Unnamed 10/26/2011

• Henoch-Schönlein Purpura Nephritis: Pathophysiology, Treatment, and Future Strategy

  • Because acute HSPN episodes are often triggered by an upper respiratory tract infection (11), the removal of any source of chronic bacterial infection should be theoretically beneficial.

• Section IV/CHAPTER 22/Definitions from Comprehensive Clinical Nephrology

  • IgA Nephropathy and Henoch-Schönlein Nephritis
  • CHAPTER 18 – Primary and Secondary (Non-Genetic) Causes of Focal and Segmental Glomerulosclerosis
  • C3 is codeposited in up to 90% of cases
  • Serum IgA levels are increased in one third of patients with IgAN and HSP
  • 40% to 50% of cases, the clinical presentation is episodic macroscopic hematuria, most frequently in the second and third decades of life.
  • HSP is most prevalent in the first decade of life but may occur at any age. A palpable purpuric rash, which may be recurrent, occurs on extensor surfaces
  • C5b-9 is found with properdin but not C4, indicating alternative complement pathway activation.
  • ynpharyngitic hematuria
  • Two distinct patterns of injury are seen in AKI. There may be tubular occlusion by red cells with acute tubular epithelial injury in macrohematuria-associated AKI (Fig. 22.7). Alternatively, glomerular injury may be the cause of AKI with necrotizing GN and cellular crescent formation. Such crescentic IgAN may develop on a histologic background of established chronic renal injury due to IgAN or may be the first presentation of IgAN.
  • There is good evidence that circulating
  • mesangial pIgA1 comes from the mucosal immune system. In IgAN, however, pIgA1 production is downregulated in the mucosa and upregulated in the bone marrow. Moreover, the pIgA response to systemic immunization with common antigens is increased, whereas the response to mucosal immunization is impaired
  • IgA1 in IgAN and HS nephritis has abnormal O-linked hinge-region sugars with reduced galactosylation because of altered IgA production in lymphocytes of patients with IgAN
  • Complement deposits are usually C3 and properdin without C1q and C4.
  • Asymptomatic urine testing identifies 30% to 40% of patients with IgAN in most reported series
  • n a few unwitting experiments, cadaver kidneys with IgA deposits have been transplanted into recipients without IgAN. In all cases, the IgA rapidly disappeared, supporting the concept that abnormalities in IgAN lie in the IgA immune system and not in the kidney.
  • . The renal prognosis is worse in adults than in children. In adults, up to 40% will have CKD or ESRD 15 years after biopsy.
  • IgA antineutrophil cytoplasmic antibodies (IgA-ANCA) have been proposed as a marker of the systemic features that differentiate HSP from IgAN. Circulating IgA-ANCA has been described in HSP, although findings are not consistent. IgA-ANCA is not found in IgAN.

• ScienceDirect - American Journal of Kidney Diseases : Human Cytomegalovirus and Kidney Transplantation: A Clinician's Update

  • Human Cytomegalovirus and Kidney Transplantation: A Clinician's Update
  • detection of viral replication by phosphoprotein 65 antigenemia or CMV DNA polymerase chain reaction

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