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434 results on '"D'Agati, V."'

68. The MEST score provides earlier risk prediction in lgA nephropathy

Author

Barbour, Sean J., Espino-Hernandez, Gabriela, Reich, Heather N., Coppo, Rosanna, Roberts, Ian S.D., Feehally, John, Herzenberg, Andrew M., Cattran, Daniel C., Bavbek, N., Cook, T., Troyanov, S., Alpers, C., Amore, A., Barratt, J., Berthoux, F., Bonsib, S., Bruijn, J., D’Agati, V., D’Amico, G., Emancipator, S., Emmal, F., Ferrario, F., Fervenza, F., Florquin, S., Fogo, A., Geddes, C., Groene, H., Haas, M., Hill, P., Hogg, R., Hsu, S., Hunley, T., Hladunewich, M., Jennette, C., Joh, K., Julian, B., Kawamura, T., Lai, F., Leung, C., Li, L., Li, P., Liu, Z., Massat, A., Mackinnon, B., Mezzano, S., Schena, F., Tomino, Y., Walker, P., Wang, H., Weening, J., Yoshikawa, N., Zhang, H., Coppo, R., Troyanov, S., Cattran, D.C., Cook, H.T., Feehally, J., Roberts, I., Tesar, V., Maixnerova, D., Lundberg, S., Gesualdo, L., Emma, F., Fuiano, L., Beltrame, G., Rollino, C., RC, Amore, A., Camilla, R., Peruzzi, L., Praga, M., Feriozzi, S., Polci, R., Segoloni, G., Colla, L., Pani, A., Angioi, A., Piras, L., JF, Cancarini, G., Ravera, S., Durlik, M., Moggia, E., Ballarin, J., Di Giulio, S., Pugliese, F., Serriello, I., Caliskan, Y., Sever, M., Kilicaslan, I., Locatelli, F., Del Vecchio, L., Wetzels, J.F.M., Peters, H., Berg, U., Carvalho, F., da Costa Ferreira, A.C., Maggio, M., Wiecek, A., Ots-Rosenberg, M., Magistroni, R., Topaloglu, R., Bilginer, Y., D’Amico, M., Stangou, M., Giacchino, F., Goumenos, D., Kalliakmani, P., Gerolymos, M., Galesic, K., Geddes, C., Siamopoulos, K., Balafa, O., Galliani, M., Stratta, P., Quaglia, M., Bergia, R., Cravero, R., Salvadori, M., Cirami, L., Fellstrom, B., Kloster Smerud, H., Ferrario, F., Stellato, T., Egido, J., Martin, C., Floege, J., Eitner, F., Lupo, A., Bernich, P., Menè, P., Morosetti, M., van Kooten, C., Rabelink, T., Reinders, M.E.J., Boria Grinyo, J.M., Cusinato, S., Benozzi, L., Savoldi, S., Licata, C., Mizerska-Wasiak, M., Martina, G., Messuerotti, A., Dal Canton, A., Esposito, C., Migotto, C., Triolo, G., Mariano, F., Pozzi, C., Boero, R., Bellur, S., Mazzucco, G., Giannakakis, C., Honsova, E., Sundelin, B., Di Palma, A.M., Ferrario, F., Gutiérrez, E., Asunis, A.M., Barratt, J., Tardanico, R., Perkowska-Ptasinska, A., Arce Terroba, J., Fortunato, M., Pantzaki, A., Ozluk, Y., Steenbergen, E., Soderberg, M., Riispere, Z., Furci, L., Orhan, D., Kipgen, D., Casartelli, D., Galesic Ljubanovic, D., Gakiopoulou, H., Bertoni, E., Cannata Ortiz, P., Karkoszka, H., Groene, H.J., Stoppacciaro, A., Bajema, I., Bruijn, J., Fulladosa Oliveras, X., Maldyk, J., and Ioachim, E.

Abstract

The Oxford Classification of IgA nephropathy (IgAN) includes the following four histologic components: mesangial (M) and endocapillary (E) hypercellularity, segmental sclerosis (S) and interstitial fibrosis/tubular atrophy (T). These combine to form the MEST score and are independently associated with renal outcome. Current prediction and risk stratification in IgAN requires clinical data over 2 years of follow-up. Using modern prediction tools, we examined whether combining MEST with cross-sectional clinical data at biopsy provides earlier risk prediction in IgAN than current best methods that use 2 years of follow-up data. We used a cohort of 901 adults with IgAN from the Oxford derivation and North American validation studies and the VALIGA study followed for a median of 5.6 years to analyze the primary outcome (50% decrease in eGFR or ESRD) using Cox regression models. Covariates of clinical data at biopsy (eGFR, proteinuria, MAP) with or without MEST, and then 2-year clinical data alone (2-year average of proteinuria/MAP, eGFR at biopsy) were considered. There was significant improvement in prediction by adding MEST to clinical data at biopsy. The combination predicted the outcome as well as the 2-year clinical data alone, with comparable calibration curves. This effect did not change in subgroups treated or not with RAS blockade or immunosuppression. Thus, combining the MEST score with cross-sectional clinical data at biopsy provides earlier risk prediction in IgAN than our current best methods.

Published
2016
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76. Podocyte injury in focal segmental glomerulosclerosis: Lessons from animal models (a play in five acts).

Author

D'Agati, V. D.

