Minimal change glomerulopathy may be seen ‘ association with all of the following except,
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Hepatitis B
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Secondary MCD wherein the extraglomerular disease process evokes, directly or indirectly, the characteristic changes in permselectivity and morphology. In this circumstance the morphology is similar, if not identical, to primary or 'idiopathic' MCD. Moreover, it is possible, even likely, that similar or identical pathogenetic mechanisms are operative. In this scenario, a distinct etiologic link is presumed to exist between the extraglomerular disease process and the occurrence of MCD. Such a linkage would be strongly suppoed if cure of the extraglomerular disease lead to the eradication of MCD and if recurrence of the extraglomerular disorder was associated with relapse. While an attempt has been made to be comprehensive, it is possible that individual repos describing an association between the specific extra-glomerular disease and MCD may have been overlooked. The majority of the instances in which MCD has been associated with an extraglomerular disease involve neoplastic processes and idiosyncratic, hyper-sensitivity or toxic reactions to drugs. Neoplasia A variety of neoplastic processes have been repoed in association with MCD (Table 2) . In some, the association is rare enough to suspect that chance alone may have been the operational mechanism underlying the association. In others, the association is clearly contemporaneous and likely causal. Among patients with glomerular disease associated with neoplasia, 40% have MCD on renal biopsy. As mentioned previously it is possible that some of the described associations between neoplasia and MCD may be the consequence of treatment of MCD (especially cytotoxic drug therapy) predisposing to the emergence of a malignancy. Hodgkin's disease and non-Hodgkin's lymphoma are among the most frequently repoed neoplastic processes associated with MCD . Interestingly, repos describing the concurrence of MCD and Hodgkin's disease have decreased in recent years, perhaps due to the more effective diagnostic and therapeutic strategies available for this and related diseases. MCD is a rare complication of Hodgkin's ppdisease occurring in from 1:2000 to 1:10 000 cases. MCD has been associated with both limited (Stage 1) and disseminated (Stage 4) forms of Hodgkin's disease.Therapy of Hodgkin's disease, either by local radio- therapy to regional lymph nodes or by systemic chemotherapy, has often resulted in remission of MCD and recurrences of Hodgkin's disease have been associated with recurrence of MCD. These observations strongly imply a causal relationship between the tumour (or a product of the abnormal neoplastic cells) and the pathophysiological abnormalities involved in MCD. Indeed, it is quite possible that the same clone of cells which are involved in the development of Hodgkin's disease are also involved in the pathogenesis of MCD in both the primary and secondary forms. Such an explanation is more difficult to conjecture for the association of MCD with theother tumours listed in Table 2, except for mycosis fungoides, angiofollicular lymph node hyperplasia, non-Hodgkin's lymphoma and chronic lymphatic leukaemia . Perhaps, in these instances, the peurbations for MCD have also triggered the oncogenic potential of cells predisposed to neoplastic transformation (e.g. lack of a wild type tumour suppressor gene). Alternatively, lymphocytes infiltrating neoplastic growths could be induced to elaborate factors responsible for abnormal permeability. Whatever the case may be, it is wohwhile to consider potential underlying neoplasia in patients with MCD when atypical features are present such as weight loss, anorexia, lymphadenopathy, haematuria, fever, pleural effusions or skin lesions. Overall, the occurrence of MCD as a complication of neoplastic disorders is quite uncommon. MCD may precede the diagnosis of neoplasia by months or years or may follow the diagnosis of neoplasia by months or years. Some repos have suggested that NK-cell deficiency is associated with the development of MCD in patients with Hodgkin's disease Ref Harrison20th edition pg 299
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