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Archive: Twitter Poll

Twitter Poll (August 7, 2019)

ANSWER: D The most common finding on kidney biopsies in patients with immune checkpoint inhibitors (ICPIs)–induced AKI is acute tubulointerstitial nephritis. Less frequently, granulomatous interstitial nephritis and TMA have also been reported. The two main ICPIs are anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and anti-programmed cell death protein 1 (PD-1). The onset of kidney injury seen with PD-1 inhibitors is usually late (3-10 months) compared to CTLA-4 antagonists-related renal injury, which happens earlier (2-3 months). PD-1 inhibitors, as opposed to CTLA-4 inhibitors, have been associated with kidney rejection in transplantation. Steroids appear to be effective in treating the immune-related adverse effects...

Twitter Poll (July 24, 2019)

ANSWER: B Decoy cells are epithelial cells containing intranuclear viral inclusions in urine. They are not specific for polyomavirus nephritis, but when present they may indicate polyoma infection of urinary tract. Decoy cells are easily identified in routine Papanicolaou stained urine cytology specimens, and can be identified in unstained sediment by phase-contrast microscopy. In Papanicolaou stained cytology smears, Decoy cells are comet-shaped with large basophilic, amorphous, homogeneous, ground-glass like intranuclear inclusion bodies and a condensed rim of chromatin. REFERENCE: Singh HK, Bubendorf L, Mihatsch MJ, Drachenberg CB, Nickeleit V. (2006) Urine Cytology Findings of Polyomavirus Infections. In: Ahsan N. (eds)...

Twitter Poll (July 10, 2019)

Answer: True About 5-10% of the patients with monoclonal gammopathy and findings consistent with C3GN by standard IF (on frozen tissue) will actually have a Membranoproliferative GN with masked monoclonal deposits. These patients require additional IF studies to be performed on protease-digested, paraffin-embedded tissue for identification of the monoclonal immunoglobulin in the deposits. References: Leung N, et al. The evaluation of monoclonal gammopathy of renal significance: a consensus report of the International Kidney and Monoclonal Gammopathy Research Group. Nat Rev Nephrol 2019; 15(1): 45-59. Larsen CP, et al. Membranoproliferative glomerulonephritis with masked monotypic immunoglobulin deposits. Kidney Int 2015; 88(4): 867-873....

Twitter Poll (June 26, 2019)

ANSWER: C Severe intimal arteritis (v2), with or without interstitial inflammation and/or tubulitis is considered acute TCMR Grade IIB based on the Banff 2017 classification. However, we now know that arterial lesions (v>0) may be indicative of ABMR, TCMR or mixed ABMR/TCMR and are not restricted to TCMR. Reference: Haas M, et al. The Banff 2017 Kidney Meeting Report: Revised diagnostic criteria for chronic active T-cell mediated rejection, antibody-mediated rejection, and prospects for integrative endpoints for next-generation clinical trials. Am J Transplant. 2018; 1-15.    

Twitter Poll (June 13, 2019)

ANSWER: D The use of anticoagulant therapy (warfarin, dabigatran, rivaroxaban, among others) can result in AKI by causing glomerular hemorrhage and renal tubular obstruction by RBC casts. This may be a serious potential complication especially in older patients with underlying chronic kidney injury. References: Glassock RJ. Anticoagulant-Related Nephropathy It's the Real McCoy. CJASN 14:935-937, 2019. Brodsky S, Eikelboom J, Hebert LA. Anticouagulant-Related Nephropathy. J Am Soc Nephrol 29:2787-2793, 2018. Brodsky S, Satoskar A, et al. Acute Kidney Injury During Warfarin Therapy Associated with Obstructive Tubular Red blood Cell Casts: A Report of Nine Cases.  Am J Kidney Dis 54(6):1121-6, 2009....

Twitter Poll (May 22, 2019)

ANSWER: C By the Oxford Classification of IgA nephropathy, the findings present are classified as "M1 E1 S1 T1 C0" (where M=Mesangial hypercellularity; E=Endocapillary proliferation; S=Segmental sclerosis; T=Tubular atrophy & interstitial fibrosis; C=Cellular/fibrocellular crescents). REFERENCE: Trimarchi H, et al. Oxford Classification of IgA Nephropathy 2016: an update from the IgA Nephropathy Classification Working Group. Kidney Int 2017; 91(5):1014-21.    

Twitter Poll (April 17, 2019)

ANSWER: D Collapsing glomerulopathy has been associated with certain infectious disease including HIV, Hepatitis C, HTLV-1, parvovirus B19, cytomegalovirus, tuberculosis, Campylobacter enteritis, and Loa loa filariasis. References: Cossey LN, Larsen CP, Liapis H. Collapsing glomerulopathy: a 30-year perspective and single, large center experience. Clin Kidney J 2017; 10(4):443-449 Cohen AH, Nast CC. HIV-associated nephropathy. A unique combined glomerular, tubular, and interstitial lesion. Mod Pathol 1988; 1: 87–97 D’Agati V, Suh JI, Carbone L, et al. Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study. Kidney Int 1989; 35: 1358–1370 Pakasa NM, Nseka NM, Nyimi LM. Secondary collapsing glomerulopathy associated...

Twitter Poll (April 3, 2019)

ANSWER: C IgAN is the most frequent diagnosis seen in kidney biopsies from patients with renal failure and history of IBD. In a retrospective study performed by Ambruzs et al., the prevalence of IgAN was 24%, followed by TIN (19%), arterionephrosclerosis, ATI, proliferative GN and MCD. Reference: Ambruzs JM, et al. The histopathologic spectrum of kidney biopsies in patients with inflammatory bowel disease. 2014 Clin J Am Soc Nephrol; 9(2):265-270.

Twitter Poll (March 7, 2019)

ANSWER: True The presence of multiple exostoses due to mutation of the EXT1 gene has been described in a family. There are few isolated reports of extrarenal involvement in patients with type III collagen glomerulopathy, suggesting that the renal lesion may be part of systemic disease in some patients.  References: Cohen AH. Collagen Type III Glomerulopathies. Adv Chronic Kidney Dis. 2012;19(2):101-6. Roberts IS, Gleadle JM. Familial nephropathy and multiple exostoses with exostosin-1 (EXT1) gene mutation. J Am Soc Nephrol. 2008;19:450-453    

Twitter Poll (February 27, 2019)

Answer: B "Endocapillary hypercellularity" is the new term recommended to be used instead of "endocapillary proliferation". This is a more accurate term as an increase in cellularity can be the result of inflammatory influx and does not necessarily requires proliferation. Reference: Bajema IM, et al. Revision of the International Society of Nephrology/Renal Pathology Society classification for lupus nephritis: clarification of definitions, and modified National Institutes of Health activity and chronicity indices. Kidney Int. 2018;93:789-796.