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Transplant Surgery
Published in Tjun Tang, Elizabeth O'Riordan, Stewart Walsh, Cracking the Intercollegiate General Surgery FRCS Viva, 2020
David van Dellen, Zia Moinuddin, Hussein Khambalia, Brian KP Goh
No. In some patients, CTD can be assumed: Pre-existing donor diseasePatients >3 years post-transplant with: Slowly progressing reduction in GFRNormal urinalysis (therefore, recurrent GN or transplant glomerulopathy unlikely)Normal urine cytology (BK virus nephropathy unlikely)No detectable donor-reactive HLA antibody (chronic antibody-mediated rejection unlikely)In such patients CNI withdrawal is likely to be safe with confirmatory biopsy at a later date.
Urinary System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Kendall S. Frazier, John Curtis Seely
Mesangiolysis refers to the partial or complete dissolution of mesangial cells and their associated matrix. It is a degenerative lesion that is usually associated with primary endothelial cell injury, subsequent complement activation, and eventual loss of capillary wall patency (Leontsini 2003). The glomerular lobules stain poorly due to edema within the tuft. The dissolving mesangial cells, therefore, become difficult to identify and lose their borders, eventually leading to dilated or cystic capillaries. There is often proteinic fluid within Bowman’s space, fibrin deposition, and/or glomerular hemorrhage. Mesangiolysis can be a feature of glomerulonephritis such as in the anti-thy-1 rat model (Kriz et al. 2003) and can occur with widespread complement activation, particularly involving activation of the common terminal pathway and formation of C5b-9. In dogs and rats, mesangiolysis has also been associated with sustained hypertension. It is uncommonly encountered in preclinical toxicity studies, but due to the nature of the lesion should suggest the potential for an agent to target glomeruli or the vasculature. In humans, mesangiolysis may occur with hemolytic uremic syndrome and in some cases with transplant glomerulopathy. Mesangiolysis is usually associated with significant morbidity and/or mortality. If the animals survive or are put on drug holiday, glomerulosclerosis or glomerular atrophy may be sequela. PAS stains are helpful in the diagnosis as is electron microscopy to help identify the vascular changes and the primary effect on mesangial cells. Differentials would include glomerulonephritis or mesangioproliferative glomerulopathy, but the key features of mesangial dissolution and edema are not present in other glomerular lesions.
Prognostic value of the 7-year protocol biopsy of adult kidney allografts: impact of mesangiosclerosis and proteinuria
Published in Renal Failure, 2023
Yoshihiro Itabashi, Hideyo Oguchi, Tetuo Mikami, Noriyuki Kounoue, Taichi Arai, Kazunobu Shinoda, Masaki Muramatsu, Seiichiro Shishido, Ken Sakai
In our study, the concomitant presence of proteinuria with mm had a strong negative impact on eGFR decline and graft survival (Table 3, Figures. 5(b), 5(c), and 6), indicating the importance of evaluating concomitant proteinuria as well as the presence of mm in the 7-year protocol biopsy. Furthermore, four of five mm-positive patients with transplant glomerulopathy and proteinuria experienced graft loss (Figure 6). A recent study of transplant glomerulopathy showed that the level of proteinuria and the presence of mm ≥ 1 affect the graft survival [15]. Electron microscopy reveals endothelial injury in glomeruli in ABMR leading to transplant glomerulopathy [19], and we also recently reported that the electron microscopic findings of glomerular endothelial injury are detected in patients with low-level proteinuria with ABMR [9]. A histological study using electron microscopy revealed that glomerular endothelial injury is the initial change leading to transplant glomerulopathy with mesangial matrix increase [14]. Taken together, these results suggest that it may be important to focus on the treatment of glomerular endothelial injury in patients with mm-positive lesions.
Contribution of Electron Microscopy to the Clinicopathologic Diagnosis in Childhood Glomerular Renal Diseases
Published in Fetal and Pediatric Pathology, 2019
Secil Arslansoyu Camlar, Mehtat Ünlü, Alper Soylu, Duygu Karaca, Sulen Sarioglu, Salih Kavukcu
EM provides additional information for other renal diseases that were not represented in our trial. Kidney transplant biopsies were not included in our study, but EM is important to distinguish transplant glomerulopathy from recurrent or de novo glomerulonephritis in patients developing proteinuria after transplantation [18]. Diagnosis of newly described C1q nephropathy depends on the demonstration of mesangial and subendothelial electron dense deposits by EM [11]. Some studies suggest that EM can provide key information in lupus nephritis [19]. EM can show thickening of GBM before the clinical signs of diabetic kidney disease [20]. EM shows widespread thinning and lamellation of the GBM that mimics Alport’s disease in the Frasier syndrome [21]. The diagnosis of Fabry disease is made by ultrastructural examination of renal biopsy that documents typical inclusion bodies in the cytoplasm with concentric lamellation and a zebra or onion skin appearance [22]. Several new glomerular diseases and variants have been described in the past 25 years. EM is considered essential for the diagnosis of HIV-related glomerulopathy, hemolytic uremic syndrome, cryoglobulinemia, amyloidosis, nonamyloid fibrillary and immunotactoid glomerulopathies, and IgG4-related kidney disease [9, 20, 22–24].