Nefropatología Desde 2006
Monitor de la Literatura
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En esta página aparecen artículos relevantes en Patología Renal, Nefrología y afectación renal en enfermedades sistémicas, publicados en los últimos meses.

Aquí aparecerán algunos de los artículos relacionados con estos temas, sin embargo, es imposible abarcarlos todos. Si usted está interesado en literatura actual de un tema específico, le sugerimos consultar otros buscadores (como PubMed)

Sethi S, D'Agati VD, Nast CC, Fogo AB, De Vriese AS, Markowitz GS, Glassock RJ, Fervenza FC, Seshan SV, Rule A, Racusen LC, Radhakrishnan J, Winearls CG, Appel GB, Bajema IM, Chang A, Colvin RB, Cook HT, Hariharan S, Herrera Hernandez LP, Kambham N, Mengel M, Nath KA, Rennke HG, Ronco P, Rovin BH, Haas M. A proposal for standardized grading of chronic changes in native kidney biopsy specimens. Kidney Int. 2017 Apr;91(4):787-789. [PubMed link]
The authors propose a semiquantitative approach to assessing chronic changes, which include glomerulosclerosis, tubular atrophy, interstitial fibrosis, and arteriosclerosis, and report these findings as an overall chronicity grade (from 0 to 11).

Rijnink EC, Teng YK, Kraaij T, Wolterbeek R, Bruijn JA, Bajema IM. Idiopathic non-lupus full-house nephropathy is associated with poor renal outcome. Nephrol Dial Transplant. 2017 Apr 1;32(4):654-662. [PubMed link]
This study include 32 cases of non-lupus full-house nephropathy (FHN). Twenty cases had non-lupus FHN, 4 cases membranous nephropathy (anti-PLA2R-positive  = 1; cancer-associated = 3), 4 cases IgA nephropathy, 2 cases infection-related glomerulonephritis, and 2 cases anti-neutrophil cytoplasmic antibody-associated glomerulonephritis. In patients with class III/IV pattern of injury, idiopathic non-lupus FHN was an independent risk factor for end-stage renal disease.

Seifert ME, Gunasekaran M, Horwedel TA, Daloul R, Storch GA, Mohanakumar T, Brennan DC. Polyomavirus Reactivation and Immune Responses to Kidney-Specific Self-Antigens in Transplantation. J Am Soc Nephrol. 2017 Apr;28(4):1314-1325. [PubMed link]
The authors conclude: "...polyomavirus reactivation may increase the risk for acute rejection through unclear mechanisms".

Champion L, Culine S, Desgranchamps F, Benali K, Verine J, Daugas E. Metastatic Renal Cell Carcinoma in a Renal Allograft: A Sustained Complete Remission After Stimulated Rejection. Am J Transplant. 2017 Apr;17(4):1125-1128. [PubMed link]
The case of a woman who recovered from a diffuse metastatic renal cell carcinoma that developed from a kidney allograft, successfully treated by the induction of tumor rejection. Immunosuppression was discontinued, and transplant nephrectomy was deliberately delayed based on the expectation that the tumor mass would trigger the alloimmune response, which was stimulated with pegylated interferon-α-2a.

Cattran DC, Brenchley PE. Membranous nephropathy: integrating basic science into improved clinical management. Kidney Int. 2017 Mar;91(3):566-574. [PubMed link]
A review.

Ravindran A, Go RS, Fervenza FC, Sethi S. Thrombotic microangiopathy associated with monoclonal gammopathy. Kidney Int. 2017 Mar;91(3):691-698. [PubMed link]
Of 146 patients with TMA, the authors detected monoclonal immunoglobulin in 20 patients (13.7%). This study underscores the importance of evaluating for a monoclonal gammopathy in patients with TMA.

Vignon M, Cohen C, Faguer S, Noel LH, Guilbeau C, Rabant M, Higgins S, Hummel A, Hertig A, Francois H, Lequintrec M, Vilaine E, Knebelmann B, Pourrat J, Chauveau D, Goujon JM, Javaugue V, Touchard G, El Karoui K, Bridoux F. The clinicopathologic characteristics of kidney diseases related to monotypic IgA deposits. Kidney Int. 2017 Mar;91(3):720-728. [PubMed link]
The authors distinguish 2 types of glomerulopathies, α-heavy chain deposition disease (5 patients) and glomerulonephritis with monotypic IgA deposits (14 patients). Similarly to IgG-proliferative glomerulonephritis with monoclonal immunoglobulin deposits, overt hematological malignancy was infrequent, but sensitive serum and bone marrow studies revealed a subtle plasma cell proliferation in most patients with IgA-proliferative glomerulonephritis with monoclonal immunoglobulin deposits.

