Clinical and pathological kidney aspects of sickle cell anemia at Dakar: study of 11 cases of renal biopsies

Few studies are devoted to the practice of renal biopsy in sickle cell nephropathy; our objective was to determine the histological and evolutionary patterns of renal lesions in sickle cell patients who underwent renal biopsy in Dakar.Methods:This was a retrospective multicentric study (conducted from December 2009 to August 2011) on renal biopsies performed on sickle cell anaemic patients at the Nephrology Department of Teaching Hospital Aristide Le Dantec and the Albert Royer Childrens Hospital. The histological, therapeutic and evolutionary data were analysed.From the 292 total renal biopsies, 11 (3.80%) were performed on sickle cell patients (6SS, 1SBth + 4 AS) with a mean age of 23.1 [13-51 years]. Nephrotic syndrome was the indication of renal biopsy in all cases. Focal segmental glomerulosclerosis was the most frequent histological finding (five cases), followed by a combination of various specific lesions (hypertrophy of glomerular and peritubular capillaries), minimal glomerular lesions (three cases), membranoproliferative glomerulonephritis (two cases) and extra-membranous glomerulonephritis (one case). Complete remission after treatment was achieved in seven cases and one patient expired. Three patients did not continue with follow-up appointments.Conclusions:Renal biopsy is not very frequent in the course of sickle cell anaemia and in most cases it is performed because of nephrotic syndrome. The histological findings are diverse with a predominance of focal segmental glomerulosclerosis

Analysis of arterial intimal hyperplasia: review and hypothesis

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background: Despite a prodigious investment of funds, we cannot treat or prevent arteriosclerosis and restenosis, particularly its major pathology, arterial intimal hyperplasia. A cornerstone question lies behind all approaches to the disease: what causes the pathology? Hypothesis: I argue that the question itself is misplaced because it implies that intimal hyperplasia is a novel pathological phenomenon caused by new mechanisms. A simple inquiry into arterial morphology shows the opposite is true. The normal multi-layer cellular organization of the tunica intima is identical to that of diseased hyperplasia; it is the standard arterial system design in all placentals at least as large as rabbits, including humans. Formed initially as one-layer endothelium lining, this phenotype can either be maintained or differentiate into a normal multi-layer cellular lining, so striking in its resemblance to diseased hyperplasia that we have to name it "benign intimal hyperplasia". However, normal or "benign " intimal hyperplasia, although microscopically identical to pathology, is a controllable phenotype that rarely compromises blood supply. It is remarkable that each human heart has coronary arteries in which a single-layer endothelium differentiates earl