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KDIGO Connections: Membranous Glomerulopathy

Welcome to the first post in our new series KDIGO Connections, a series in which we are asking our nephrologist colleagues to educate us in real-world experiences treating kidney disease. In this series, Dr. David Bourne will be kicking it off with KDIGO guidelines for a kidney disease in visual abstract form. Our hope is that these posts will foster discussion regarding these diseases and how different providers approach them. Please share any points, pearls, questions, caveats, thoughts, or experience you have on the presented disease letting us all learn from your experience!  

A tale of two cores…

Core “A” and “B” were taken from the same patient during the same biopsy procedure. The red blood cells within the tubules in core “B” represent a biopsy artifact sometimes seen when multiple passes are made during the same biopsy procedure. One confirmatory clue is the presence of red blood cells surrounding the periphery of core “B” – these are not present in core “A” which was likely the first core taken during the biopsy.    

Where is the normal kidney tissue?

This kidney biopsy shows the histologic features characteristic of malakoplakia, which includes a dense, often obliterative, inflammatory infiltrate rich in histiocytes (Fig. 1 and 2) with numerous small intracytoplasmic concretions known as Michaelis-Gutmann bodies (these are best identified using histochemical staining for calcium as in Fig. 3). Malakoplakia is thought to result from chronic bacterial infection of the urinary tract (the most common causative organism is E. coli). Many cases are associated with the formation of small plaques and/or mass lesions. The bladder is the most common site of involvement, but kidney involvement occurs in about 15% of cases. The...

Arteriole Transition

The image captures the transition of an arteriole as it loses its internal elastic lamina (black arrow).  Note that the smaller arteriole branch, while lacking this elastic layer, still retains smooth muscle cells (red arrow).  The elastic tissue adds structural integrity to arterial and larger arteriolar walls during pulsatile distension from higher intravascular pressure, and the retained muscular layer in small arterioles helps provide an important component of the pre-capillary sphincter mechanism, whereby regulation of blood flow to capillary beds occurs.    

IgA nephropathy with something extra…

The biopsy is from a 61-year-old man with a history of intermittent microscopic hematuria for many years who presents with recent 18-pound weight loss and nephrotic syndrome.  His creatinine is mildly elevated at 1.3 mg/dL.  He has 12.5 g of proteinuria and his serum albumin is 2.6 mg/dL.  The biopsy shows diffuse mild mesangial matrix expansion with no necrosis or proliferative lesions (Fig. 1).  Immunofluorescence microscopy shows extensive granular mesangial IgA deposits (3+) (Fig. 2), compatible with IgA nephropathy.  Interestingly, the Jones methenamine silver stain also shows argyrophilic spikes involving capillary loops, which are most suggestive of spicular amyloid deposits...

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...

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...

A source of myoglobinuria…

The image shows a frozen cross section of skeletal muscle from a patient with rhabdomyolysis, which included the full clinical syndrome of muscle pain, weakness, dark urine, and markedly elevated serum creatine kinase.  The image shows three necrotic fibers engulfed by macrophages (arrow).  So what causes such muscle injury?  The broad differential diagnosis includes trauma, drugs (e.g. statins, alcohol, heroin, cocaine), toxins (e.g. metabolic poisons, animal venom), inflammatory myopathy, immune-mediated necrotizing myopathy (e.g. anti-HMG CoA reductase associated myopathy), infection (e.g. EBV, influenza), paraneoplastic myopathy, and metabolic myopathy (e.g. disorders of glycolysis, lipid metabolism, mitochondria).

Fungus Microabscess

Cortical microabscess formation is a clue to the presence of an infectious organism.  Various bacteria, viruses, fungi, and even parasites may cause similar appearing lesions.  This biopsy is taken from a renal transplant patient with acute kidney injury and microscopic hematuria.  The low-power image shows a densely mixed cellular infiltrate involving the tubulointerstitium (Fig. 1).  Higher magnification shows tubulitis with intratubular leukocytes and rare structures suspicious for fungal elements (Fig. 2).  Gomori methenamine silver staining confirms the presence of budding yeast forms (Fig. 3 arrow) with hyphae and pseudohyphae.  Fungal isolates from urine culture showed colony morphology characteristics consistent with...