Increased genetic risk of hypertension in glomerulonephritis?

Schmid, Marcel; Meyer, Susanne; Wegner, Renate; Ritz, Eberhard

doi:10.1097/00004872-199006000-00011

Cited by 24 publications

(7 citation statements)

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“…testosterone; 5␣-dihydrotestosterone; 17␤-estradiol; sexual dimorphism AS EARLY AS 1846, BRIGHT (4) noted that patients with renal disease develop hypertension and in 1923, Vohard (25) recognized the "vicious circle" in postulating that hypertension causes renal insufficiency. Direct evidence of hypertension causing renal disease arises from studies in patients with glomerulonephritis (23) and diabetic nephropathy (5), in which a genetic predisposition to hypertension increases the risk of developing renal disease, and from clinical trials showing that antihypertensive treatments slow the progression of renal disease (13).…”

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confidence: 99%

Gonadal steroid regulation of renal injury in renal wrap hypertension

Menini²,

Mok³

et al. 2005

American Journal of Physiology-Renal Physiology

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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 17beta-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; microm3 x 10(6): 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 (microm3 x 10(6): 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 x 10(6) microm3), 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.

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confidence: 99%

Gonadal steroid regulation of renal injury in renal wrap hypertension

Menini²,

Mok³

et al. 2005

American Journal of Physiology-Renal Physiology

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“…Parents of type 1 diabetic patients had higher BP values than parents of patients without diabetic nephropathy [11]. Higher BP values were found in parents of type 1 diabetic patients with as compared to parents of patients without diabetic nephropathy [12].…”

Section: Introductionmentioning

confidence: 82%

Renoprotection with Anti-Hypertensives: Reduction of Proteinuria and Improvement of Oxygenation via Inhibition of the Renin-Angiotensin System

Nangaku¹,

Ohse²,

Tanaka³

et al. 2005

CHYR

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Hypertension is a common cause of chronic kidney disease (CKD) and even more common sequelae of CKD. While strict control of blood pressure is essential to preserve residual renal function, numerous clinical trials have demonstrated that inhibitors of the renin-angiotensin system (RAS), i.e. angiontensin converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARB), reduce the progression of CKD. These studies have examined type I and type II diabetic as well as non-diabetic nephropathies, utilizing end points such as serum creatinine, glomerular filtration rate, time to end-stage renal disease (ESRD), and death. These observations suggest that drugs blocking the RAS offer advantages beyond lowering blood pressure in diabetic and non-diabetic CKD. Therefore, guidelines recommend antihypertensives that block RAS in patients with CKD.Previous studies emphasized amelioration of glomerulosclerosis induced by glomerular hypertension as a renoprotective mechanism of inhibition of RAS. It should also be noted that progression to ESRD is mediated by two final common pathways; tubulointerstitial injury induced by proteinuria, and chronic hypoxia in the tubulointerstitium. Recent research indicates that reduction of proteinuria and improvement of oxygenation of the kidney are crucial mechanisms by which inhibition of RAS mediates renoprotection providing additional rationale for the use of ACEi and ARB to protect the kidney.

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“…It has been proposed that parental hypertension is more prevalent in patients with glomerulonephritis [13] or IgAN [6] than in the general population, but its role as predictor of poor outcome, and in particular of progression rate, has not been clearly elucidated previously. To our knowledge, only three studies have looked for association between outcome and family history of hypertension in patients with IgAN [6,14,15].…”

Section: Discussionmentioning

confidence: 99%

“…An increased frequency of parental hypertension has been reported also in patients with glomerulonephritis, with respect to the general population. Some, [6,13,14], but not all [15] have reported that, besides hypertension, positive family history for hypertension affects renal outcome. Such studies were performed on a small number of individuals [13,14] or in heterogeneous cohorts including patients with advanced renal failure at presentation [6].…”

Section: Introductionmentioning

confidence: 99%