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Fellowing Joel – Episode 14

Visitors, and journal clubs, and lectures! Oh, my! Dr. Murphy breaks down what's been happening in this week's Fellowing Joel episode.  [video width="1920" height="1080" mp4=""][/video]      

Dr. Jai Radhakrishnan Visit

We're so excited to have Dr. Jai Radhakrishnan of Columbia University visiting this week! He joined the Arkana Journal Club last night and gave a lecture on lupus nephritis this morning.

Fellowing Joel – Episode 13

We caught up with Dr. Murphy as he was getting a tour of the Arkana Fish Lab in this week's Fellowing Joel episode. [video width="1920" height="1080" mp4=""][/video]    

Arkana Employee Spotlight: Daniel

Meet Daniel McPherson. Daniel joined our client development team in 2012, and he has become not only a valuable asset to our practice but also an all-around great person to know.  His colleagues describe him as incredibly caring, creative, curious and inquisitive, helpful, and annoyingly chipper in the mornings.  The staff at Arkana frequently see Daniel moving heavy things around the office. This is primarily because he has a servant's heart and is always willing to help, but his background as a certified strength and conditioning coach doesn't hurt either. That certification has allowed him to greatly influence and impact...

Fellowing Joel – Episode 12

We caught up with Dr. Murphy this week to see what's been happening in his world. [video width="1920" height="1080" mp4=""][/video]    

Twitter Poll (December 11, 2019)

Answer: D Anti-GBM disease presents with rapidly progressive glomerulonephritis (GN) with or without pulmonary hemorrhage. On biopsy typical disease displays bright polytypic linear GBM staining for IgG by immunofluorescence and diffuse crescentic/necrotizing GN on light microscopy. Anti-glomerular basement membrane (GBM) nephritis is clinically and pathologically one of the most aggressive form of glomerulonephritis. Patients typically present with nephritic syndrome and rapidly progressive acute kidney injury. Lung involvement in the form of alveolar hemorrhage occurs in 34% to 62% of patients. Anti-GBM disease is due to circulating autoantibodies directed against cryptic epitopes in the NC1 domain of the alpha-3 chain of...

Art of Medicine: Proliferative Glomerulonephritis

The above painting shows endocapillary hypercellularity with mononuclear cells and neutrophils, as well as hyaline deposits within glomeruli.  Red blood cell casts are seen within focal tubular lumens, and the tubules are widely spaced due to interstitial edema and inflammation.  These findings can be seen within acute proliferative glomerulonephritis.  Other proliferative changes within glomeruli seen in acute proliferative glomerulonephritis include mesangial hypercellularity and crescent formation. The differential diagnosis for proliferative glomerulonephritis is broad and includes infection-associated glomerulonephritis including post-streptococcal glomerulonephritis, focal or diffuse lupus nephritis, shunt nephritis, cryoglobulinemic glomerulonephritis, hepatitis-associated glomerulonephritis, and IgA nephropathy (or Henoch-Schonlein purpura nephritis).   Other considerations...

Disease Week: Alport Syndrome

Alport syndrome (AS) is a heterogeneous genetic disorder caused by mutations in the α-chain (3, 4 or 5) of the collagen IV genes. Collagen IV is a major component of basement membranes and comprises six genetically distinct α-chains: α1(IV) through α6(IV). Human collagen IV genes are arranged in three pairs with head-to-head orientation: COL4A1 and COL4A2 (chromosome 13), COL4A3 and COL4A4 (chromosome 2) and COL4A5 and COL4A6 (X-chromosome). Each α-chain contains three domains: a short 7S N-terminal domain, a midsection collagenous domain and a C-terminal noncollagenous domain (NC1). α-chains form heterotrimeric molecules called promoters. While 56 theoretical combinations exist, only...