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Comparative analysis of hypertensive nephrosclerosis in animal models of hypertension and its relevance to human pathology. Glomerulopathy

“…Some studies have found an immediate increase during the first week after clipping which was followed by a gradual decrease to baseline blood pressure [ 15 , 57 ]. The clipped kidney weight, an indicator of ischemia severity, was found to vary from 10 to 90% [ 32 , 38 , 57 ]. In the clipped kidney, many studies identified severe glomerulosclerosis [ 15 , 32 , 57 ], while others found only mild glomerulopathy that was less than in the nonclipped kidney [ 58 , 59 , 99 ], or even absent [ 60 , 99 , 101 ].…”

“…Therefore some studies have tried to increase effectiveness by using a cylindrical probe [ 32 ], special clamp [ 103 ], spiral [ 107 ], intra-arterial coil [ 9 ], and specially designed clip [ 106 ]. A second important reason for data variation is a wide SBP baseline to consider animals being hypertensive, ranging from >120 [ 58 ], >140 [ 38 , 57 , 100 ], >150 [ 27 ], >160 [ 60 ], or >170 [ 12 ] mm Hg. Third, the arterial wall and lumen at the clip side could be compromised by scar formation, or muscular and endothelial proliferative response but analysis of this issue is absent.…”

“…Other studies have analyzed ischemic, acute hypertensive injury, or segmental sclerosis [ 31 ], glomerular collapse, hypertrophy, and sclerosis [ 32 ], glomerular basement membrane (GBM) thickening, or mesangial hypertrophy and capillary occlusion [ 33 ]. Moreover, there are many formulas to quantify glomerular lesion score, with values ranging from 0–2 [ 16 ], 0–3 [ 27 ], 0–4 [ 34 ], 0–5 [ 35 ], 0–100 [ 36 ], 0–400 [ 12 , 37 ], or with yes/no binary variables [ 38 ] ( S1 Table ). Different criteria/parameters for semi-quantitative scoring and quantification make it difficult to properly validate the severity of hypertensive nephropathy in each study, and make comparison within animal studies, and with human data ( Tables 1 and 2 ).…”