Recurrent HIV-associated immune complex glomerulonephritis with lupus-like features after kidney transplantation.

A spectrum of kidney diseases besides classic human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) exists in HIV-infected patients. Immune complex-mediated glomerulonephritis has emerged as a significant contributor to the burden of kidney disease in this population, particularly in patients of non-African descent. Lupus-like nephritis, a form of immune complex glomerulonephritis with histologic features identical to lupus nephritis in the absence of clinical or serologic markers of lupus, is well recognized as a cause of end-stage renal disease in HIV-infected patients. None of the HIV-associated kidney lesions, whether classic HIVAN or non-HIVAN, has been reported to recur in kidney transplants. We report here for the first time clinical and histologic recurrence of HIV-associated lupus-like nephritis after successful kidney transplantation, causing proteinuria, hematuria, and impaired kidney transplant function.

Erythema elevatum diutinum with unusual clinical appearance.

Erythema elevatum diutinum is a rare chronic inflammatory skin disease of unknown etiology with a histopathology of a leukocytoclastic vasculitis. Clinical findings involve symmetrical livid-erythematous to red-brown papules and plaques or nodules which are initially soft but become firmer. The skin lesions are located over extensor surfaces and often over joints. Early treatment with dapsone, corticosteroids and antibiotics is sometimes effective. A patient with multiple myeloma displayed unusual lesions of erythema elevatum diutinum.

[Immune complexes in suppurative surgical infection]. / Immunnye kompleksy pri gnoinoi khirurgicheskoi infektsii.

The authors examined 56 patients with various forms of purulent surgical infection. The number of T- and B-lymphocytes and the level of immunoglobulins, complement, and immune complexes was determined. It was established that the level of circulating immune complexes reflects the clinical situation most authentically. Five- or six-fold increase in immune complexes is a constant sign of a persisting and severe inflammatory process marked by the predominance of destructive changes and tendency to generalization.

[Circulating immune complexes in chronic thrombocytopenic purpura in adults before and after splenectomy]. / Krazace kompleksy immunologiczne w przewleklej maloplytkowosci samoistnej doroslych przed i po splenektomii.

Circulating immune complexes (cic) were determined by means of the immunoenzymatic method in a group of 16 adults with immune thrombocytopenic purpura (ITP) before and after splenectomy. The recurrence of immune thrombocytopenic purpura after splenectomy was observed in 9 patients, in 6 out of them there co-existed non-specific inflammatory process and cic were present in the serum. In 7 patients in whom the number of thrombocytes after splenectomy was normal, no circulating immune complexes were found. A significant decrease in the medium level of IgM after splenectomy should be attributed rather to splenectomy than to the consuming of IgM in the formation of circulating complexes. The role of circulating complexes in the pathogenesis of ITP in adults still remains not fully solved, but the authors' experience suggests that non-specific inflammatory processes may lead to their appearance.

The dense deposits disease of the renal basement membranes.

Dense-deposits disease is characterized by an original morphological aspect of the renal basement membranes which have an electron-dense appearance. The immunofluorescence studies showed C3 alone in kidney. Low serum C3 levels and the presence of C3 NF activity have been detected in this disease, demonstrating an activation of the complement alternative pathway. The observation of recurrence in transplanted kidneys contributed to establish the sequence of the morphological events and showed the dissociation between the serological complement profiles and the lesions. Although the nature of the dense deposits remains still unknown, the altered membranes are recognized by at least some anti-GBM antibodies.