Autological platelet-rich fibrin sealant for anterior horseshoe anal fistula in female patient: A video vignette.

INTRODUCTION: Nowadays many techniques have been developed for the treatment of complex anorectal fistulas. Biological substances are used for minimally invasive treatment of anorectal fistulas, especially for complex anal fistulas. Insertion of autological fibrin substance into the fistula tract is one of the types of such procedures. CLINICAL CASE: Here, we present a case of insertion of platelet-rich fibrin sealant into a horseshoe fistula in a female patient. The follow-up period was 10 months with no signs of clinical or MRI recurrence.

Negative Regulation of TGFß Signaling by Stem Cell Antigen-1 Protects against Ischemic Acute Kidney Injury.

Acute kidney injury, often caused by an ischemic insult, is associated with significant short-term morbidity and mortality, and increased risk of chronic kidney disease. The factors affecting the renal response to injury following ischemia and reperfusion remain to be clarified. We found that the Stem cell antigen-1 (Sca-1), commonly used as a stem cell marker, is heavily expressed in renal tubules of the adult mouse kidney. We evaluated its potential role in the kidney using Sca-1 knockout mice submitted to acute ischemia reperfusion injury (IRI), as well as cultured renal proximal tubular cells in which Sca-1 was stably silenced with shRNA. IRI induced more severe injury in Sca-1 null kidneys, as assessed by increased expression of Kim-1 and Ngal, rise in serum creatinine, abnormal pathology, and increased apoptosis of tubular epithelium, and persistent significant renal injury at day 7 post IRI, when recovery of renal function in control animals was nearly complete. Serum creatinine, Kim-1 and Ngal were slightly but significantly elevated even in uninjured Sca-1-/- kidneys. Sca-1 constitutively bound both TGFß receptors I and II in cultured normal proximal tubular epithelial cells. Its genetic loss or silencing lead to constitutive TGFß receptor-mediated activation of canonical Smad signaling even in the absence of ligand and to KIM-1 expression in the silenced cells. These studies demonstrate that by normally repressing TGFß-mediated canonical Smad signaling, Sca-1 plays an important in renal epithelial cell homeostasis and in recovery of renal function following ischemic acute kidney injury.