Atypical Presentation of Novel Coronavirus Disease 2019 in a Peritoneal Dialysis Patient.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a rapidly spreading disease causing increased morbidity and mortality across the globe. There is limited available knowledge regarding the natural history of the SARS-CoV-2 infection. Other factors that are also making this infection spread like a pandemic include global travelers, lack of proven treatment, asymptomatic carriers, potential reinfection, underprepared global health care systems, and lack of public awareness and efforts to prevent further spread. It is understood that certain preexisting medical conditions increase the risk of mortality with COVID-19; however, the outcome of this disease in traditionally vulnerable chronic illnesses such as end-stage renal disease is not well documented. We present a case of a 56-year-old African American lady with end-stage renal disease on the peritoneal dialysis who presented predominantly with nausea, vomiting, and subsequently found to have COVID-19. We use this case to illustrate an atypical presentation of the COVID-19 in a vulnerable patient and discuss the literature.

Hydralazine-associated antineutrophil cytoplasmic antibody vasculitis with pulmonary-renal syndrome.

Hydralazine, a vasodilator, is commonly used as an adjunctive treatment for moderate to severe hypertension, heart failure and hypertensive emergencies in pregnancy. Hydralazine-induced lupus was first described in 1953. Clinical presentation ranges from arthralgia, myalgia, petechiae, or rash to single or multiorgan involvement. An occurrence of systemic vasculitis is a rare complication. When presented as the pulmonary-renal syndrome, it could have a rapidly progressive course which can be fatal. Here, we describe a case of hydralazine-associated rapidly progressive glomerulonephritis and pulmonary haemorrhage. We use this case to review the current literature and discuss and highlight the importance of a high degree of clinical acumen, early diagnosis and prompt treatment for better clinical outcomes.

Differential responsiveness of early- and late-passage endothelial cells to shear stress.

BACKGROUND: The incidence of vascular disease increases with age. Because atherosclerosis and neointimal hyperplasia colocalize in areas of disturbed shear stress, the effects of orbital shear stress (SS) on endothelial cell proliferation, protein kinase B (Akt) activation, and functional activity were analyzed using a senescence model. METHODS: Early- (p3 to 7) and late- (p28 to 32) passage bovine aortic endothelial cells were exposed to orbital SS (210 rpm) or static conditions (0 to 5 days). Cell proliferation was directly counted and confirmed with proliferating cell nuclear antigen reactivity. Phosphorylated and total Akt were assessed with Western blotting. Endothelial cell-induced smooth muscle cell migration was assessed with a Boyden chamber. RESULTS: Late-passage endothelial cells demonstrated no increase in orbital SS stimulated proliferation compared with early-passage cells (P = .42). Late-passage endothelial cells demonstrated decreased Akt phosphorylation in response to SS compared with early passage cells (n = 6, P = .01). Late-passage cells induced 26% less smooth muscle cell migration than early-passage cells (n = 3, P = .03). CONCLUSIONS: Late-passage endothelial cells demonstrate decreased proliferation, Akt phosphorylation, and secretion of smooth muscle cell chemoattractants in response to orbital SS compared with early passage cells. These results suggest that late-passage endothelial cells respond to SS differently than early-passage cells and confirm the utility of the in vitro senescence model.