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

We describe a 14 year old boy with antiphospholipid syndrome who initially presented at the age of 10 with recurrent loin pain, fever, weight loss, leucocytosis, thrombocytopenia, hypertension and haematuria. He had primary adrenal insufficiency with bilaterally enlarged adrenals on computed tomographic (CT) scan consistent with adrenal infarction. Renal and liver biopsies showed microthrombi in the glomerular capillaries and hepatic sinusoids respectively. The case is unusual in that hypertension rather than hypotension was dominant and a CT scan was consistent with bilateral adrenal infarction without haemorrhage. He represented with evidence of persistent hypertension with glomerulosclerosis and glomerular microthrombi on repeat renal biopsy. He continues to have permanent adrenal insufficiency with complete atrophy of his adrenals.
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PMID:Addison's disease, hypertension, renal and hepatic microthrombosis in 'primary' antiphospholipid syndrome. 206 36

The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain to be established. However, there is now evidence that renal disease clusters in families and that genetic factors are of central importance in determining liability. A predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Genetically controlled hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. This suggestion derives from the observation that the fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first sign of renal damage is the appearance of microalbuminuria and of a small elevation in arterial pressure, changes associated with significant mesangial expansion. Microalbuminuria is associated with abnormalities of lipoprotein profiles possibly as a consequence of insulin-resistance-induced hyperinsulinemia. It could be postulated that the environmental changes brought about by diabetes lead in susceptible individuals to increased systemic and intraglomerular pressure on the one hand and mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities would further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered of reduction in renal function, more hypertension, more proteinuria, more glomerular obsolence, more hyperlipidemia and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Mechanisms of diabetic renal and cardiovascular disease. 207 90

A study was undertaken to estimate the incidence of glomerular sclerosis in the normal population in Hong Kong. The percentage glomerular sclerosis in 100 cadavers without clinical evidence of kidney disease or hypertension was determined by histologic examination of the kidneys. The mean percentage values in the normal population at all age groups were calculated based on this sample. The subcapsular cortical area generally had a higher proportion of sclerotic glomeruli than the deeper cortex. Statistical analysis showed that 95% of the normal population up to 40 years of age would be expected to have less than 6% sclerotic glomeruli. After the age of 55, the upper limit containing 95% of the normal population would exceed 10% sclerosis. A broad scatter of observed percentage glomerular sclerosis was present in the elderly after the age of 70 years. The data obtained provide the baseline values of glomerular scarring that would allow age-related involutional changes to be distinguished from those due to disease.
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PMID:Age-related glomerular sclerosis: baseline values in Hong Kong. 178 Jan 98

Similarities between atherosclerosis and glomerulosclerosis suggest that hyperlipidaemia may contribute to glomerular injury. Dietary supplementation with 4% cholesterol + 1% cholic acid was administered to rats 4 weeks after 1 1/3 nephrectomy and continued for 7 weeks. There was a significant increase in serum cholesterol (peak = 11.52 +/- 1.09 mmol l-1 vs. 4.73 +/- 0.31 on control diet, P less than 0.001) and triglyceride concentrations (peak = 2.31 +/- 0.27 mmol l-1 vs. 1.41 +/- 0.29, P less than 0.05) and a marked increase in beta-migrating lipoproteins. The severity of hypercholesterolaemia was significantly correlated with proteinuria (control diet: r = 0.600, cholesterol diet: r = 0.672, P less than 0.0001) as was hypertriglyceridaemia (control diet: r = 0.544, cholesterol diet: r = 0.678, P less than 0.0001). The percentage of glomeruli containing lipid deposits was increased from 21% to 60% (P less than 0.05). The kidney total cholesterol content was increased from 29.2 +/- 0.8 to 47.7 +/- 3.3 mumols g-1 dry weight (P less than 0.0001), with esterified cholesterol increasing from 7.5 +/- 0.4% to 14.5 +/- 2.1% of total (P less than 0.01). Serum cholesterol concentration was significantly correlated with both glomerular lipid deposition (rs = 0.7195, P less than 0.0001) and tissue total cholesterol content (rs = 0.6053, P less than 0.001). Lipid vacuolation was prominent in the paramesangium and within mesangial cells. Despite these changes hypertension, uraemia, proteinuria and glomerulosclerosis were not significantly increased on the cholesterol diet. Cholesterol deposition in the glomeruli occurs secondary to hyperlipidaemia in rats following subtotal nephrectomy but over 7 weeks no exacerbation of glomerulosclerosis is detectable.
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PMID:The role of lipids in the pathogenesis of glomerulosclerosis in the rat following subtotal nephrectomy. 210 41

