FERNANDA FLORENCIA FREGNAN ZAMBOM

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LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina

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  • article 30 Citação(ões) na Scopus
    NF-kappa B System Is Chronically Activated and Promotes Glomerular Injury in Experimental Type 1 Diabetic Kidney Disease
    (2020) FORESTO-NETO, Orestes; ALBINO, Amanda Helen; ARIAS, Simone Costa Alarcon; FAUSTINO, Viviane Dias; ZAMBOM, Fernanda Florencia Fregnan; CENEDEZE, Marcos Antonio; ELIAS, Rosilene Motta; MALHEIROS, Denise Maria Avancini Costa; CAMARA, Niels Olsen Saraiva; FUJIHARA, Clarice Kazue; ZATZ, Roberto
    High glucose concentration can activate TLR4 and NF-kappa B, triggering the production of proinflammatory mediators. We investigated whether the NF-kappa B pathway is involved in the pathogenesis and progression of experimental diabetic kidney disease (DKD) in a model of long-term type 1 diabetes mellitus (DM). Adult male Munich-Wistar rats underwent DM by a single streptozotocin injection, and were kept moderately hyperglycemic by daily insulin injections. After 12 months, two subgroups - progressors and non-progressors - could be formed based on the degree of glomerulosclerosis. Only progressors exhibited renal TLR4, NF-kappa B and IL-6 activation. This scenario was already present in rats with short-term DM (2 months), at a time when no overt glomerulosclerosis can be detected. Chronic treatment with the NF-kappa B inhibitor, pyrrolidine dithiocarbamate (PDTC), prevented activation of renal TLR4, NF-kappa B or IL-6, without interfering with blood glucose. PDTC prevented the development of glomerular injury/inflammation and oxidative stress in DM rats. In addition, the NF-kappa B p65 component was detected in sclerotic glomeruli and inflamed interstitial areas in biopsy material from patients with type 1 DM. These observations indicate that the renal NF-kappa B pathway plays a key role in the development and progression of experimental DKD, and can become an important therapeutic target in the quest to prevent the progression of human DKD.
  • article 2 Citação(ões) na Scopus
    NF-kappa B blockade during short-term L-NAME and salt overload strongly attenuates the late development of chronic kidney disease
    (2020) OLIVEIRA, Karin Carneiro; ZAMBOM, Fernanda Florencia Fregnan; ALBINO, Amanda Helen; ARIAS, Simone Costa Alarcon; AVILA, Victor Ferreira; FAUSTINO, Viviane Dias; MALHEIROS, Denise Maria Avancini Costa; CAMARA, Niels Olsen Saraiva; FUJIHARA, Clarice Kazue; ZATZ, Roberto
    Nitric oxide synthase inhibition by N-omega-nitro-L-arginine methyl ester (L-NAME) plus a high-salt diet (HS) is a model of chronic kidney disease (CKD) characterized by marked hypertension and renal injury. With cessation of treatment, most of these changes subside, but progressive renal injury develops, associated with persistent low-grade renal inflammation. We investigated whether innate immunity. and in particular the NF-kappa B system, is involved in this process. Male Munich-Wistar rats received HS + L-NAME (32 mg.kg(-1).day(-1)), whereas control rats received HS only. Treatment was ceased after week 4 when 30 rats were studied. Additional rats were studied at week 8 (n = 30) and week 28 (n = 30). As expected, HS + L-NAME promoted severe hypertension, albuminuria, and renal injury after 4 wk of treatment, whereas innate immunity activation was evident. After discontinuation of treatments, partial regression of renal injury and inflammation occurred, along with persistence of innate immunity activation at week 8. At week 28, glomerular injury worsened, while renal inflammation persisted and renal innate immunity remained activated. Temporary administration of the NF-kappa B inhibitor pyrrolidine dithiocarbamate, in concomitancy with the early 4-wk HS + L-NAME treatment, prevented the development of late renal injury and inflammation, an effect that lasted until the end of the study. Early activation of innate immunity may be crucial to the initiation of renal injury in the HS + L-NAME model and to the autonomous progression of chronic nephropathy even after cessation of the original insult. This behavior may be common to other conditions leading to CKD.