Goodship TH, Cook HT, Fakhouri F, Fervenza FC, Frémeaux-Bacchi V, Kavanagh D, Nester CM, Noris M, Pickering MC, Rodríguez de Córdoba S, Roumenina LT, Sethi S, Smith RJ. Atypical hemolytic uremic syndrome and C3 glomerulopathy: conclusions from a "Kidney Disease: Improving Global Outcomes" (KDIGO) Controversies Conference. Kidney Int. 2017 Mar;91(3):539-551. [PubMed link]
Areas addressed included renal pathology, clinical phenotype and assessment, genetic drivers of disease, acquired drivers of disease, and treatment strategies.

Luque Y, Louis K, Jouanneau C, Placier S, Esteve E, Bazin D, Rondeau E, Letavernier E, Wolfromm A, Gosset C, Boueilh A, Burbach M, Frère P, Verpont MC, Vandermeersch S, Langui D, Daudon M, Frochot V, Mesnard L. Vancomycin-Associated Cast Nephropathy. J Am Soc Nephrol. 2017 doi: 10.1681/ASN.2016080867. [Epub ahead of print] [PubMed link]
The authors describe obstructive tubular casts composed of noncrystal nanospheric vancomycin aggregates entangled with uromodulin; they developed a immunohistologic staining technique to detect vancomycin in renal tissue.

Shima Y, Nakanishi K, Sato M, Hama T, Mukaiyama H, Togawa H, Tanaka R, Nozu K, Sako M, Iijima K, Suzuki H, Yoshikawa N. IgA nephropathy with presentation of nephrotic syndrome at onset in children. Pediatr Nephrol. 2017 Mar;32(3):457-465. [PubMed link]
Among 426 patients, 30 (7.0 %) had nephrotic syndrome at onset of the IgAN. The authors analyzed and compared with non nephrotic syndrome IgAN.

Loupy A, Haas M, Solez K, Racusen L, Glotz D, Seron D, Nankivell BJ, Colvin RB, Afrouzian M, Akalin E, Alachkar N, Bagnasco S, Becker JU, Cornell L, Drachenberg C, Dragun D, de Kort H, Gibson IW, Kraus ES, Lefaucheur C, Legendre C, Liapis H, Muthukumar T, Nickeleit V, Orandi B, Park W, Rabant M, Randhawa P, Reed EF, Roufosse C, Seshan SV, Sis B, Singh HK, Schinstock C, Tambur A, Zeevi A, Mengel M. The Banff 2015 Kidney Meeting Report: Current Challenges in Rejection Classification and Prospects for Adopting Molecular Pathology. Am J Transplant. 2017 Jan;17(1):28-41. [PubMed Link]
Newly introduced concepts include the i-IFTA score, comprising inflammation within areas of fibrosis and atrophy and acceptance of "chronic allograft arteriopathy" within the descriptions of chronic active T cell-mediated rejection (TCMR) or chronic antibody mediated rejection (ABMR). The pattern of mixed TCMR and ABMR was increasingly recognized.

De Vriese AS, Glassock RJ, Nath KA, Sethi S, Fervenza FC. A Proposal for a Serology-Based Approach to Membranous Nephropathy. J Am Soc Nephrol. 2017 Feb;28(2):421-430. [PubMed link]
The presence or absence of anti-PLA2R and anti-THSD7A antibodies adds important information to clinical and immunopathologic data in discriminating between primary and secondary MN. Levels of anti-PLA2R antibodies and possibly, anti-THSD7A antibodies tightly correlate with disease activity.

Haas M, Verhave JC, Liu ZH, Alpers CE, Barratt J, Becker JU, Cattran D, Cook HT, Coppo R, Feehally J, Pani A, Perkowska-Ptasinska A, Roberts IS, Soares MF, Trimarchi H, Wang S, Yuzawa Y, Zhang H, Troyanov S, Katafuchi R. A Multicenter Study of the Predictive Value of Crescents in IgA Nephropathy. J Am Soc Nephrol. 2017 Feb;28(2):691-701. [PubMed link]
The authors propose "adding the following crescent scores to the Oxford Classification: C0 (no crescents); C1 (crescents in less than one fourth of glomeruli), identifying patients at increased risk of poor outcome without immunosuppression; and C2 (crescents in over one fourth of glomeruli), identifying patients at even greater risk of progression, even with immunosuppression".

Cosio FG, Cattran DC. Recent advances in our understanding of recurrent primary glomerulonephritis after kidney transplantation. Kidney Int. 2017 Feb;91(2):304-314. [PubMed link]
A review.