The relation between hypertensive glomerular damage and arteriolar diameter was examined in a microvascular cast study in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The blood pressure and urinary protein excretion increased progressively in the DOCA rats. In controls afferent arteriolar diameters increased during the course of the experiment, and efferent arteriolar diameters remained unchanged. In the DOCA rats, however, afferent arteriolar diameters did not change significantly, while efferent arteriolar diameters increased. Histological studies showed severe arteriolosclerosis and glomerulosclerosis in the DOCA rats. The results show that these arteriolar changes might contribute to the reduction of glomerular capillary pressure in the development of DOCA-salt hypertension. However, they are not sufficient to protect glomeruli from hypertensive damage.
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PMID:Variations in renal arteriolar diameter in deoxycorticosterone acetate-salt hypertensive rats. A microvascular cast study. 212 85

Previous studies have demonstrated that inhibition of thromboxane A2-dependent platelet aggregation by the thromboxane A2 synthase inhibitor, OKY 1581, ameliorated the progressive kidney disease of rats with subtotal renal ablation. OKY 1581 also decreased the excessive renal thromboxane A2 synthesis and lowered systemic blood pressure. In the same model, a low dose aspirin and a specific thromboxane A2 receptor antagonist failed to influence proteinuria, glomerulosclerosis, and hypertension, thus excluding a role for either platelet or renal thromboxane A2 in renal disease progression. The aims of this study were to establish (1) whether a thromboxane A2 synthase inhibitor different from OKY 1581 could retard the progression of glomerular disease in rats with remnant kidney and (2) whether this effect was associated with an increase in renal synthesis of the vasodilatory prostacyclin. Treatment of rats with renal mass ablation with FCE 22178 (100 mg/kg by gavage and 200 mg/kg in the drinking water) for 35 days starting 10 days after surgical ablation was associated with an improvement in renal function in comparison with rats receiving the vehicle alone. Proteinuria was significantly lower, and rats were partially protected from the development of glomerulosclerosis. Systolic blood pressure was significantly lower than in animals given the vehicle. Urinary thromboxane B2 excretion was significantly decreased, and urinary 6-keto-prostaglandin F1 alpha increased in respect to vehicle-treated rats. We conclude that FCE 22178 limits glomerular injury in rats with remnant kidney.
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PMID:Thromboxane synthesis inhibition increases renal prostacyclin and prevents renal disease progression in rats with remnant kidney. 213 29

Coexistent renal pathology with diabetic glomerulosclerosis was found in 38 of 136 (28%) consecutive renal biopsies performed primarily for proteinuria in individuals with diabetes mellitus. The histological lesions found were glomerulonephritis (14), focal tubulointerstitial disease (23), and amyloidosis (1). Significant microscopic haematuria was present in 66% of all patients and did not help to distinguish non-diabetic disease. The severity of diffuse diabetic glomerular disease was independently associated with duration of diabetes, raised plasma creatinine, the presence of hypertension, clinical retinopathy and neuropathy, but not with type of diabetes, degree of proteinuria or glycosylated haemoglobin at the time of biopsy. Diffuse interstitial fibrosis was related to the severity of glomerular disease and, if severe, also with a significantly (p less than 0.01) higher plasma creatinine. Coexisting renal disease was found to be associated with a significantly higher plasma creatinine (p less than 0.01) independent of the severity of diabetic glomerulopathy. Coexistent pathology is a not uncommon finding in renal biopsies from diabetic patients with proteinuria. These lesions and their underlying causes may not only influence the renal function and natural history of renal disease in diabetic individuals, but may also determine the response of proteinuria to therapy.
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PMID:A clinical-histological study of individuals with diabetes mellitus and proteinuria. 213 92

