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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 28 year old woman, with diabetes since age 18, had the nephrotic syndrome, hypertension and renal insufficiency. The initial renal biopsy specimen revealed diffuse glomerulosclerosis with early nodular changes. After an initial decline in renal function, her creatinine clearance progressively improved and has remained normal. Within 2 years she had a spontaneous remission of the nephrotic syndrome despite the presence of more pronounced nodular glomerular lesions. Although the renal hemodynamic functions were normal, certain tubular functions were impaired. Since we found no etiology for the nephrotic syndrome other than diabetic glomerulopathy, the complete remission of the nephrotic syndrome and improvement in renal function were very unusual events.
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PMID:Spontaneous remission of the nephrotic syndrome in diabetic nephropathy. 116 52

We wished to clarify the effects of a newly developed calcium antagonist, manidipine hydrochloride (HCl), on renal microcirculation in hypertensive rats by using the micropuncture technique. Oral administration of manidipine HCl for 2 months reduced systemic blood pressure (BP), did not change the single-nephron glomerular filtration rate (SNGFR), but increased the SNG plasma flow (SNGPF). Moreover, the glomerular transcapillary hydraulic pressure difference (delta P), which is assumed to be the parameter most related to development of glomerulosclerosis, was significantly reduced. Both afferent and efferent arteriolar resistance (RA and RE) were reduced. Intravenous (i.v.) infusion of manidipine HCl (20 micrograms/kg) decreased systemic BP but did not change SNGFR, SNGPF, or delta P. Both RA and RE were also significantly decreased. These results indicate that chronic administration of manidipine HCl increases renal blood flow (RBF) by dilating the afferent arterioles and improves glomerular hypertension by dilating the efferent arterioles. Thus, manidipine HCl might be a beneficial antihypertensive agent for patients with renal diseases. Because acute i.v. infusion of manidipine HCl did not change delta P, apparently time must elapse before glomerular hypertension is corrected.
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PMID:Effects of manidipine hydrochloride on the renal microcirculation in spontaneously hypertensive rats. 128 91

Organ protection is the main goal in the treatment of high blood pressure. Consequently, this protective capacity should be one of the main characteristics of any drug used in the treatment of hypertension. A renal protective agent should protect the kidney from intrinsic renal vasoconstrictors and exogenous agents, and should also protect, or at least delay, the decline in renal function in the presence of renal insufficiency, by mechanisms other than increasing glomerular filtration pressure. Verapamil protects mesangial cells from the reduction in surface area induced by endothelin in vitro. In human subjects, it minimises the renal impairment provoked by the administration of cisplatin, and in mice it protects superficial cortical blood flow from the vasoconstriction elicited by cyclosporin. Finally, verapamil may protect from glomerulosclerosis as a result of its capacity to inhibit mesangial cell replication.
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PMID:Is renal protection with calcium antagonists possible? 128 92

Eicosapentaenoic acid (EPA) can induce a shift in prostaglandin and leukotriene synthesis. The effects of EPA supplementation of the diet on the progression of chronic renal failure (CRF) were evaluated in a model of 5/6 renal mass ablation in rats. After 30 or 60 days of CRF, elevation in single-nephron glomerular filtration rate due to an increase in glomerular plasma flow and hydraulic pressure was observed. These hemodynamic alterations were followed by a rise in proteinuria and glomerular sclerosis. EPA treatment for 30 or 60 days did not substantially modify the hemodynamic or morphological profiles induced by renal mass ablation. In the present non-immune model of CRF, preglomerular vasodilation with glomerular hyperperfusion and hypertension were responsible, at least in part, for the presence of proteinuria and glomerular sclerosis. No additional vasodilation was observed in the present model of CRF, and, thus, hemodynamic effects induced by EPA did not modify renal damage, in contrast to the EPA effects observed in immune-mediated models of CRF.
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PMID:Effect of eicosapentaenoic acid on the progression of chronic renal failure in rats. 130 Apr 41

