A primer of urinalysis

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Monoclonal antibody identification of infiltrating mononuclear leukocytes in lupus nephritis

Monoclonal antibody identification of infiltrating mononuclear leukocytes in lupus nephritis (LN). Populations of mononuclear inflammatory cells infiltrating the renal interstitium in LN were studied by means of an avidin–biotin immunoperoxidase technique applied to cryostat sections of 26 renal biopsies (3 WHO class IIb; 4 class III; 8 class IV; 4 class V; 4 class III and V; and 3 class IV and V). The majority of interstitial leukocytes were T cells (mean 65.7 ± 14.1). The number of cells reactive with OKT8 (47.3 ± 11.0) exceeded the number of OKT4 positive cells (32.5 ± 11.3) in 22 of 26 biopsies. Cells reactive with antimonocyte antibodies OKM1 and OKM5 (6.7 ± 5.9 and 7.9 ± 5.9, respectively) and B lymphocytes (OKB2 3.9 ± 3.5) were a minor component of the interstitial infiltrates. Monocytes were the predominant cell type among stained cells in glomerular tufts and crescents. Tissue T4/T8 ratios varied widely (range 0.31 to 1.81), and were less than 1 in 22 of 26 patients. There was no correlation between tissue T4/T8 ratios and simultaneous peripheral blood T4/T8 ratios. Using stepwise multivariate linear regression, tissue T4/T8 ratio was found to correlate highly with renal histologic activity (P < 0.001) but was not independently predictive of any other histopathologic or clinical variable studied. Mean tissue T4/T8 ratio in LN was significantly lower than that of other glomerular and interstitial diseases studied (P < 0.001), a finding which may reflect differences in the pathogenesis of renal injury. These findings suggest that local cellular immune mechanisms may be important in the modulation of disease activity in LN

Histological and Clinical Evolution of Lupus Nephritis

In recent years, lupus nephritis has become the major complication and the most pressing problem in patients suffering from lupus erythematosus disseminatus. The clinical course of the disease was different 15 years ago, when Keith (1940) wrote that &quot;renal insufficiency does not play an important role in causing death&quot;. At that time patients usually died of a &quot;lupus crisis &quot; or as a result of concurrent infection. However, the use of anti-biotics, blood transfusions, balanced water and electrolyte therapy, steroid hormone therapy, and injections of corticotropin has, apparently, pro-longed life in those afflicted with systemic lupus erythematosus (S.L.E.). With present methods of care many such patients can usually be kept free of symptoms for a considerable length of time, only to succumb to a rapidly progressive renal failure. Because of the problems raised by the increased incidence of lupus nephritis, a study of the histo-logical evolution of renal involvement in S.L.E. was begun, using serial percutaneous renal biopsies (Kark and Muehrcke, 1954; Muehrcke and others, 1955a). Histological data were correlated with changing clinical status, clinical laboratory data, and renal function tests in a continuing study of the patho-physiology and natural history of lupus nephritis. Preliminary observations have been reported else-where (Pirani and others, 1954; Muehrcke and others, 1955b). This communication outlines some observations on 34 patients studied intensively during the past 18 months