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

Posted from Diigo. The rest of my favorite links are here.

Technology in (Medical) Education: A 50 dollar Smart Board?

Technology in (Medical) Education: A 50 dollar Smart Board?: "While reading a recent article in Edutopia ' Why integrate technology into the curriculum? The reasons are many. ' I found a post by Chris w..."

Targeted inhibition of complement activation prevents features of preeclampsia in mice

Targeted inhibition of complement activation prevents features of preeclampsia in mice: "

Targeted inhibition of complement activation prevents features of preeclampsia in mice

Kidney International 79,
331 (February (1) 2011). doi:10.1038/ki.2010.393

Authors: Xiaoping Qing, Patricia B Redecha, Melissa A Burmeister, Stephen Tomlinson, Vivette D D'Agati, Robin L Davisson
& Jane E Salmon

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Angiotensin II: breathtaking in the renal medulla

Angiotensin II: breathtaking in the renal medulla: "

Angiotensin II: breathtaking in the renal medulla

Kidney International 79,
269 (February (1) 2011). doi:10.1038/ki.2010.434

Author: Volker H Haase

"

Serum Iron Markers Are Inadequate for Guiding Iron Repletion in Chronic Kidney Disease

Serum Iron Markers Are Inadequate for Guiding Iron Repletion in Chronic Kidney Disease: "Background and objectives

Iron (Fe) overload may complicate parenteral Fe therapy used to enhance the efficacy of erythropoietic-stimulating agents in the treatment of anemia of chronic kidney disease. However, serum Fe markers are influenced by inflammation or malignancy and may not accurately reflect the amount of body Fe.

Design, setting, participants, & measurements

We studied the relationship between parenteral Fe therapy, conventional serum Fe markers, and liver iron concentration (LIC) measured using magnetic resonance R2 relaxometry (FerriScan) in 25 Fe-deficient predialysis chronic kidney disease patients before and 2 and 12 weeks after single high-dose intravenous Fe and in 15 chronic hemodialysis patients with elevated serum ferritin (>500 µg/L).

Results

In predialysis patients, there was strong dose dependency between the administered Fe dose and changes in LIC at weeks 2 and 12; however, no dose dependency between Fe dose and changes in ferritin or transferrin saturation (TSAT) were observed. In hemodialysis patients, LIC correlated with the cumulative Fe dose and duration of dialysis but not with current ferritin or TSAT. The cumulative Fe dose remained a significant independent predictor of LIC in a multiple regression model. Two dialysis patients who received >6 g parenteral Fe had substantially elevated LIC >130 µmol/g, which is associated with hemochromatosis.

Conclusions

In Fe-deficient predialysis patients, intravenous Fe therapy is associated with increases in LIC unrelated to changes in conventional Fe markers. In hemodialysis patients, TSAT and ferritin are poor indicators of body Fe load, and some patients have LICs similar to those found in hemochromatosis.

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Beyond genetics: epigenetic code in chronic kidney disease

Beyond genetics: epigenetic code in chronic kidney disease: "

Beyond genetics: epigenetic code in chronic kidney disease

Kidney International 79,
23 (January (1) 2011). doi:10.1038/ki.2010.335

Authors: Rama S Dwivedi, James G Herman, Timothy A McCaffrey
& Dominic S C Raj

The best succinct review of epigenetics

Theory of gastric CO(2) ventilation and its control during respiratory acidosis: implications for central chemosensitivity, pH regulation, and diseases causing chronic CO(2) retention Gastric CO(2) ventilation during respiratory acidosis.

Theory of gastric CO(2) ventilation and its control during respiratory acidosis: implications for central chemosensitivity, pH regulation, and diseases causing chronic CO(2) retention Gastric CO(2) ventilation during respiratory acidosis.: "

Theory of gastric CO(2) ventilation and its control during respiratory acidosis: implications for central chemosensitivity, pH regulation, and diseases causing chronic CO(2) retention Gastric CO(2) ventilation during respiratory acidosis.

Respir Physiol Neurobiol. 2010 Dec 6;

Authors: Dean JB

The theory of gastric CO(2) ventilation describes a previously unrecognized reflex mechanism controlled by neurons in the caudal solitary complex (cSC) for non-alveolar elimination of systemic CO(2) during respiratory acidosis. Neurons in the cSC, which is a site of CO(2) chemosensitivity for cardiorespiratory control, also control various gastroesophageal reflexes that remove CO(2) from blood. CO(2) is consumed in the production of gastric acid and bicarbonate in the gastric epithelium and then reconstituted as CO(2) in the stomach lumen from the reaction between H(+) and HCO(3)(-). Respiratory acidosis and gastric CO(2) distension induce cSC/vagovagal mediated transient relaxations of the lower esophageal sphincter to vent gastric CO(2) upwards by bulk flow along an abdominal-to-esophageal (= intrapleural) pressure gradient the magnitude of which increases during abdominal (gastric) compression caused by increased contractions of respiratory muscles. Esophageal distension induces cSC/nucleus ambiguus/vagovagal reflex relaxation of the upper esophageal sphincter and CO(2) is vented into the pharynx and mixed with pulmonary gas during expiration or, alternatively, during eructation. It is proposed that gastric CO(2) ventilation provides explanations for 1) the postprandial increase in expired CO(2) and 2) the negative P(blood-expired)(CO)difference that occurs during increased metabolic CO(2) production. Furthermore, it is postulated that gastric CO(2) ventilation and alveolar CO(2) ventilation are coordinated under dual control by CO(2) chemosensitive neurons in the cSC. This new theory, therefore, presupposes a level of neural control and coordination between two previously presumed dissimilar organ systems and supports the notion that different sites of CO(2) chemosensitivity address different aspects of whole body pH regulation. Consequently, not all sites of central chemosensitivity are equal regarding the mechanism(s) activated for CO(2) elimination. A distributed CO(2) chemosensitive network-at least nine different areas in the CNS, including the cSC, have been reported to date-may reflect the complexity and dynamic nature of the fundamental neural circuitry required to achieve CO(2)/pH regulation across multiple organ systems under various states of arousal, oxygenation, pH status, and redox state. Moreover, coordination of respiratory and digestive control networks through the cSC could also account for the frequent co-expression of pulmonary diseases that cause chronic respiratory acidosis (and overstimulation of cSC neurons) with peptic ulcer disease or gastroesophageal reflux disease.

PMID: 21144912 [PubMed - as supplied by publisher]

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