In minimal-change nephropathy

Patients with renal diseases leading to the nephrotic syndrome often present complex problems in volume management. These patients may exhibit fluid retention in the form of ascites or edema but have reduced plasma volume due to reduced plasma oncotic pressures. This is very often the case in patients with "minimal change" nephropathy. In these patients, diuretic use may cause further reductions in plasma volume that can impair GFR and may lead to orthostatic hypotension. Most other causes of nephrotic syndrome are associated with primary retention of salt and water by the kidney, leading to expanded plasma volume and hypertension despite the low plasma oncotic pressure. In these cases, diuretic therapy may be beneficial in controlling the volume-dependent component of hypertension. 

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. 

Gil. Guasch, A., and Myers, B. D., Determinants of glomerular hypofiltration in nephrotic patients with minimal change nephropathy. J. Am. Soc. Nephrol. 4, 1571-1581 (1994). 

Proximal renal tubnlar proteinuria is a possible complication in patients treated with high doses of mesalazine, and it is clearly important to monitor renal function in these patients (SEDA-22, 394) (75). Two studies in 21 (76) and 95 (77) patients with ulcerative colitis and Crohn s disease have shown that proteinuria of tubular marker proteins is common and is related to disease activity rather than to treatment with mesalazine. Thus, tubular proteins are not useful predictors of an adverse renal response to the drug. Nephrotic syndrome with minimal change nephropathy has been described with sulfasalazine and mesalazine (SEDA-16, 427). 

Renal papillary necrosis and interstitial nephritis with the nephrotic syndrome have been documented (27,28). Other cases of the nephrotic syndrome, with or without renal insufficiency, which were apparently due to minimal-change nephropathy (which is relatively more common in NSAID users), have been reported (29,30). The unusual feature of diclofenac-associated renal interstitial mucinosis has been described (SEDA-17, 109). 

Isenring P, de Cotret PR, Delage C, Kingma I, Lebel M. d-Penicillamine induced reversible minimal change nephropathy in rheumatoid arthritis. J Nephrol 1991 4 245-8. 

Interferon Proteinuria in up to 5 to 20% patients Rarely nephritic syndrome or/and acute renal failure (acute interstitial nephrotoxicity and minimal change nephropathy ... 

Among all the types of glomerulonephritis, minimal-change nephropathy is most responsive to treatment. Steroids can induce good responses in most patients during initial treatment as well as relapse. 

The immunosuppressive effect of cytotoxic agents, with or without the concurrent use of steroids, can result in serious infections, which are the primary cause of death in patients with minimal-change nephropathy. Other toxicities associated with cyclophosphamide include gonadal fibrosis, which results in sterility, hemorrhagic cystitis, alopecia, and a potential to develop malignancy in those on long-term treatment. Patients on chronic steroid therapy often develop growth retardation, osteoporosis, obesity, and cataracts. ... 

The presenting clinical features in nephrotic adults with minimal-change nephropathy can be indistinguishable from that of FSGS, and renal biopsy is therefore critical in the treatment of adults with nephrotic syndrome. FSGS is two to four times more common in black patients than in white patients. They tend to present with proteinuria more frequently in the nephrotic range and are more likely to experience a rapid decline in renal function. 

The cytoplasmic part of nephrin interacts also with ZO-1 protein and actin (K10). Interaction of the antibody or toxin with the extracellular part of nephrin could thus also result in intracellular signaling (phophorylation of tyrosine residues in the cytoplasmic part of nephrin), change of the actin cytoskeleton, and foot process fusion. Indeed, increased levels of phosphotyrosine were demonstrated in renal biopsies of patients with minimal change disease and membranous nephropathy (B2). 

In the following we concentrate mainly on the pathogenesis of minimal change disease, focal and segmental glomerulosclerosis, and idiopathic membranous nephropathy. These three diseases are responsible for about 60-95% of nephrotic syndromes and their prevalence depends on age. 

In 54 patients, a kidney biopsy was performed 13.2 8.9 days after onset (n = 32). In all patients, the findings suggested either acute tubular necrosis or its recovery phase. The underlying diseases included kidney diseases such as IgA nephropathy [138], minimal change nephrotic syndrome [139], autosomal dominant polycystic kidney disease (ADPKD) [140], and cystinuria [67]. 

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