Subjects
*RECOMBINANT proteins, *HIV infections, *ANIMAL models in research, *KIDNEY diseases, *GENETIC engineering, *GENETIC recombination, *VIRUS diseases
Abstract

Genetic engineering in the mouse has ushered in a new era of disease modeling that has advanced our understanding of podocyte injury in the pathogenesis of focal segmental glomerulosclerosis. Historically, the major animal models of focal segmental glomerulosclerosis involve direct podocyte injury (exemplified by toxin models) and indirect podocyte injury due to adaptive responses (exemplified by renal ablation models). In both paradigms, recent evidence indicates that podocyte depletion is a major pathomechanism mediating proteinuria and glomerulosclerosis. Podocyte-specific toxin models support that podocyte loss is sufficient to cause focal segmental glomerulosclerosis in a dose-dependent manner. Knockout and transgenic models have provided proof of concept that mutations in specific podocyte proteins mediate genetic forms of focal segmental glomerulosclerosis. Transgenic models of HIV-associated nephropathy have helped to elucidate the role of direct viral infection and podocyte expression of viral gene products in the pathogenesis of this form of collapsing glomerulopathy. Taken together, emerging data support that injury directed to or inherent within the podocyte constitutes the critical event in diverse pathways to glomerulosclerosis.Kidney International (2008) 73, 399–406; doi:10.1038/sj.ki.5002655; published online 7 November 2007 [ABSTRACT FROM AUTHOR]

Published
2008
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83. Differential activities of the RET tyrosine kinase receptor isoforms during mammalian embryogenesis.

Author

de Graaff, E, Srinivas, S, Kilkenny, C, D'Agati, V, Mankoo, B S, Costantini, F, and Pachnis, V

Abstract

The RET receptor tyrosine kinase has a critical role in kidney organogenesis and the development of the enteric nervous system. Two major isoforms, RET9 and RET51, differ in the amino acid sequence of the C-terminal tail as a result of alternative splicing. To determine the roles of these isoforms in vivo, we used targeted mutagenesis to generate mice that express either RET9 or RET51. Monoisoformic RET9 mice, which lack RET51, are viable and appear normal. In contrast, monoisoformic RET51 animals, which lack RET9, have kidney hypodysplasia and lack enteric ganglia from the colon. To study the differential activities of the two RET isoforms further, we generated transgenic mice expressing ligand-dependent and constitutively active forms of RET9 or RET51 under the control of the Hoxb7 regulatory sequences. Such RET9 transgenes are capable of rescuing the kidney agenesis in RET-deficient mice or causing kidney hypodysplasia in wild-type animals. In contrast, similar RET51 transgenes fail to rescue the kidney agenesis or cause hypodysplasia. Our findings show that RET9 and RET51 have different signaling properties in vivo and define specific temporal and spatial requirements of c-Ret function during renal development and histogenesis of the enteric nervous system.

Published
2001
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84. HepatitisBAssociated Glomerulonephritis

Author

VENKATASESHAN, V. S., LIEBERMAN, K., KIM, D. U., THUNG, S. N., DIKMAN, S., D'AGATI, V., SUSIN, M., VALDERRAMA, E., GAUTHIER, B., PRAKASH, A., and CHURG, J.

Published
1990

86. Glycation and diabetes: The RAGE connection

Author

Hudson, B. I., Hofmann, M. A., Bucciarelli, L., Wendt, T., Bernhard Moser, Lu, Y., Qu, W., Stern, D. M., D Agati, V., Yan, S. D., Yan, S. F., Grant, P. J., and Schmidt, A. M.

94. Supersized kidneys: Lessons from the preclinical obese kidney.

Author

D'Agati, V. D. and Markowitz, G. S.

Subjects
*BODY weight, *OBESITY, *KIDNEY diseases, *URINARY organs
Abstract

The worldwide prevalence of obesity continues to rise. Obesity has been shown to increase the risk of both the development and the progression of renal failure, even after correction for other comorbid conditions. The ability of nephrologists to intervene will require greater understanding of obesity's renal physiologic effects. Kidney biopsies and functional studies performed on morbidly obese patients without overt renal disease who presented for bariatric surgery have helped to elucidate the earliest obesity-related structural and functional responses.Kidney International (2008) 73, 909–910. doi:10.1038/ki.2008.42 [ABSTRACT FROM AUTHOR]

Published
2008
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99. A young man with Propionibacterium acnes-induced shunt nephritis.

Author

Kiryluk, K., Preddie, D., D'Agati, V. D., and Isom, R.

Subjects
*GLOMERULONEPHRITIS, *KIDNEY diseases, *CHRONIC kidney failure, *PROTEINURIA, *CLINICAL trials
Abstract

The article presents a case study of a 23-year-old man recommended for a second opinion regarding chronic glomerulonephritis. He had a history of a rectal pilocytic astrocytoma which was diagnosed in 1992. In 1999, he developed mild renal insufficiency with nephrotic-range proteinuria and mirohematuria. On physical examination, he was afebrile with a pulse of 68 bpm and a blood pressure of 130/82mm Hg. A repeat kidney biopsy was performed.

Published
2008
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100. Infantile nephropathic cystinosis.

Author

Stokes, M. B., Jernigan, S., and D'Agati, V. D.

Subjects
*CYSTINOSIS, *INFANT diseases, *FEVER, *DEHYDRATION in infants, *RENAL tubular transport disorders
Abstract

The article discusses the case of a Caucasian girl with infantile nephropathic cystinosis who was delivered after a full-term uneventful pregnancy. She had no history of fevers, dehydration, or photophobia and there was no family history of renal or other medical disease. The patient was treated for the next

Published
2008
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