Pediatric KT in children up to 15 kg: A single-center experience.

BACKGROUND: KT is the preferred treatment for ESRD in pediatrics. However, it may be challenging in those weighing ≤15 kg with potential complications that impact on morbidity and graft loss. METHODS: This retrospective review reports our experience in KT in children, weighing ≤15 kg, and the strategies to reduce morbidity and mortality. RESULTS: All patients were on RRT prior to KT. Patients reached ESRD mainly due to urologic malformations (54.54%). LD was performed in 82% of patients. The recipient's median age was 2.83 years, and median weight 12.280 kg. Male sex was predominant (73%). All patients required transfusions of PRBCs. There was a high requirement for ventilated support in patients post-KT with no relation to weight, amount of resuscitation used intra-operatively or ml/kg of PRBCs. One patient presented with stenosis of the native renal artery. No patients presented DGF, graft thrombosis, or surgical complications. No association was found between cold ischemia and eGFR at 1 year (p = .12). In univariate analysis, eGFR at 1 year is related to AR. eGFR at 3 years is related to the number of UTI. Median follow-up was 1363 days. Patient and graft survival were 100%. CONCLUSIONS: KT in children ≤15 kg can be challenging and requires a meticulous perioperative management and surgical expertise. Patient and graft survival are excellent with low rate of complications.

Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS).

Hemolytic uremic syndrome (HUS) is defined as a triad of noninmune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. The most frequent presentation is secondary to Shiga toxin (Stx)-producing Escherichia coli (STEC) infections, which is termed postdiarrheal, epidemiologic or Stx-HUS, considering that Stx is the necessary etiological factor. After ingestion, STEC colonize the intestine and produce Stx, which translocates across the intestinal epithelium. Once Stx enters the bloodstream, it interacts with renal endothelial and epithelial cells, and leukocytes. This review summarizes the current evidence about the involvement of inflammatory components as central pathogenic factors that could determine outcome of STEC infections. Intestinal inflammation may favor epithelial leakage and subsequent passage of Stx to the systemic circulation. Vascular damage triggered by Stx promotes not only release of thrombin and increased fibrin concentration but also production of cytokines and chemokines by endothelial cells. Recent evidence from animal models and patients strongly indicate that several immune cells types may participate in HUS physiopathology: neutrophils, through release of proteases and reactive oxygen species (ROS); monocytes/macrophages through secretion of cytokines and chemokines. In addition, high levels of Bb factor and soluble C5b-9 (sC5b-9) in plasma as well as complement factors adhered to platelet-leukocyte complexes, microparticles and microvesicles, suggest activation of the alternative pathway of complement. Thus, acute immune response secondary to STEC infection, the Stx stimulatory effect on different immune cells, and inflammatory stimulus secondary to endothelial damage all together converge to define a strong inflammatory status that worsens Stx toxicity and disease.