Role of Lipids in Progressive Renal Disease: Insights from the Analbuminemic Rat

1997 ◽  
pp. 120-131
Author(s):  
J.A. Joles ◽  
T.J. Rabelink ◽  
H.A. Koomans
Keyword(s):  
Renal Disease ◽  
Progressive Renal Disease

Role of Tubular Cells in Progressive Renal Disease

1999 ◽  
Vol 22 (1-2) ◽  
pp. 53-61 ◽  
Author(s):  
Cees van Kooten ◽  
Alexandra M.J. Langers ◽  
Jan A. Bruijn ◽  
Mohamed R. Daha
Keyword(s):  
Renal Disease ◽  
Tubular Cells ◽  
Progressive Renal Disease

Hypertension

2021 ◽  
pp. 43-61
Keyword(s):  
Renal Disease ◽  
Renal Artery ◽  
Treatment Options ◽  
Treatment Strategies ◽  
Western World ◽  
Interventional Treatment ◽  
Lifestyle Modifications ◽  
Artery Disease ◽  
Progressive Renal Disease

Hypertension (HTN) is a common condition and a risk factor for numerous comorbidities, including cardiovascular disease, cerebrovascular disease, and progressive renal disease. In many people the aetiology of HTN is unknown, but in some a triggering “secondary” cause can be identified, e.g. renal disease, endocrine, or other underlying condition. For most people the treatment of HTN is straightforward, but in a small number the blood pressure can become “malignant or accelerated” and require urgent treatment or hospitalization. The chapters in this section provide an overview of the clinical assessment and investigation of a hypertensive patient, the recommended lifestyle modifications and pharmacological treatment options available, and potential complications of HTN. Renal artery stenosis a common cause of HTN that can be caused by atheromatous renovascular disease (ARVD) or other rarer pathologies, including fibromuscular disease, Takayasu’s arteritis, or other syndromes. ARVD is the commonest cause of renal artery disease in the Western world and in this section the authors focus upon the epidemiology and clinical presentation of ARVD and the potential diagnostic and treatment strategies. A particular focus is given to the role of medical and interventional treatment of ARVD, including potential outcomes, complications, and prognosis.

Role of Mesangial Cell Damage in Progressive Renal Disease

1999 ◽  
Vol 22 (1-2) ◽  
pp. 5-12 ◽  
Author(s):  
F. Shimizu ◽  
H. Kawachi ◽  
M. Orikasa
Keyword(s):  
Renal Disease ◽  
Mesangial Cell ◽  
Cell Damage ◽  
Progressive Renal Disease

scholarly journals Progressive renal disease: Role of race and antihypertensive medications

1990 ◽  
Vol 37 (4) ◽  
pp. 1113-1119 ◽  
Author(s):  
Peter C. Brazy ◽  
James F. Fitzwilliam
Keyword(s):  
Renal Disease ◽  
Antihypertensive Medications ◽  
Progressive Renal Disease

scholarly journals Gonadal steroid regulation of renal injury in renal wrap hypertension

2005 ◽  
Vol 288 (3) ◽  
pp. F513-F520 ◽  
Author(s):  
Hong Ji ◽  
Stefano Menini ◽  
Koby Mok ◽  
Wei Zheng ◽  
Carlo Pesce ◽  
...  
Keyword(s):  
Renal Disease ◽  
Renal Injury ◽  
Gonadal Steroids ◽  
Female Rats ◽  
Tubular Damage ◽  
Gonadal Steroid ◽  
Ovx Rats ◽  
17Β Estradiol ◽  
Progressive Renal Disease

