Kidney failure is common in patients with Coronavirus Disease-19 (COVID-19) resulting in increased morbidity and mortality. In an international collaboration, 284 kidney biopsies were evaluated to improve understanding of kidney disease in COVID-19. Diagnoses were compared to five years of 63,575 native biopsies prior to the pandemic and 13,955 allograft biopsies to identify diseases increased in patients with COVID-19. Genotyping for APOL1 G1 and G2 alleles was performed in 107 African American and Hispanic patients. Immunohistochemistry for SARS-CoV-2 was utilized to assess direct viral infection in 273 cases along with clinical information at the time of biopsy. The leading indication for native biopsy was acute kidney injury (45.4%), followed by proteinuria with or without concurrent acute kidney injury (42.6%). There were more African American patients (44.6%) than patients of other ethnicities. The most common diagnosis in native biopsies was collapsing glomerulopathy (25.8%) which associated with high-risk APOL1 genotypes in 91.7% of cases. Compared to the five-year biopsy database, the frequency of myoglobin cast nephropathy and proliferative glomerulonephritis with monoclonal IgG deposits was also increased in patients with COVID-19 (3.3% and 1.7%, respectively), while there was a reduced frequency of chronic conditions (including diabetes mellitus, IgA nephropathy, and arterionephrosclerosis) as the primary diagnosis. In transplants, the leading indication was acute kidney injury (86.4%), for which rejection was the predominant diagnosis (61.4%). Direct SARS-CoV-2 viral infection was not identified. Thus, our multi-center large case series identified kidney diseases that disproportionately affect patients with COVID-19, demonstrated a high frequency of APOL1 high-risk genotypes within this group, with no evidence of direct viral infection within the kidney.
The majority of cases of primary membranous nephropathy (MN) are associated with auto-antibodies against the podocyte antigen M-type phospholipase A2 receptor (PLA2R). This particular subset of MN can be diagnosed by identifying anti-PLA2R within patient sera or by detecting PLA2R antigen within glomerular immune complexes in renal biopsy tissue. Since the discovery of anti-PLA2R in 2009, there has been an abundance of literature regarding PLA2R testing as a tool in the diagnosis and management of MN, and these tests are increasingly being implemented in clinical practice. However, questions still remain about a variety of issues such as PLA2R testing in the setting of presumably secondary MN and the significance of PLA2R negative primary MN. The goal of this review is to summarize the current PLA2R testing methods and highlight special features of anti- PLA2R-associated MN.
BackgroundBone marrow transplant-associated thrombotic microangiopathy (TA-TMA) is a relatively frequent but under-recognized and under-treated hematopoietic stem cell transplant (HSCT) complication that leads to significant post-transplant morbidity and mortality. Classic TMA-defining laboratory abnormalities appear at different times in the course of TA-TMA development, with schistocytes often appearing later in the disease course. In some severe TMA cases, schistocytes may be absent due to increased endothelial permeability. Unfortunately, many clinicians continue to perceive the presence of schistocytes as an absolute requirement for TA-TMA diagnosis, which leads to delayed recognition and treatment of this potentially fatal transplant complication.MethodsPatient chart review and PubMed literature search using the term, “transplant-associated thrombotic microangiopathy”.Case presentationA 54-year-old male IgG kappa multiple myeloma underwent a reduced intensity allogeneic HSCT from a 9/10 HLA-matched unrelated donor after conditioning with fludarabine and melphalan. On day + 27, the patient developed acute kidney injury followed by repeated episodes of diarrhea and gastrointestinal bleeding attributed to graft versus host disease (GVHD) and cytomegalovirus (CMV) colitis. Repeated colonic biopsies suggested CMV infection and GVHD. Despite appropriate treatment with antiviral therapy and immunosuppressants, the patient’s condition continued to deteriorate. He experienced concomitant anemia and thrombocytopenia as well as elevated lactate dehydrogenase and low haptoglobin levels, but a TA-TMA diagnosis was not made due to an absence of schistocytes on peripheral smear. The patient expired secondary to uncontrolled gastrointestinal bleeding. A post-mortem analysis of the resection specimen revealed extensive TMA involving numerous arteries and arterioles in the ileal and colonic submucosa as well as in the muscularis propria and deep lamina propria of the mucosa.ConclusionsTA-TMA can occur in the absence of peripheral blood schistocytes. Our experience underscores the importance of considering the diagnosis of intestinal TA-TMA in patients with refractory post-transplant diarrhea and GI bleeding, even if all classic features are not present.
Highlights Fabry is an X-linked lysosomal storage disease with deficiency in α-galactosidase. This deficiency results in the accumulation of glycosphinogolipids. Diagnosis is often made by analysis of globotriaosylceramide in fluids and tissues. Fabry is often misdiagnosed in female patients due to residual enzyme activity. Lipidomics by LC-HRMS enables identification of new biomarkers in Fabry.
Once thought to be limited mainly to lesions involving deposition of monoclonal paraproteins, glomerular diseases associated with hematologic neoplasms now include forms in which manifestations are probably mediated through cytokines or chemokines. Said et al. studied one such lesion, myeloproliferative neoplasm-related glomerulopathy, and found it to be a late complication of these neoplasms, with a generally poor renal outcome. Whether earlier recognition of glomerular diseases associated with hematopoietic neoplasms can result in more effective treatment remains an important question.
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