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A new revised version of the Banff scheme for allograft kidney rejection has been published (April 2008)

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)

 

Berns JS, Bloom RD. Viral nephropathies: core curriculum 2008. Am J Kidney Dis. 2008 Aug;52(2):370-81. [PubMed link][Free full text]
An usefull article.

Howie AJ, Agarwal A, Sebire NJ, Trompeter RS. Glomerular tip changes in childhood minimal change nephropathy. Pediatr Nephrol. 2008 Aug;23(8):1281-6. [PubMed link]
The authors reviewed 50 consecutive biopsies (49 children) diagnosed as minimal change nephropathy. Four biopsies (4 patients) showed only tip changes. Three patients were in remission. The authors conclude: "This should make little difference in clinical practice, because the clinical course should resemble that of minimal change nephropathy".

Zarkhin V, Li L, Sarwal M. "To B or not to B?" B-cells and graft rejection. Transplantation. 2008 Jun 27;85(12):1705-14. [PubMed link]
In this review, the authors discusse the possible roles of B-cells in graft rejection, whether involved as antigen presenting, as indirect effector, or antibody producing cells.

Haas M, Racusen LC, Bagnasco SM. IgA-dominant postinfectious glomerulonephritis: a report of 13 cases with common ultrastructural features. Hum Pathol. 2008 Jul 10. [Epub ahead of print] [PubMed link]
Each case was characterized by subepithelial humps at various stages of resolution. There were 6 patients who had recent Staphylococcus aureus infections. IgA-dominant postinfectious glomerulonephritis resembles poststreptococcal glomerulonephritis in its histologic spectrum and electron microscopy findings, is often associated with staphylococcal infections, occurs in diabetics and nondiabetics, and may resolve if renal failure at presentation is not severe.

Dunér F, Patrakka J, Xiao Z, Larsson J, Vlamis-Gardikas A, Pettersson E, Tryggvason K, Hultenby K, Wernerson A. Dendrin expression in glomerulogenesis and in human minimal change nephrotic syndrome. Nephrol Dial Transplant. 2008 Aug;23:2504-11. [PubMed link]
Dendrin is an 81-kD cytosolic protein hitherto described in the brain, where it is associated with the actin cytoskeleton, and it was found in foot processes of mouse glomerular podocytes. "The expression of dendrin during glomerulogenesis and in the normal human kidney is similar to that previously shown for nephrin, which suggests that dendrin associates with the slit diaphragm complex. In MCNS patients, dendrin and ZO-1 are re-distributed within the podocytes. Whether this is a cause or a consequence of FPE remains unclear".

Haas M, Rahman MH, Cohn RA, Fathallah-Shaykh S, Ansari A, Bartosh SM. IgA Nephropathy in children and adults: comparison of histologic features and clinical outcomes. Nephrol Dial Transplant. 2008 Aug;23:2537-45. [PubMed link]
"In patients with proliferative IgA nephropathy, the clinical course is more likely to be benign when the disease is diagnosed in childhood versus adulthood. This difference can be accounted for only in part by more advanced disease at the time of biopsy in adults".

Gwinner W, Hinzmann K, Erdbruegger U, Scheffner I, Broecker V, Vaske B, Kreipe H, Haller H, Schwarz A, Mengel M. Acute Tubular Injury in Protocol Biopsies of Renal Grafts: Prevalence, Associated Factors and Effect on Long-Term Function. Am J Transplant. 2008 Jun 12. [Epub ahead of print] [PubMed link]
The authors analyze 612 protocol biopsies and 151 indication biopsies. Acute tubular injury is linked to inferior long-term graft function. While this suggests lack of recovery from ATI with permanent allograft damage, the underlying molecular mechanisms need yet to be uncovered.

Hughson MD, Gobe GC, Hoy WE, Manning RD Jr, Douglas-Denton R, Bertram JF. Associations of Glomerular Number and Birth Weight With Clinicopathological Features of African Americans and Whites. Am J Kidney Dis. 2008 Jul;52(1):18-28. [PubMed link]
This works suggests that the more severe hypertension found in African Americans could not be attributed to racial differences in glomerular number or birth weight.