Renal injury is greater in male compared with female rats after renal wrap (RW) hypertension. We investigated the role of gonadal steroids in the sex differences in RW disease severity in male (M) and female (F), castrated (Cast), and ovariectomized (OVX) rats and after dihydrotestosterone (DHT) and 17β-estradiol (E2) treatment. Male castration attenuated the severity of RW-induced glomerulosclerosis (GS) [GS index (GSI): RW-M, 2.1 ± 0.2; RW-Cast, 1.3 ± 0.2; RW-Cast+DHT, 2.4 ± 0.4], mean glomerular volume (MGV; μm3 × 106: RW-M, 1.9 ± 0.1; RW-Cast, 1.45 ± 0.15; RW-Cast+DHT, 1.91 ± 0.15), tubular damage, and proteinuria (mg/day: RW-M, 130 ± 8; RW-Cast, 105 ± 5; RW-Cast+DHT, 142 ± 9), whereas DHT treatment abrogated these effects. Ovariectomy increased the GSI (RW-F, 0.69 ± 0.05; RW-OVX, 1.2 ± 0.1; RW-OVX+E2, 0.65 ± 0.05), tubular damage, and MGV (μm3 × 106: RW-F, 1.0 ± 0.06; RW-OVX, 1.5 ± 0.05; RW-OVX+E2, 0.96 ± 0.06), whereas E2 treatment prevented these effects. Furthermore, DHT treatment of RW-OVX animals exacerbated the GSI (1.9 ± 0.19), MGV (1.7 ± 0.2 × 106 μm3), and proteinuria (171 ± 21 mg/day) even further. Our data show that the lack of E2 and presence of androgens contribute to progressive renal disease induced by RW hypertension, suggesting that gonadal steroid status is an independent factor in the greater susceptibility men exhibit toward hypertension-associated renal disease compared with women.

The role of chemokines in progressive renal disease

10.2741/3343 ◽  
2009 ◽  
Vol Volume (14) ◽  
pp. 1815 ◽  
Author(s):  
Carla Zoja
Keyword(s):  
Renal Disease ◽  
Progressive Renal Disease

scholarly journals Impaired Angiogenesis in the Remnant Kidney Model: I. Potential Role of Vascular Endothelial Growth Factor and Thrombospondin-1

2001 ◽  
Vol 12 (7) ◽  
pp. 1434-1447 ◽  
Author(s):  
DUK-HEE KANG ◽  
ALISON H. JOLY ◽  
SE-WOONG OH ◽  
CHRISTIAN HUGO ◽  
DONTSCHO KERJASCHKI ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Renal Disease ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Endothelial Growth Factor ◽  
Progressive Renal Disease ◽  
Remnant Kidney ◽  
Impaired Angiogenesis

Abstract. Few studies have examined the role of the microvasculature in progressive renal disease. It was hypothesized that impaired angiogenesis might occur in the diseased kidney and could contribute to renal scarring. Progressive renal disease was induced in rats by 5/6 renal ablation and those rats were compared with sham-operated control animals at multiple time points, for examination of changes in the microvasculature and the expression of angiogenic factors. An early angiogenic response was documented in remnant kidneys, with increases in the proliferation of peritubular (1 wk) and glomerular (2 wk) endothelial cells. Subsequently, however, there was a decrease in endothelial cell proliferation, which was reduced to levels below those of sham-treated animals, in conjunction with interstitial expression of the antiangiogenic factor thrombospondin-1 (TSP-1) and decreased tubular expression of the proangiogenic factor vascular endothelial growth factor (VEGF). Both the increase in TSP-1 expression and the loss of VEGF expression were correlated with capillary loss and the development of glomerulosclerosis and interstitial fibrosis. Progressive macrophage infiltration was correlated both spatially and quantitatively with the sites of absent or diminished VEGF expression. In addition, macrophage-associated cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α) inhibited VEGF mRNA expression and protein secretion by cultured tubular epithelial cells of the medullary thick ascending limb, under both normoxic and hypoxic conditions. Impaired angiogenesis characterizes the remnant kidney model and is correlated with progression. The impaired angiogenesis may be mediated by alterations in the renal expression of TSP-1 and VEGF, with the latter being regulated by macrophage-associated cytokines.

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