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Archive: October 2018

Infection-Associated Glomerulonephritis

This biopsy is taken from a 39-year-old woman who presents with abdominal pain, ascites, and lower extremity edema. Her serum creatinine is 3.9 mg/dL and her complete blood count shows leukocytosis (14,500). Initial serologic workup is negative. The biopsy shows a diffuse proliferative glomerulonephritis characterized by global endocapillary hypercellularity with prominent neutrophils, best visualized using methenamine silver staining (Fig. 1). No crescents, necrotizing lesions, or significant double contours are identified. By immunofluorescence, there is coarsely granular (3+) capillary wall and less prominent mesangial staining for IgG, C3, kappa, and lambda (Fig. 2). Electron microscopy shows global endocapillary proliferation and numerous...

Diagnose This (October 29, 2018)

What class of disease does this patient have and how did they present clinically?           ​   ​ ​   ​   ​ ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​ ​   ​ ​...

All in a day’s work

Less than a week until American Society of Nephrology's #kidneywk! This year we are asking what "All in a day's work" means to you.   ​   ​ ​   ​   ​ ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​...

How “omnioma” virus became “polyoma” virus…

The arrow points to an intranuclear viral inclusion characteristic of BK virus, one species of non-enveloped dsDNA viruses belonging to the polyoma virus family.  Sarah Stewart (see inset), a physician and research scientist, studied viral oncogenesis (she was the first woman to earn an M.D. degree from Georgetown Medical School).  Dr. Stewart and her collaborator, Dr. Bernice Eddy (Ph.D. virologist), renamed the parotid tumor virus originally discovered by Ludwik Gross “SE polyoma virus” (the “SE” was for “Stewart-Eddy”).  Interestingly, Dr. Stewart like the name “omnioma” virus, but Eddy suggested the term “polyoma” virus since not all viral infections caused tumors...

Cystinosis

Cystinosis is an autosomal recessive lysosomal storage disease caused by CTNS gene mutations.  The normal product of the CTNS gene is cystinosin, a transport protein that moves the amino acid cystine out of the lysosome.  CTNS gene mutations (more than 80 have been described thus far) result in the accumulation of cystine within lysosomes.  Cystine crystals, which accumulate in various tissues such as the kidney and eye, can be detected using polarization or electron microscopy (Fig. 1).  In the kidney, multinucleated podocytes (Fig. 2-3) and increased numbers of atubular glomeruli (not shown) may be identified by routine light microscopy.  In...

Lunch & Learn

We always love it when our Journey2Health team comes to town for a visit. Dr. Lawson is pictured reminding us to eat real food! 

Polyomavirus Nephropathy in Native Kidney

Polyomavirus nephropathy (PVN), predominantly caused by BK virus reactivation in the urogenital tract, is an important complication of renal allografts (reference 1). While it rarely affects the native kidney, it may be seen in the setting of chronic immunosuppression, including bone marrow transplantation, HIV infection, chemotherapy and in the setting of other solid organ transplants (reference 2). The case shown is from a 69-year-old female with a history of sarcoidosis and cirrhosis who is now 5 years post liver transplant. The patient is currently being evaluated for a progressive increase in serum creatinine. The biopsy shows significant, non-specific tubulointerstitial scarring...