antibodies [ 181] in the BN rat. In PVG/C rats [192, 193], mercuric chloride also induced glomerulopathi and antinuclear antibodies directed against non-histone nucleoprotein. 

Renal function impairment Proteinuria and hematuria may develop and may be a warning sign of membranous glomerulopathy, which can progress to a nephrotic syndrome. 

The glomerular capillary wall has a very high hydraulic permeability and the glomerular basement membrane and the slit diaphragm probably contribute approximately 50% each to the total hydraulic resistance of the capillary wall (D8). Foot process effacement found both in experimental models of nephrotic syndrome and in human glomerulopathies dramatically reduces the hydraulic permeability of the glomerular capillary wall (Gil). 

Pathogenesis of foot process fusion in various human glomerulopathies may be different. On one hand, in membranous nephropathy, foot process fusion may be the consequence of complement-induced podocyte damage (Cl 1) on the other hand, in minimal change disease, proteinuria may be caused by direct damage to the slit diaphragm with consequent foot process fusion. In any case, foot process fusion results in the formation of large pores and proteinuria. 

Slusarczyk, J., Michalak, T., Mazarewicz-de Mezer, T., Krawczynski, K., and No-woslawski, A., Membranous glomerulopathy associated with hepatitis B core antigen immune complexes in children. Am. J. Pathol. 98, 29-43 (1980). 

Membranous nephropathy is rare and causes the nephrotic syndrome, usually with minimal-change glomerulopathy, with or without interstitial nephritis (SEDA-11, 85). A retrospective study provided more data on the frequency and clinical characteristics of membranous nephropathy associated with NSAIDs (158). It confirmed that it is rare (13 of 125 patients diagnosed during the last 20 years met the strict criteria for NSAID-associated membranous nephropathy), and the nephrotic syndrome is reversible after prompt withdrawal. The pathogenesis is unknown but seems to be immune-mediated, given the characteristic deposition of IgG and C3. 

Serious renal injury can develop as a late complication of pre-existing benign penicillamine nephropathy (220,225). Unfortunately, microscopic hematuria has limited predictive value for imminent serious renal injury, since in most patients who take penicillamine it is a transient or coincidental finding (SEDA-7, 260). The diagnosis of penicillamine-induced renal injury is often difficult because of the frequent association of rheumatoid arthritis with renal disorders (198,204,226-228), including spontaneous membranous glomerulopathy (229), or with injury caused by concomitant analgesics (230). 

Textor SC, Gephardt GN, Bravo EL,Tarazi RC, Fouad FM,Tubbs R,and McMahon JT. Membranous glomerulopathy associated with captopril therapy. The American Journal of Medicine 74 705-712,1983. 

Non-steroidal anti-inflammatory drugs are known to induce a nephrotic syndrome in addition to acute tubulointerstitial nephritis (discussed in [77]). Glomerulopathies include minimal change disease, focal glomerulosclerosis that could represent a continuum with the former entity and membranous glomerulopathy. A review of 97 patients with non-steroidal anti-in-... 

Histopathological examinations of the renal biopsy specimens from patients with proteinuria show predominantly membranous glomerulopathy [10, 22,... 

In this chapter we first will discuss the undesirable aspects of these effects of ACEI and will show how most of these effects may be prevented by cautious use of the agents. Since the mechanisms of the ACEI-induced membranous glomerulopathy and interstitial nephritis are different from those causing the fall in GFR, we will discuss each separately. 

Thus far, no reports have been published on membranous glomerulopathy or acute interstitial nephritis in relation to the use of angiotensin It receptor antagonists. Whether this is due to the relatively short experience with these agents, or the fact that these ACET induced side effects are specific for ACEl and thus not related to the interference in the renin angiotensin system in general, cannot be concluded as yet. 

Sturgill BC, Shearlock KT. Membranous glomerulopathy and nephrotic syndrome after captopril therapy. JAMA 1983 250 2343-2345. 

Smit AJ, Hoorntje SJ, Weening JJ, Donker AM, Hoedemaeker PJ. Unilateral membranous glomerulopathy during captopril treatment. Neth J Med 1985 28 23-27. 

Markowitz GS, Falkowitz DC, Isom R, Zaki M, Imaizumi S, Appel GB, et al. Membranous glomerulopathy and acute interstitial nephritis following treatment with celecoxib. Clin Nephrol 2003 59 137-42. 

Fritsche L, Budde K, Farber L, et al. Treatment of membranous glomerulopathy with cyclosporin A How much patience is required Nephrol Dial Transplant 1999 14 1036-1038. 

Human membranous glomerulopathies and possibly minimal change disease... 

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