Cattran DC, Reich HN, Beanlands HJ, Miller JA, Scholey JW, Troyanov S; for the Genes, Gender and Glomerulonephritis Group. The impact of sex in primary glomerulonephritis. Nephrol Dial Transplant. 2008 Jul;23(7):2247-53. [PubMed link]
"Women have a better outcome than men in membranous GN and focal segmental glomerulosclerosis but not in IgA nephropathy".

Hoy WE, Bertram JF, Denton RD, Zimanyi M, Samuel T, Hughson MD. Nephron number, glomerular volume, renal disease and hypertension. Curr Opin Nephrol Hypertens. 2008 May;17(3):258-65. [PubMed link]
The authors discuss studies evaluating associations of glomerular number (Nglom) and glomerular volume with hypertension and kidney disease. They conclude "Higher mean glomerular volume and individual glomerular volume heterogeneity mark glomerular stress. Low Nglom is an important determinant of hypertension and renal disease. Many 'missing' nephrons have probably been lost during life, leaving little trace".

Albaqumi M, Barisoni L. Current Views on Collapsing Glomerulopathy. J Am Soc Nephrol. 2008 Jul;19(7):1276-81. [PubMed link]
Historical background, terminology, morphologic and phenotypic features, and suggested mechanisms are reviewed in this manuscript.

Nasr SH, D'Agati VD, Park HR, Sterman PL, Goyzueta JD, Dressler RM, Hazlett SM, Pursell RN, Caputo C, Markowitz GS. Necrotizing and crescentic lupus nephritis with antineutrophil cytoplasmic antibody seropositivity. Clin J Am Soc Nephrol. 2008 May;3(3):682-90. [PubMed link]
Antineutrophil cytoplasmic antibodies are detected in 20% of patients with systemic lupus erythematosus. The authors report 10 cases of necrotizing and crescentic lupus nephritis with antineutrophil cytoplasmic antibody seropositivity.

Fogazzi GB, Verdesca S, Garigali G. Urinalysis: core curriculum 2008. Am J Kidney Dis. 2008 Jun;51(6):1052-67. [PubMed link][Free full text]
An interesting issue. It is also important for pathologist.

Hinkes BG. NPHS3: new clues for understanding idiopathic nephrotic syndrome. Pediatr Nephrol. 2008 Jun;23(6):847-850. [PubMed link]
The autosomal recessive nephrotic syndrome type 3 (NPHS3) has been recently identified. It is caused by mutations in the phospholipase PLCE1 gene. This nephrotic syndrome shows steroid responsiveness.

Hiramatsu N, Kuroiwa T, Ikeuchi H, Maeshima A, Kaneko Y, Hiromura K, Ueki K, Nojima Y. Revised classification of lupus nephritis is valuable in predicting renal outcome with an indication of the proportion of glomeruli affected by chronic lesions. Rheumatology (Oxford). 2008 May;47(5):702-7. [PubMed link]
This study showed that in Class IV-G cases, renal outcome differed in the presence of chronicity. Chronicity could be a critical factor in predicting outcome.

Tøndel C, Bostad L, Hirth A, Svarstad E. Renal biopsy findings in children and adolescents with Fabry disease and minimal albuminuria. Am J Kidney Dis. 2008 May;51(5):767-76. [PubMed link]
Glomerular and vascular changes are present before progression to overt proteinuria and decreased glomerular filtration rate. Electron microscopy shows lesions in all patients.

Solez K, Colvin RB, Racusen LC, et al. Banff 07 classification of renal allograft pathology: updates and future directions. Am J Transplant. 2008 Apr;8(4):753-60. [PubMed link] A new version of the Banff classification
Major updates from the 2007 Banff Conference were: inclusion of peritubular capillaritis grading, C4d scoring, interpretation of C4d deposition without morphological evidence of active rejection, application of the Banff criteria to zero-time and protocol biopsies and introduction of a new scoring for total interstitial inflammation (ti-score).

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