Bisalbuminemia is a rare electrophoretic abnormality of the albumin fraction, characterized by a doubling of this fraction on the electrophoretic trace of serum proteins, reflecting the presence in the same individual of normal plasma albumin and structurally altered albumin, which may be of acquired etiology, rarely hereditary. The aim of this article is to study the etiologies and prevalence of bisalbuminemias associated with nephropathies discovered on serum protein electrophoresis at the biochemistry laboratory of the university hospital Ibn Rochd in Casablanca. This is a retrospective study of serum protein electrophoretic capillary tracings revealing bisalbuminemia in patients hospitalized in the nephrology department at university hospital Ibn Rochd in Casablanca over an 18-month period. 29 electrophoretic profiles out of 242 showed bisalbuminemia, i.e. 12% of all electrophoretic tracings in 29 patients presenting with acute or chronic nephropathy. The average age was 45±22 years, with a sex ratio (M/F) of 2.22. The etiologies of the nephropathies were dominated by renal amyloidosis with 24.14%, followed by minimal glomerular lesion nephropathies, extramembranous glomerulonephritis and lupus nephropathies with 17.24% each, and finally membranoproliferative glomerulonephritis with 6.9%. Among secondary etiologies, betalactam use was highlighted in 13.8% of cases, no patient in the series had a labelled pancreatopathy, and the presence of a monoclonal gammapathy was objectified in only one case in the series. This study illustrates the varied etiologies of bisalbuminemia associated with nephropathy, requiring detailed knowledge to enable proper interpretation of electrophoretic profiles.

We report two cases of patients with COVID-19. Clinical and biological features of the two patients confirm severe form of COVID-19 associated with cytokine storm. High levels of IL-6 and IL-17 were found. Unfortunately the patients died because of the multi-organ failure secondary to the cytokine storm. Cytokine storm is a systemic inflammatory syndrome which leads to aberrant release of cytokines. IL-6 is the most frequently reported cytokine to be increased in COVID-19 patients. Naïve T CD4+ cells in the presence of TGF β and IL-6 will differentiate into T helper 17 cells responsible for secreting IL-17A and IL-17F, which target macrophages, dendritic cells, endothelial cells, and fibroblasts to increase the production of cytokines. IL-6 and IL-17 have been shown to play a role in increasing risk of airway disease. They synergistically promote viral persistence by protecting virus-infected cells from apoptosis. Immune hyperactivation in cytokine storm amplified levels of cytokines that will have systemic effects and cause collateral damage to vital organ systems. Immunotherapy can play a crucial role in COVID-19 managing. Tocilizumab an anti-IL6 receptor antibody was used with clinical improvement. The possibility of inhibiting IL17 as therapy for COVID-19 should be also considered.