Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to purify and identify a plasma protein fraction (PreR-Co) involved in renal prorenin activation and to explore its capacity to process plasma prorenin. PreR-Co was obtained from plasma as a single electrophoretic band by (NH(4))(2)SO(4) precipitation, Sephacryl S-200 HR gel filtration, anti-rat albumin immunoaffinity, and ion-exchange chromatography. The amidase, esterase, and kallikrein activities of PreR-Co were studied, as was its N-terminal amino acid sequence. Rat kidney extract or plasma (normal or previously treated with acid to pH 2.8) were incubated with PreR-Co for 15 minutes at 37 degrees C. Renin concentration was measured by incubation with homologous angiotensinogen. The same protocol was repeated with samples activated by trypsin. The N-terminal amino acid sequence was IIGGSMDAKGSFP, which had a homology of 90% with the beta-chain of haptoglobin, 69% with serine-proteases, and 65% with kallikreins. The renin concentration in rat kidney extract was 34+/-4 ng of angiotensin I (Ang I). mg of tissue(-1). h(-1). After PreR-Co or trypsin treatments, renin concentrations were 211+/-7 and 110+/-11 ng of Ang I. mg of tissue(-1). h(-1), respectively. The plasma renin concentration in normal plasma was 67.6+/-13.3 ng of Ang I. mL(-1). h(-1), and no significant difference was observed after PreR-Co treatment. However, a significant increase (202.8+/-7.8 ng of Ang I. mL(-1). h(-1); P<0.01) was found after trypsin treatment. The isolated PreR-Co acts on renal prorenin but not on plasma prorenin. These results suggest that active renin is processed in the kidney by a circulating enzyme that may have a role in the regulation of circulating renin.
Hypertension 1999 Sep
PMID:Rat renal and plasma prorenin are activated in vitro by different mechanisms. 1048 4

Fifty patients with stable slight and moderate uncomplicated essential hypertension, treated by ramipril, atenolol, or isradipine, were examined. Total protein and urinary excretion of individual proteins were studied before and after treatment. Urinary concentrations of apolipoproteins A1 and B1, alpha 1-acid glycoprotein, alpha 1-antitrypsin, prealbumin, albumin, beta 2-microglobulin, transferrin, haptoglobin, IgG and IgA, and C3 and C4 complement components were measured. Index of proteinuria selectiveness was calculated for each portion of urine. All three drugs exerted a nephroprotective effect, atenolol being the most active of them. Apolipoproteins, IgG, and complement components were the most valuable for diagnosis. Their excretion correlated with the severity of arterial hypertension and efficiency of treatment. Use of protein markers helps reliably assess the renal function and monitor the treatment efficiency.
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PMID:[Protein markers in evaluation of nephroprotective effects of antihypertensive drugs in patients with arterial hypertension]. 1098 85

HELLP syndrome is a serious, life-threatening form of pre-eclampsia with a typical laboratory triad. The incidence of the disease is reported as being 0.17-0.85% of all live births. There has been, to date, neither reliable early recognition nor effective prevention of HELLP syndrome. As a result of endothelial dysfunction, activation of intravascular coagulation occurs with fibrin deposition in the capillaries and consecutive microcirculation disorders. The disease manifests itself on average between 32-34 weeks' gestation. HELLP syndrome will occur postpartum in up to 30% of the cases. The clinical cardinal symptom of the disease is right upper quadrant pain or epigastric pain accompanied with nausea, vomiting and malaise. In 20% of the cases with HELLP syndrome there is no hypertension and 5-15% of the pregnant patients present a low level of proteinuria or none at all. The early recognition of hemolysis is most sensitively managed by the determination of the serum haptoglobin. The increase of the aspartate transaminase (AST) and the alanine transaminase (ALT) often precedes a decrease in platelets. The course of HELLP syndrome is incalculable. It is universally agreed that a pregnancy from 32-34 weeks should be immediately delivered. Before 32-34 weeks, expectant management is generally possible in a perinatal center. The frequency for a repeated hypertensive disease in pregnancy ranges from 27% to 48%.
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PMID:HELLP syndrome. 1103 96

Renal failure occurring in pregnancy or post partum is an unusual but well-described complication. Acute renal failure seems to be associated more often with HELLP syndrome rather than with pre-eclampsia or chronic hypertension. Probable overlapping of HELLP and hemolytic uremic syndrome in pregnancy or postpartum should be taken into consideration when treating pregnant women who show signs of proteinuria, hypertension, hematuria, increase of reticulocytes, decrease of haptoglobin with thrombocytopenia and microangiopathic hemolytic anemia. Our case refers to a 32 year old woman at 32 weeks gestation in twin pregnancy who presented with HELLP syndrome and renal failure. Immediately postpartum oliguria was noted and the laboratory analyses suggested the coexistence of HELLP and hemolytic uremic syndrome. In patients with gestosis and/or HELLP syndrome presenting oliguria combined with a decrease of hemoglobin level not due to intraoperative hematic leaks it is always necessary to ask for haptoglobin dosage. In treating hemolytic uremic syndrome it is very important to use a high dosage of plasma and sometimes plasmapheresis. HELLP syndrome contributes to various complications which are sometimes responsible for kidney or maternal mortality. In treating these patients early diagnosis combined with a specific treatment can considerably reduce kidney and maternal mortality.
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PMID:[Hemolytic uremic syndrome in twin pregnancy at 32 weeks gestation with HELLP syndrome. Case report]. 1143 43