Mesangial cells play an important role in physiological and pathophysiological regulation of glomerular functions. To explore the involvement of deranged mesangial cell functions in the pathogenesis of hypertension, the growth activity of mesangial cells was compared in stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto rats (WKY). Upon exposure to fetal calf serum, the growth rate was significantly higher in mesangial cells cultured from glomeruli of 4-week old SHRSP than in those of age-matched WKY. This abnormally high growth of SHRSP mesangial cells was significantly inhibited by dihydropyridine calcium antagonists. Of the three antagonists tested, manidipine was the most potent inhibitor. Significant growth inhibition occurred at a concentration as low as 10(-12) M; inhibition as high as 65% was found at 10(-6) M. Calcium antagonists, particularly manidipine, may prevent or delay the development of hypertension not only through vasodilation but also through inhibition of mesangial cell growth. By slowing mesangial cell proliferation, calcium antagonists also may slow the progression of hypertension-induced glomerular sclerosis.
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PMID:Mesangial cell growth in genetically hypertensive rats and effect of calcium antagonists upon this growth. 134 84

Systemic hypertension is an important risk factor for the progression of diabetic glomerular disease. Recognition of this detrimental aspect has prompted intensive investigation into the mechanisms by which systemic hypertension promotes diabetic glomerulopathy, as well as into potential benefits of antihypertensive therapy. Studies in diabetic rats, both normotensive and hypertensive, have established that certain antihypertensive regimens effectively slow the development of albuminuria and glomerular sclerosis. Most consistently effective have been angiotensin-converting enzyme inhibitors, which may act to protect the kidney by several different mechanisms. Other antihypertensive regimens have been less consistent.
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PMID:Antihypertensive therapy in experimental diabetes. 136 Aug 46

Over a 16-year period, 205 patients with hypertension were shown to have a renovascular aetiology. Of these, 125 (61 per cent) had Takayasu's arteritis, 58 (28.3 per cent) had fibromuscular dysplasia, 16 (7.8 per cent) had atherosclerosis, five (2.4 per cent) had polyarteritis nodosa and one (0.5 per cent) had renal artery aneurysm. Among patients with Takayasu's arteritis, males were affected as commonly as females. The mean age of these patients at the time of detection was 26.8 +/- 8.6 years (range 5-52 years). Type I arteritis was seen in nine (7.2 per cent), Type II in 40 (32 per cent) and Type III in 76 (60.8 per cent) patients. The abdominal aorta was involved in 117 (93.3 per cent) patients. Takayasu's arteritis was associated with ulcerative colitis in two patients and with renal amyloidosis and focal segmental glomerulosclerosis with a nephrotic syndrome in one patient each. Surgical intervention consisting of bypass procedures, autotransplantation or nephrectomy was performed in 17 (13.6 per cent) and angioplasty in nine (7.2 per cent) patients. Cure and improvement in blood pressure was observed in 82.4 per cent and 77.8 per cent respectively. Adequate control of blood pressure was achieved with drugs only in 22 (22.2 per cent) patients. A definite cause and effect relationship could not be established between any infective or immunological disorder and Takayasu's arteritis. Takayasu's arteritis is a far more common cause of renovascular hypertension in Indian population than fibromuscular dysplasia or atherosclerosis, which are more common in the western population.
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PMID:Renovascular hypertension due to Takayasu's arteritis among Indian patients. 136 62

Hypertension and diabetes mellitus are strongly associated conditions from epidemiologic, genetic, and pathophysiologic points of view. The prevalence of hypertension is high in patients with diabetes, and, conversely, many patients with essential hypertension are glucose intolerant. Proteinuria appears in 40-50% of patients with insulin-dependent diabetes mellitus and 20-30% of patients with non-insulin-dependent diabetes mellitus. Progressive renal failure occurs in 30-40 and 3-8% of patients, respectively, hypertension being a leading factor in its rate of progression. In various animal experiments, ACE inhibitors are able to prevent proteinuria and glomerular sclerosis, presumably by lowering transglomerular capillary pressure. In the diabetic human, ACE inhibitors are powerful antihypertensive drugs, devoid of metabolic side effects. Clinical studies indicate that ACE inhibitors reduce proteinuria and possibly slow the rate of decline in renal function. Such an effect is not observed with beta-blockers. Large-scale studies are needed to confirm this very important hypothesis.
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PMID:Angiotensin-converting enzyme inhibition and diabetic nephropathy. 138 63

