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Hypertension and the Kidney
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Roberto Pontremoli, Giovanna Leoncini, Francesca Viazzi
The lack of specific criteria to define a histological diagnosis often limits a clear demonstration that hypertension causes the development of renal damage and makes it difficult to correctly estimate the impact of hypertension in renal dysfunction. In fact, regardless of the underlying etiology of CKD, the increase in systemic blood pressure accelerates per se the rate of glomerular filtration rate deterioration, especially in the presence of proteinuria. However, many aspects of hypertension-related renal damage, such as the individual susceptibility to hypertensive renal damage and the different renoprotective effect of various antihypertensive drug classes, are still incompletely understood (43). The renal pathology typically observed in the vast majority of individuals with primary hypertension is benign nephrosclerosis, a condition characterized by accelerated ageing of the renal vasculature with a slow progressive thickening and sclerosis of the renal resistance vessels, with a substantial sparing of glomerular capillaries (Figure 3.3a). Therefore, it is not surprising that primary hypertension rarely leads to advanced stages of renal damage. In fact, except for genetically susceptible groups, such as blacks, the only individuals with primary hypertension who develop severe hypertension-induced renal damage to reach ESRD are those with very high levels of BP that result in the development of malignant nephrosclerosis, characterized by acute disruptive injury and fibrinoid necrosis of small arteries, arterioles and glomerular capillaries, with a prevalent glomerular ischemia. In these cases, acute renal failure develops over days, and despite treatment is often followed by progressive renal damage leading to CKD or even ESRD.
Glomerular solidification is associated with nephritis-related clinical parameters in IgA nephropathy
Published in Renal Failure, 2019
Tsutomu Inoue, Yankun Luo, Takeru Seto, Hiromichi Suzuki, Hirokazu Okada
This was a single center, cross-sectional, observational study. Subjects were enrolled for 5 years from October 2009 until September 2014. During this period, 400 renal biopsies were performed and patients aged ≥16 years with biopsy-proven IgA nephropathy (n = 116) were enrolled. The diagnosis was made using light microscopy and immunofluorescence. Patients for whom the biopsy included fewer than 10 glomeruli were excluded from the analysis. All biopsy specimens with periodic acid-Schiff (PAS) staining were independently reevaluated by the authors YL and HO. The presence of the two types of global glomerulosclerosis was assessed and quantified as a percentage of the total number of glomeruli for each biopsy. Results were obtained as the average of the data from both YL and HO. Before histologic evaluation of IgA nephropathy, several hypertensive nephrosclerosis tissue specimens were used to confirm mutual recognition of the characteristics of two types of global glomerulosclerosis. The method described above was based on a previous report [5]. Solidified glomeruli were defined as glomeruli in which the entire tuft was solidified in the absence of collagenous changes in the capsular space. This can be described by the term ‘decompensated benign nephrosclerosis.’ Obsolescent glomeruli were defined as glomeruli in which the Bowman’s space was occupied by collagenous, PAS-positive material, and the tuft was retracted. Figure 1 shows representative findings for two types of global glomerulosclerosis in IgA nephropathy in our patients.
Changes in the diagnosis of glomerular diseases in east China: a 15-year renal biopsy study
Published in Renal Failure, 2018
Qin Zhou, Xin Yang, Meifang Wang, Huiping Wang, Jie Zhao, Yan Bi, Xiayue Wang, Jihong Yao, Ying Chen, Chuan Lin, Xishao Xie, Hong Jiang, Jianghua Chen
All biopsies were categorized for the purpose of this analysis as PGN, SGN, hereditary nephropathy (HN), tubulointerstitial nephropathy (TIN), or other miscellaneous or undefined histological diagnoses. In this study, we analyzed only the common categories of PGN and SGN. PGN included IgA N, MN, non-IgA mesangial proliferative glomerulonephritis (MsPGN), minimal change disease (MCD), and focal segmental glomerulosclerosis (FSGS). SGN included LN, HSN, DN, systemic vasculitis (SV), hepatitis B virus-associated glomerular nephropathy (HBV-GN), benign nephrosclerosis (BANS) and amyloidosis nephropathy (AMYN).