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Archive: Twitter Poll

Twitter Poll: October 30, 2019

ANSWER: D ADPKD is genetically heterogeneous with two major genes, PKD1 and PKD2 (~90% families), and a rare third locus, GANAB lately discovered. Less than 10% of ADPKD families are negative for these genes. More recently, DNAJB11 has been identified in those patients from ADPKD-negative pedigrees. For the blog: ADPKD is the most common inherited kidney disorder. Two genes PKD1 and PKD2, coding for membrane proteins involved in the primary cilium, account for more than 90% of typical cases of ADPKD. A third gene, GANAB coding for the α-subunit of the endoplasmic reticulum-resident enzyme glucosidase II, has been associated with...

Twitter Poll (September 26, 2019)

ANSWER: C APOL1-risk alleles have been reported only on African-derived chromosomes, including individuals from West Africa and recently admixed individuals from the United States or the Caribbean. Approximately 13% of the US African American population carries the APOL1 high-risk genotype. Recent data suggest that this risk is strongly associated with two common variants (G1 and G2) in the last exon of APOL1 that confer resistance to Trypanosoma brucei infections. The highest G1 and G2 allelic frequencies were described in Western, sub-Saharan Africa, with frequencies >40% for G1 in Ghana and Nigeria, and 24% for G2 in Nigeria. REFERENCES: Parsa A, Kao WHL, Xie D,...

Twitter Poll (September 12, 2019)

ANSWER: B In a case series by Boils et al. which included 49 patients with GN due to IE, the most common biopsy finding was necrotizing and crescentic GN which was found in 53% of the cases. This was followed by endocapillary proliferative GN in 37% of the biopsies. Reference: Boils CL, et al. Update on endocarditis-associated glomerulonephritis. Kidney Int. 2015; 87(6):1241-1249.  

Twitter Poll (August 28, 2019)

ANSWER: A Dr. Albert Hewett Coons was an American physician, pathologist, and immunologist who conceptualized and developed the immunofluorescence technique for labeling antibodies in the early 1940s. Renal pathologists acquired this technique for the assessment of medical kidney biopsies, and since then it has become the gold standard on routine evaluation. References: Coons, AH, et al. The demonstration of pneumococcal antigen in tissues by the use of fluorescent antibody. J Immunol 1942; 45: 159-170. Coons, AH. The beginnings of immunofluorescence. J Immunol 1961; 97: 499-503.        

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.