In order to investigate the effects of atrial natriuretic polypeptides (ANP) on hypertensive glomerular lesions, ANP was administered intravenously by osmotic minipumps to 20 15-week-old male spontaneously hypertensive rats (SHRs) in a sustained hypertensive stage. ANP was infused at the rate of 100 ng/hour/rat (the ANP group). Saline was similarly administered to 19 age-matched SHRs (the control group). The rats were sacrificed on the seventh day. Semiquantitative evaluation of the renal tissue revealed no significant difference in glomerular sclerosis between the 2 groups. However, segmental hyalinosis in glomeruli was more accentuated in the ANP group than in the control group. As it is suggested that hyalinosis in glomeruli is related to the elevated intracapillary pressure, the results of the present work were in accordance with reports that ANP increases glomerular capillary pressure by preglomerular vasodilation and postglomerular vasoconstriction. It should be determined whether endogenous ANP works as an aggravating factor for glomerular injuries in the natural course of hypertension.
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PMID:Effects of chronic administration of atrial natriuretic polypeptide on glomerular lesions in spontaneously hypertensive rats. 214 67

A 12 year-old girl with a family of Charcot-Marie-Tooth neuropathy was referred to us with mild proteinuria without hematuria or renal insufficiency; a renal biopsy specimen showed focal glomerulosclerosis. Two years later, proteinuria and renal function were quite stable and there was no arterial hypertension. Of 13 other cases in the literature, the outcome of renal involvement has the same profile:proteinuria at onset with or without microhematuria, sometimes with nephrotic syndrome; the prognosis is often poor, since 9 out of 13 patients have end-stage renal failure after 6 months to 17 years of follow-up. The pathological examination show focal glomerulosclerosis in most cases. Nerve deafness is uncommon in Charcot-Marie-Tooth disease but was present in 7 out of 13 patients with the nephritis. Such an association may be a variant of the dominant autosomal form of the disease, whose gene is located on chromosome 1.
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PMID:[Nephropathy and Charcot-Marie-Tooth disease. A case report]. 216 44

Nephron loss is a common progression of a diverse range of kidney diseases. Recent experimental models of chronic renal disease have suggested that hemodynamic and nonhemodynamic mechanisms play key roles in progressive renal injury. Extensive renal ablation in the rat was followed by development of altered glomerular hemodynamics. Albuminuria and histologic damage leading to focal glomerulosclerosis were preceded by the development of increased glomerular pressures and were prevented by interventions such as severe dietary protein restriction and angiotensin-converting enzyme (ACE) inhibitor therapy. Both experimental interventions ameliorated glomerular hypertension. It was therefore concluded that these interventions ameliorated injury by glomerular hemodynamic effect. Similar findings were obtained in a rat model of type I diabetes mellitus induced by streptozotocin in which glomerular hemodynamic factors appeared important to the development of progressive renal disease. Recent studies have suggested that nonhemodynamic factors have important roles in the progression of glomerular injury. For example, although the predominant effects of ACE inhibitor therapy appear to be hemodynamically mediated, data are emerging which suggest that these agents may also influence growth/proliferation of glomerular cells. Because hyperplasia/hypertrophy may influence glomerular susceptibility to injury, this may also be a potential mechanism whereby ACE inhibitor therapy influences glomerular damage. In addition, a variety of studies have suggested that hyperlipidemia, which is frequent accompaniment of glomerular disease, is an important modulator of glomerular injury independent of glomerular hemodynamic effects. Coagulation factors, calcium phosphorus balance, as well as the genetic susceptibility of the glomerulus to injury, all appear to contribute to progressive nephron destruction.
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PMID:Renal protective effects of angiotensin-converting enzyme inhibition. 218 11


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