The aim of this study was to investigate the effects of hemorheological factors on the development of hypertension in diabetic children without retinopathy and persistent microalbuminuria. Arterial blood pressures were measured in 46 diabetic children and were compared with those of 29 healthy non-obese and 32 obese age- and sex-matched children. Higher systolic (SBP) (109.0 +/- 13.0 mmHg) and diastolic blood pressure (DBP) (74.3 +/- 9.5 mmHg) were obtained in diabetics (independent of age, sex, duration, and control degree of diabetes), when compared with non-obese children (SBP: 97.9 +/- 10.3 mmHg, DBP: 74.3 +/- 9.5 mmHg; p < 0.01, p < 0.05, respectively). No significant DBP and SBP difference was found between diabetics and obese children. When compared with non-obese children, blood viscosity, plasma viscosity, serum viscosity, serum albumin, and plasma fibrinogen values were found elevated in diabetics and were correlated with SBP and DBP. Serum haptoglobin levels and lipid profile were normal. The multivariate discriminant analysis demonstrated plasma viscosity and fibrinogen to be the most important variables related to the development of hypertension. The results of this study revealed that: (1) arterial blood pressures are high in diabetic patients independent of age, sex, duration of diabetes, control degree of diabetes, and lipid profiles; (2) arterial blood pressure levels in diabetic children are affected primarily from changes of plasma viscosity and fibrinogen; and (3) a common mechanism might play a role in the pathogenesis of hypertension in obese and diabetic children.
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PMID:Effects of hemorheological factors on the development of hypertension in diabetic children. 1284 7

Adipose tissue plays an active role in energy balance because it is not only a lipid storing and mobilizing tissue but consists of functionally specialized tissues able to produce heat (in brown adipose tissue) and to produce or release a vast number of so called adipokines or adipocytokines. These consist of polypeptides but also non-protein factors and are metabolically active molecules belonging to different functional categories like immunity (complement factors, haptoglobin), endocrine function (leptin, sex steroids, various growth factors), metabolic function (fatty acids, adiponectin, resistin), and cardiovascular function (angiotensinogen, PAI-1). Recent advances using genomic and proteomic approaches have identified numerous new adipocyte secreted factors whose function remain to be established. Too little as well as too much adipose tissue leads to metabolic disturbances like insulin resistance. Visceral obesity is especially strongly correlated with the development of diabetes, hypertension and cardio-vascular disease. Thermogenesis in brown adipose tissue is a means to dissipate excess energy, but in adult humans brown fat is very scarce and probably not functional. However, human white adipose tissue contains mesenchymal stem cells, and if these could be stimulated to differentiate into brown adipocytes, increased energy expenditure in white fat could help to shift energy balance towards a more negative state.
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PMID:Adipose tissue as a regulator of energy balance. 1505 10

We report the case of a 47-year-old man with the simultaneous occurrence of clinical and laboratory features consistent with acute poststreptococcal glomerulonephritis (APSGN), hemolytic uremic syndrome (HUS), and nephrotic syndrome. Acute nephritic syndrome occurred 3 weeks after having pharyngeal pain and diarrhea. He presented with edema and hypertension on admission. Laboratory evaluation showed hemolytic anemia with fragmentation, thrombocytopenia, elevated lactic dehydrogenase level, low haptoglobin level, low complement C3 level, and elevated antistreptolysin-O titer. Serum creatinine level was 1.22 mg/dL (108 micromol/L), and urinalysis showed marked proteinuria, with protein of 8.7 g/d, and hematuria. The renal biopsy specimen was characteristic of APSGN, but not HUS. Moderate expansion of the mesangial matrix, moderate proliferation of epithelial and endothelial cells, and marked infiltration of neutrophils was seen by means of light microscopy, and many subepithelial humps were seen by means of electron microscopy. Neither fibrin deposition nor evidence of thrombotic microangiopathy was found. Complement C3 deposition along the capillary wall and tubules was seen in an immunofluorescence study. The patient was administered plasma infusion at 320 mL/d and antihypertensive drugs. Serum complement C3 and haptoglobin levels returned to normal within 3 weeks. This is a rare case of the simultaneous occurrence of APSGN, HUS, and nephrotic syndrome.
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PMID:An adult with acute poststreptococcal glomerulonephritis complicated by hemolytic uremic syndrome and nephrotic syndrome. 1618 9

