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APOL1: Why Is It Important?

I have been working at Arkana Laboratories (formerly Nephropath) for close to seven years as the Molecular Diagnostics Laboratory Supervisor. One of my first projects here was to isolate DNA from formalin-fixed, paraffin-embedded tissue and get an assay set up to determine variants in the APOL1 gene. At that time, these variants were recently discovered and there was great excitement in the scientific community as to their role in kidney disease, especially in African Americans, which is the population with the highest frequency of these gene variants in America. Our project involved the role of these variants in collapsing glomerulopathy...

Art of Medicine: Minimal Change Disease

The above painting shows podocytes with foot processes extending along the glomerular basement membrane of neighboring capillary loops.  Effacement of podocyte foot processes occurs in primary podocytopathies, including minimal change disease (see electron photomicrograph below). Minimal change disease is the most common etiology of idiopathic nephrotic syndrome in children and is the third most common cause in adults, after focal segmental glomerulosclerosis and membranous glomerulopathy.  A majority of cases are “primary”, require no additional workup, and are due to a circulating permeability factor.   Several possible secondary causes have also been identified.  Although these are rare, these should be considered in...

Disease Week: C3 Glomerulonephritis

C3 glomerulonephritis is a recently described entity which is due to dysregulation in the alternative complement pathway. Patients typically present with hematuria and/or proteinuria in the face of persistently low serum levels of C3. The annual incidence of biopsy-proven disease is 1 to 2 per million with both sexes affected equally. The median age of diagnosis is 21 years of age, but there is a second spike after the age of 50 due to paraprotein-associated disease. The most common glomerular disease pattern is a membranoproliferative pattern. The hallmark of the disease is dominant C3 staining on immunofluorescence which is defined...

Here Comes Another Bride

There must be something in the Spring air.  A second bride-to-be on our transcription team was showered with gifts today!  Best wishes to Hillary and her groom!     

Dr. Wael Abukwaik Visit

We were thrilled to have Dr. Abukwaik visit us this week.  He is currently a PGY-3 Nephrology Fellow at Children's Hospital of Michigan.  We hope he takes some extra knowledge of kidney disease back with him!       

Membranous Nephropathy After Transplantation

The biopsy shows a recurrent membranous nephropathy within a transplant. Figure 1 shows "spikes" and "holes." Figure 2 shows mild interstitial fibrosis. Figures 3, 4, 5, and 6 shows IgG, kappa, lambda, and PLA2r, respectively. Figure 7 shows subepithelial and intramembranous deposits. Membranous nephropathy can arise in the graft from recurrence of the original disease, a de novo disease, and rarely as a donor-derived disease. Recurrence of the original disease can be seen as early as one week post transplant. Most cases of recurrent membranous nephropathy occur within the first few months following transplantation, whereas de novo membranous nephropathy usually...

Art of Medicine: Lysozyme Nephropathy

The painting above shows acute tubular injury with numerous intracytoplasmic inclusions within proximal tubular epithelium, which can be seen in lysozyme-associated nephropathy.  Lysozyme-induced nephropathy is a rare cause of acute tubular injury seen in patients with hematologic malignancies, most commonly with chronic myelomonocytic leukemia (CMML) and acute monocytic leukemia (Santoriello et al, 2017).   Malignancy associated overproduction of lysozyme can lead to acute kidney injury and proteinuria.  Lysozyme is freely filtered by the glomerulus and reabsorbed by the proximal tubular epithelium.  While this happens at a low level physiologically, over-reabsorption of lysozyme induces toxic acute tubular injury. Lysozyme-induced nephropathy is one...

Crescentic IgA nephropathy

The patient is a 17-year-old white female who presents with 2.85 grams/24 hr proteinuria, microscopic hematuria, and a creatinine of 3.2 mg/dl. She was in her normal state of health and was incidentally found to have abnormal lab values and urinalysis at a routine sport's physical. She reports that she had noticed a little more fatigue the last few months, but had blamed this on being busy at her job after school. Figure 1 shows focal fibrinoid necrosis. Figure 2 shows moderate tubular atrophy and interstitial fibrosis. Figures 3 & 4 show a segmental cellular crescent. Figure 5 shows several...

Diagnose This (April 22, 2019)

What is this finding and what diagnoses does it imply?       ​ ​   ​   ​ ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​   ​ ​   ​ ​   ​ ​   ​ ​    ...