Disease relevance of Nephrosclerosis

• The underlying diseases included glomerulopathies (in 192 patients), interstitial nephritis (in 105), nephrosclerosis (in 97), polycystic kidney disease (in 64), diabetic nephropathy (in 21), and miscellaneous or unknown disorders (in 104) [1].
• Evaluation of serum creatinine for estimating glomerular filtration rate in African Americans with hypertensive nephrosclerosis: results from the African-American Study of Kidney Disease and Hypertension (AASK) Pilot Study [2].
• CML and PENT were also identified in areas of glomerulosclerosis and arteriosclerosis in idiopathic and secondary focal segmental glomerulosclerosis, hypertensive nephrosclerosis, and lupus nephritis [3].
• All had azotemia, presumable from nephrosclerosis, and had serum creatinine concentrations ranging from 2.3 to 4.9 mg/dl [4].
• Adverse effect of the calcium channel blocker nitrendipine on nephrosclerosis in rats with renovascular hypertension [5].

High impact information on Nephrosclerosis

• Effect of ramipril vs amlodipine on renal outcomes in hypertensive nephrosclerosis: a randomized controlled trial [6].
• Elevated levels of endogenous angiotensin can cause hypertensive nephrosclerosis as a result of the potent vasopressor action of the peptide [7].
• It is suggested that the vascular changes of nephrosclerosis, which may be seen in both hypertensive and normal subjects, result in a reduction of afferent arteriolar distensibility, with impairment of basal renin secretion and responsiveness [8].
• Thus, in patients with hypertensive nephrosclerosis and early impairment of glomerular filtration, alterations of glucose metabolism become evident only when creatinine clearance is < 50 ml.min(-1).1.73 m(-2) and are not related to microalbuminuria and cardiovascular complications [9].
• Thus, the T-type (mibefradil) and L-type (amlodipine) calcium antagonists each prevented and reversed the pathophysiological alterations of L-NAME-exacerbated hypertensive nephrosclerosis in SHR [10].

Chemical compound and disease context of Nephrosclerosis

• Although other dihydropyridine calcium antagonists have been found to reduce experimental glomerular injury, these data suggest that amlodipine may not prevent hypertensive nephrosclerosis [11].
• Thus, the calcium antagonist felodipine, alone or in combination with an ACE inhibitor, not only prevented but also reversed L-NAME-exacerbated hypertensive nephrosclerosis in SHR [12].
• Several lines of experimental evidence demonstrate that selective blockade of aldosterone, independent of renin-angiotensin blockade, reduces proteinuria and nephrosclerosis in the spontaneously hypertensive stroke-prone rat model and reduces proteinuria and glomerulosclerosis in the subtotally nephrectomized rat model (i.e. remnant kidney) [13].
• CONCLUSIONS: Three weeks of treatment with L-arginine improved systemic hemodynamics, renal function and renal histologic changes in aged SHR with naturally occurring nephrosclerosis [14].
• Imidapril improves L-NAME-exacerbated nephrosclerosis with TGF-beta 1 inhibition in spontaneously hypertensive rats [15].

Biological context of Nephrosclerosis

• L-NAME rats developed severe hypertensive nephrosclerosis with significantly elevated blood pressure, markedly increased urinary protein excretion and serum creatinine levels, and more severe glomerulosclerosis and tubulo-interstitial changes [15].
• CONCLUSION : Cilnidipine not only prevented, but reversed, the severe renal hemodynamic and glomerular dynamic changes, including apoptosis and glomerular cellular proliferation, in l-NAME/SHR-exacerbated nephrosclerosis [16].
• They suggest that both ACE inhibition and angiotensin II blockade decrease renal cell proliferation and suppress the infiltration of mononuclear cells that may trigger expression of extracellular matrix proteins and progressive nephrosclerosis [17].
• After 32 weeks the renal blood flow was significantly lower in th FO group 2.8+/-1.1 vs. 4.6+/-1.9 ml/min/g, (p<0.05), and the rats had an accelerated development of nephrosclerosis, with sclerotic lesions in 60.3+/-6.6% of the glomeruli as compared with 46.5+/-9.8% in the cholesterol and 39.8+/-5.9 in the control group (p<0.05) [18].
• In diabetic animals, ALT-711 improved left ventricular function, decreased ventricular collagen content and improved its solubility, reduced aortic stiffness, ameliorated diabetic nephrosclerosis, and improved renal function [19].

Anatomical context of Nephrosclerosis

• Experimental studies on the role of intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1 in hypertensive nephrosclerosis [20].
• The mechanism for this association between C3 and properdin deposition and hyaline arteriolar nephrosclerosis is not clear at present, but our findings suggest possible involvement of the alternative pathway of the complement system [21].
• We report a 19-year-old male with Seckel syndrome (bird-like dwarfism) who presents with malignant hypertension associated with hypertensive nephrosclerosis, dilated cardiomyopathy, and a ruptured cerebral artery aneurysm [22].
• However, acute renal insufficiency or overt renal failure occurs in some patients with underlying critical renal artery stenosis (RAS), hypertensive nephrosclerosis, autosomal dominant polycystic kidney disease, diabetes mellitus, and chronic congestive heart failure [23].
• Ang II, via its AT1 receptor, is also involved in cell proliferation, left ventricular hypertrophy, nephrosclerosis, vascular media hypertrophy, endothelial dysfunction, neointima formation and processes leading to athero-thrombosis [24].

Gene context of Nephrosclerosis

• CRP was higher in patients with a previous history of cardiovascular disease (P<0.01), as well as in patients in whom ischaemic nephropathy or nephrosclerosis was the cause of end-stage renal disease (P<0.01) [25].
• CONCLUSION: In the remnant kidney model, the time course and localization of TSP-1 are consistent with its playing a role as a local activator of TGF-beta1, thereby potentially participating in the development of nephrosclerosis [26].
• We studied the expression of TSP-1 mRNA and protein during the development of glomerular and tubulointerstitial nephrosclerosis in the renal ablation model particularly in relation to TGF-beta1 expression [26].
• In human patients with essential hypertension, atherosclerosis, and nephrosclerosis, plasma ET-1 levels are increased compared with patients with uncomplicated essential hypertension [27].
• L-PGDS was stained in the tubules and the interstitium of the kidney in nephrosclerosis [28].

Analytical, diagnostic and therapeutic context of Nephrosclerosis

• Early impairment of renal function (creatinine clearance, 30 to 89 ml/min per 1.73 m2 of body surface area) caused by arteriolar nephrosclerosis was found in 172 patients [29].
• CONCLUSION: HCTZ administration exacerbated the changes in renal and micropuncture dynamics, proteinuria and histopathological nephrosclerosis produced by L-NAME in SHR [30].
• These findings suggested that the renal function loss was not only caused by the nephron mass reduction due to the nephrectomy but was also caused by nephrosclerosis [31].
• Forty patients with biopsy-proven nephrosclerosis were divided into two groups by the 75-g oral glucose tolerance test (OGTT): group A, 2-hr plasma glucose concentration > 140 mg/dL (n = 25); group B, 140 < or = 2-hr plasma glucose < 200 mg/dL (n = 15) [32].
• Clinical trials report. The effect of Ramipril versus Amlodipine on renal outcomes in hypertension nephrosclerosis [33].

References