Hypertension has been associated with increased case-fatality rates among individuals who subsequently suffer from acute coronary events. It is unknown whether inflammation modifies this relationship. This population-based study explored the effects of inflammation and hypertension on incidence of coronary event, and on the fatality of the future events. Blood pressure (BP) and five inflammation-sensitive plasma proteins (ISPs, fibrinogen, orosomucoid, alpha 1-antitrypsin, haptoglobin and ceruloplasmin) were determined in 6071 healthy men. During the mean follow-up of 19 years, 679 men had a first coronary event (non-fatal myocardial infarction or death from coronary heart disease). Of them, 197 (29%) were fatal cases (death during the first day). As expected, hypertension was associated with increased incidence of coronary events and increased proportion of fatal cases. At all levels of BP, high ISPs (> or =2 ISPs in top quartile) significantly added to the incidence of events. Men with high ISPs had the highest case-fatality rates. The difference in case-fatality rate between men with and without high ISPs was, however, significant only in men with normal BP (<130/85 mm Hg) (33 vs 19%, P < 0.05), and not in men with moderate or severe hypertension (> or =160/100 mm Hg) (40 vs 35%, P = 0.32). High ISPs add to the incidence of coronary events at all levels of BP. Hypertension and inflammation are both independently associated with increased case-fatality in subjects who later have an acute coronary event. The influence of ISPs on the case-fatality rate seems to be most important in men with normal BP.
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PMID:Fatality of acute coronary events in relation to hypertension and low-grade inflammation: a population-based cohort study. 1667 12

We report a patient with homozygous factor H deficiency leading to permanent alternate complement activation and early onset of the hemolytic uremic syndrome. He was successfully treated with weekly infusions of fresh frozen plasma over 4 years, displaying normal blood pressure while only treated with an angiotensin converting enzyme (ACE) inhibitor, a steady level of haptoglobin, low-range proteinuria and normal creatinine clearance. By the end of the fourth year of treatment, he dramatically developed a relapse of hemolytic and uremic syndrome, displaying undetectable haptoglobin, nephrotic range proteinuria and progressive renal failure. Despite a ten-fold increase in the dosage of plasma infusion through daily plasma exchange, haptoglobin remained undetectable while circulating antigenic factor H levels reached 22-24% (normal values 65-140%). Three months following the biological onset of the relapse, a bilateral nephrectomy was performed owing to uncontrolled hypertension and rapidly progressive renal failure. The molecular mechanism of plasma resistance remained unclear while antifactor H antibodies were not detected in the plasma. We suggest that protracted administration of exogenous factor H might not be a long-term strategy in homozygous factor H deficiency.
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PMID:Secondary failure of plasma therapy in factor H deficiency. 1690 42

The white adipose tissue, especially of humans, is now recognized as the central player in the mild inflammatory state that is characteristic of obesity. The question is how the increased accumulation of lipid seen in obesity causes an inflammatory state and how this is linked to the hypertension and type 2 diabetes that accompanies obesity. Once it was thought that adipose tissue was primarily a reservoir for excess calories that were stored in the adipocytes as triacylglycerols. In times of caloric deprivation these stored lipids were mobilized as free fatty acids and the insulin resistance of obesity was attributed to free fatty acids. It is now clear that in humans the expansion of adipose tissue seen in obesity results in more blood vessels, more connective tissue fibroblasts, and especially more macrophages. There is an enhanced secretion of some interleukins and inflammatory cytokines in adipose tissue of the obese as well as increased circulating levels of many cytokines. The central theme of this chapter is that human adipose tissue is a potent source of inflammatory interleukins plus other cytokines and that the majority of this release is due to the nonfat cells in the adipose tissue except for leptin and adiponectin that are primarily secreted by adipocytes. Human adipocytes secrete at least as much plasminogen activator inhibitor-1 (PAI-1), MCP-1, interleukin-8 (IL-8), and IL-6 in vitro as they do leptin but the nonfat cells of adipose tissue secrete even more of these proteins. The secretion of leptin, on the other hand, by the nonfat cells is negligible. The amount of serum amyloid A proteins 1 & 2 (SAA 1 & 2), haptoglobin, nerve growth factor (NGF), macrophage migration inhibitory factor (MIF), and PAI-1 secreted by the adipocytes derived from a gram of adipose tissue is 144%, 75%, 72%, 37%, and 23%, respectively, of that by the nonfat cells derived from the same amount of human adipose tissue. However, the release of IL-8, MCP-1, vascular endothelial growth factor (VEGF), TGF-beta1, IL-6, PGE(2), TNF-alpha, cathepsin S, hepatocyte growth factor (HGF), IL-1beta, IL-10, resistin, C-reactive protein (CRP), and interleukin-1 receptor antagonist (IL-1Ra) by adipocytes is less than 12% of that by the nonfat cells present in human adipose tissue. Obesity markedly elevates the total release of TNF-alpha, IL-6, and IL-8 by adipose tissue but only that of TNF-alpha is enhanced in adipocytes. However, on a quantitative basis the vast majority of the TNF-alpha comes from the nonfat cells. Visceral adipose tissue also releases more VEGF, resistin, IL-6, PAI-1, TGF-beta1, IL-8, and IL-10 per gram of tissue than does abdominal subcutaneous adipose tissue. In conclusion, there is an increasing recognition that adipose tissue is an endocrine organ that secretes leptin and adiponectin along with a host of other paracrine and endocrine factors in addition to free fatty acids.
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PMID:Release of interleukins and other inflammatory cytokines by human adipose tissue is enhanced in obesity and primarily due to the nonfat cells. 1702 26


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