A significant proportion of renal allografts fail within several months or years after transplantation, primarily because of chronic rejection. The etiology and pathophysiology of this condition remain unclear. We studied the renal function, morphology, and immunohistology, in parallel, among F344-to-Lewis allografts (n = 23) and isografts (n = 13) over the course of 24 weeks. Only an initial 10-day course of CsA (5 mg/kg/day) was given to both groups to prevent acute rejection. Hypertension did not develop, although awake systolic blood pressure was significantly higher in allografts at the end of the study. Significant differences in urine albumin excretion (UalbV) between isografts and allografts were evident as early as 4 weeks after engraftment but rose dramatically by 20 weeks (3.3 +/- 0.7 vs. 21.2 +/- 3.7 mg/day, respectively, P < .001). This pattern continued until the conclusion of the study (5.0 +/- 1.1 vs. 53.5 +/- 7.6 mg/day, P < .001). Serum creatinine values were only significantly elevated in allografts at 16 weeks, which temporally corresponded to the dramatic increase in UalbV. However, renal blood flow and glomerular filtration rate, measured by paraaminohippurate and inulin clearances, respectively, were significantly lower in allografted organs, at 24 weeks. The frequency of glomerulosclerosis lesions was significantly increased in allografted kidneys at 24 weeks and correlated with UalbV values. Glomerular localization of mononuclear leukocyte subsets were equivalent between allografts and isografts; however, the numbers of interstitial macrophages, CD8+, and pan-T-cells were all significantly greater in allografts at 24 weeks. The infiltration of significantly greater numbers of macrophages and lymphocytes into the tubulointerstitium of the allograft group suggests a mononuclear leukocyte effector cell mediation of the progressive glomerular abnormalities in this model of chronic renal allograft rejection in the rat.
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PMID:Progressive albuminuria and glomerulosclerosis in a rat model of chronic renal allograft rejection. 141 63

To evaluate the contribution of systemic hypertension in the progression of nephropathies to glomerular sclerosis, a mild form of puromycin aminonucleoside (PAN) nephrosis was associated with Goldblatt hypertension and studied after 18 weeks. We studied four groups: Group I, controls; Group II, Goldblatt hypertension; Group III, PAN nephrosis; and Group IV, both conditions. Systolic blood pressure, 24-h proteinuria, serum cholesterol, triglycerides, glomerular hemodynamics, and histological studies were compared among the groups. Rats in groups II and IV developed systemic hypertension, but only group IV rats showed persistent proteinuria. No alterations in lipid metabolism were present in any of the groups. The most striking findings in the micropuncture studies were a significant increase of glomerular capillary pressure in group IV rats (63.15 +/- 1.34 mm Hg) as compared to controls (48.74 +/- 0.97 mm Hg) and to groups II and III (55.31 +/- 2.11 and 48.17 +/- 1.23 mm Hg, respectively), and a marked fall in Kf in groups III and IV. Only group IV showed significant histological alterations such as glomerular sclerosis, interstitial damage, and increased glomerular area. These results suggest that, in the presence of an underlying nephropathy, a greater fraction of systemic pressure is transmitted to the glomerular capillaries when systemic hypertension is present; the resulting elevation in glomerular pressure and proteinuria seems to be responsible for the progression to glomerular sclerosis.
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PMID:Mechanisms involved in the progression to glomerular sclerosis induced by systemic hypertension during mild puromycin aminonucleoside nephrosis. 141 51


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