Nephropathology Since 2006
Literature Monitor
Up to date
Versión en Español


Articles about kidney pathology, nephrology, and renal affectation in systemic diseases, published in the last months.

Here there are some articles, but if you are interested in a specific issue, please search in a more complete site (as PubMed)


Bajema IM, Wilhelmus S, Alpers CE, Bruijn JA, Colvin RB, Cook HT, D'Agati VD, Ferrario F, Haas M, Jennette JC, Joh K, Nast CC, Noël LH, Rijnink EC, Roberts ISD, Seshan SV, Sethi S, Fogo AB. 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 Feb 16. [Epub ahead of print] [PubMed link]
The authors report detailed recommendations on issues for which they propose adjustments based on existing evidence and current consensus opinion.

Ponticelli C, Locatelli F. Corticosteroids in IgA Nephropathy. Am J Kidney Dis. 2018 Feb;71(2):160-162 [PubMed link]
The authors believe that patients with eGFRs > 30 mL/min/1.73 m2 and proteinuria with protein excretion > 1 g/d merit treatment with corticosteroids. To reduce the risk for side effects, they prefer to use the protocol based on pulse methylprednisolone and alternate-day prednisone.

Huerta A, Arjona E, Portoles J, Lopez-Sanchez P, Rabasco C, Espinosa M, Cavero T, Blasco M, Cao M, Manrique J, Cabello-Chavez V, Suñer M, Heras M, Fulladosa X, Belmar L, Sempere A, Peralta C, Castillo L, Arnau A, Praga M, Rodriguez de Cordoba S. A retrospective study of pregnancy-associated atypical hemolytic uremic syndrome. Kidney Int. 2017 Feb;93(2);450-459. [PubMed link]
Cases included: 22. Identification of inherited complement abnormalities explained nine of the cases. In thirteen of the cases, pregnancy complications were sufficient to trigger a thrombotic microangiopathy in the absence of genetic or acquired complement alterations. Ten patients received eculizumab with an excellent renal response in all, independent of carrying or not inherited complement abnormalities.

Furuichi K, Yuzawa Y, Shimizu M, Hara A, Toyama T, Kitamura H, Suzuki Y, Sato H, Uesugi N, Ubara Y, Hisano S, Ueda Y, Nishi S, Yokoyama H, Nishino T, Kohagura K, Ogawa D, Mise K, Shibagaki Y, Kimura K, Haneda M, Makino H, Matsuo S, Wada T. Nationwide multicentre kidney biopsy study of Japanese patients with type 2 diabetes. Nephrol Dial Transplant. 2018 Jan;33(1):138-148. [PubMed link]
This study of 600 cases with type 2 diabetes revealed that pathologic findings (presence of nodular lesions, exudative lesions and mesangiolysis) were strong predictors of kidney events in low-risk patients.

Rijnink EC, Teng YKO, Kraaij T, Dekkers OM, Bruijn JA, Bajema IM. Validation of the Systemic Lupus International Collaborating Clinics classification criteria in a cohort of patients with full house glomerular deposits. Kidney Int. 2018 Jan;93(1):214-220. [PubMed link]
Compared with the American College of Rheumatology classification, the SLICC classification had better sensitivity (100 vs. 94%); although, this was at the expense of specificity (91 vs. 100%). Application of this stand-alone renal criterion resulted in mistaken classification of SLE in some cases with antinuclear antibody.

Stokes MB, D'Agati VD. Full-house glomerular deposits: beware the sheep in wolf's clothing. Kidney Int. 2018 Jan;93(1):18-20. [PubMed link]
A comment on the previos paper.

Lusco MA, Fogo AB, Najafian B, Alpers CE. AJKD Atlas of Renal Pathology: Adenovirus Infection. Am J Kidney Dis. 2018 Jan;71(1):e1-e2. [PubMed link]
With a mini-review.

Dasari S, Alexander MP, Vrana JA, Theis JD, Mills JR, Negron V, Sethi S, Dispenzieri A, Highsmith WE Jr, Nasr SH, Kurtin PJ. DnaJ Heat Shock Protein Family B Member 9 Is a Novel Biomarker for Fibrillary GN. J Am Soc Nephrol. 2018 Jan;29(1):51-56. [PubMed link]
The authors propose that DNAJB9 is a strong biomarker for rapid diagnosis of FGN in renal biopsy specimens.

Andeen NK, Yang HY, Dai DF, MacCoss MJ, Smith KD. DnaJ Homolog Subfamily B Member 9 Is a Putative Autoantigen in Fibrillary GN. J Am Soc Nephrol. 2018 Jan;29(1):231-239. [PubMed link]
In this work, the results identify DNAJB9 as a putative autoantigen in fibrillary GN and suggest IgG1 and classic complement effector pathways as likely mediators of the destructive glomerular injury in this disease.