Arias LF, Taborada-Murillo A. Mesangial proliferative glomerulonephritis: A glomerular disease or a non-specific morphological change? Nephrology (Carlton). 2017 Jul;22(7):575. [PubMed link]
Isolated mesangial proliferation is a frequent and nonspecific change that should prompt a search for better characterized glomerulopathies. When no other morphological, immunopathological or ultrastructural alterations are found, the non-specific and controversial diagnosis of “mesangial proliferative glomerulonephritis” might be considered; however, this descriptive histological term does not aid in determining the aetiology or pathogenesis of a renal disease.
Park E, Ahn YH, Kang HG, Yoo KH, Won NH, Lee KB, Moon KC, Seong MW, Gwon TR, Park SS, Cheong HI. COQ6 Mutations in Children With Steroid-Resistant Focal Segmental Glomerulosclerosis and Sensorineural Hearing Loss. Am J Kidney Dis. 2017 Jul;70(1):139-144. [PubMed link]
In this report of 10 children with SR-FSGS and sensorineural hearing loss, the authors found 6 patients with biallelic COQ6 mutations. Median age at the onset of nephrotic syndrome was 29 months. All patients progressed to end-stage renal disease within a median of 13 months after the onset. Kidney biopsy revealed abnormal mitochondrial proliferation in podocytes in all 6 patients.
Malyszko J, Kozlowska K, Kozlowski L, Malyszko J. Nephrotoxicity of anticancer treatment. Nephrol Dial Transplant. 2017 Jun 1;32(6):924-936. [PubMed link]
Chemotherapeutic agents can affect the glomerulus, tubules, interstitium and renal microvasculature. The most nephrotoxic chemotherapeutic drug is cisplatin, which is often associated with acute kidney injury. A review.
Timmermans SAMEG, Abdul-Hamid MA, Vanderlocht J, Damoiseaux JGMC, Reutelingsperger CP, van Paassen P; Limburg Renal Registry. Patients with hypertension-associated thrombotic microangiopathy may present with complement abnormalities. Kidney Int. 2017 Jun;91(6):1420-1425. [PubMed link]
The authors evaluated the role of complement in nine patients with biopsy-proven renal TMA attributed to severe hypertension. In six out of nine patients, they found mutations C3 in three, CFI in one, CD46 in one, and/or CFH in two patients either with or without the risk CFH-H3 haplotype in four patients.
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 Jun;28(6):1723-1728. [PubMed link]
In renal tissue there is obstructive tubular casts composed of noncrystal nanospheric vancomycin aggregates entangled with uromodulin. The authors developed a new immunohistologic staining technique to detect vancomycin in renal tissue.
Einecke G, Reeve J, Halloran PF. Hyalinosis Lesions in Renal Transplant Biopsies: Time-Dependent Complexity of Interpretation. Am J Transplant. 2017 May;17(5):1346-1357. [PubMed link]
In this study, ah0 was associated with increased risk of T cell-mediated rejection and graft loss, "probably because of underimmunosuppression and nonadherence"; "ah lesions often indicate adequate CNI exposure, not toxicity, and unexpected ah0 should increase vigilance for nonadherence and underimmunosuppression". "The absence of hyalinosis is actually a risk for graft loss, probably reflecting nonadherence". A very interesting article.
Kozakowski N, Eskandary F, Herkner H, Bond G, Oberbauer R, Regele H, Böhmig GA, Kikić Ž. Diffuse Extent of Peritubular Capillaritis in Late Antibody-Mediated Rejection: Associations With Levels of Donor-Specific Antibodies and Chronic Allograft Injury. Transplantation. 2017 May;101(5):e178-e187. [PubMed link]
Diffuse ptc and ptc score of 2 or greater were independently related to cg, however lost their independent relation after adjusting for total microcirculation scores. Diffuse ptc was the only ptc characteristic independently related to chronic lesion score.
Wijkström J, González-Quiroz M, Hernandez M, Trujillo Z, Hultenby K, Ring A, Söderberg M, Aragón A, Elinder CG, Wernerson A. Renal Morphology, Clinical Findings, and Progression Rate in Mesoamerican Nephropathy. Am J Kidney Dis. 2017 May;69(5):626-636. [PubMed link]
Kidney biopsies showed glomerulosclerosis, glomerular hypertrophy, and signs of chronic glomerular ischemia. Mild to moderate tubulointerstitial damage and mostly mild vascular changes were seen.
Maas RJ, Deegens JK, Beukhof JR, Reichert LJ, Ten Dam MA, Beutler JJ, van den Wall Bake AWL, Rensma PL, Konings CJ, Geerse DA, Feith GW, Van Kuijk WH, Wetzels JF. The Clinical Course of Minimal Change Nephrotic Syndrome With Onset in Adulthood or Late Adolescence: A Case Series. Am J Kidney Dis. 2017 May;69(5):637-646. [PubMed link]
"Progression to end-stage renal disease occurred in a few patients and was explained by focal segmental glomerulosclerosis".
Connor TM, Aiello V, Griffith M, Cairns T, Roufosse CA, Cook HT, Pusey CD. The natural history of immunoglobulin M nephropathy in adults. Nephrol Dial Transplant. 2017 May 1;32(5):823-829. [PubMed link]
The authors report 57 cases. Thirty-nine per cent of nephrotic patients achieved complete remission. Focal segmental glomerulosclerosis was diagnosed in 80% of those undergoing repeat renal biopsy, despite ongoing mesangial IgM deposition.
Marinozzi MC, Roumenina LT, Chauvet S, Hertig A, Bertrand D, Olagne J, Frimat M, Ulinski T, Deschênes G, Burtey S, Delahousse M, Moulin B, Legendre C, Frémeaux-Bacchi V, Le Quintrec M. Anti-Factor B and Anti-C3b Autoantibodies in C3 Glomerulopathy and Ig-Associated Membranoproliferative GN. J Am Soc Nephrol. 2017 May;28(5):1603-1613. [PubMed link]
Among 141 patients with C3G and Ig-associated membranoproliferative GN (Ig-MPGN) for anti-FB and anti-C3b autoantibodies using ELISA. The authors identified seven patients with anti-FB IgG, three patients with anti-C3b IgG, and five patients with anti-FB and anti-C3b IgG. Of these 15 patients, ten were diagnosed with Ig-MPGN. In conclusion, the prevalence of anti-C3b/anti-FB Abs and alternative pathway activation is similar in Ig-MPGN and C3G, suggesting similar pathogenic mechanisms. Identification of the underlying defect in Ig-MPGN could lead to improved treatment.
Bierzynska A, Soderquest K, Dean P, Colby E, Rollason R, Jones C, Inward CD, McCarthy HJ, Simpson MA, Lord GM, Williams M, Welsh GI, Koziell AB, Saleem MA; NephroS.; UK study of Nephrotic Syndrome. MAGI2 Mutations Cause Congenital Nephrotic Syndrome. J Am Soc Nephrol. 2017 May;28(5):1614-1621. [PubMed link]
A novel disease-causing mutation. Another more!
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]