Podocytes in Glomerular InjuryOf the various cells comprising the glomerulus (endothelial, mesangial, resident macrophages, and visceral glomerular epithelial cells also known as podocytes), the latter are most vulnerable to various forms of glomerular injury (Diabetes, Hypertension, immune-mediated, etc.) that frequently progress to end-stage kidney disease (ESKD).This is due to their non-replicative, terminally differentiated highly specialized nature.Specifically, they exhibit a high rate of vesicular traffic as evidenced by multiple coated vesicles and coated pits along with their basolateral domain and have a high capacity for protein synthesis and posttranslational modifications because of a well-developed endoplasmic reticulum and a large Golgi apparatus [1].Podocyte depletion consequent to injury is a well-established mechanism underlying glomerular scarring (sclerosis) while progressive glomerulosclerosis leads to ESKD [2].It is, therefore, not surprising that strategies assessing ways to protect podocytes against injury are being explored.
Sarcina are gram-positive anaerobic bacteria found to be associated with delayed gastric emptying and gastric outlet obstruction. We describe two cases of Sarcina co-existing with Helicobacter pylori organisms in pediatric siblings presenting within four months of each other with pyloric obstruction secondary to severe gastritis/duodenitis. The co-existence of Sarcina and Helicobacter pylori has not, to our knowledge, been previously reported. Its characteristic tetrad packeted morphology permits Sarcina to be readily identified on routine sections. Detection of these organisms in gastric biopsies should prompt consideration of gastric outlet obstruction and/or delayed gastric emptying as a possible etiologic factor.
