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)

Transgenic mice containing a ren-2 promoter T-antigen fusion construct (TAG+) develop renal vascular hypertrophy and hyperplasia associated with markedly suppressed renal renin mRNA, renal renin content, and plasma renin concentration. These animals are normotensive. In the present study, the renal and cardiovascular systems are characterized, revealing some surprising findings. Not only are the TAG+ mice normotensive in the face of pronounced renal pathology but also in the presence of an increase in plasma volume. These data raise interesting questions about blood pressure physiology and renal function of the TAG+ mice. Blood nitrogen urea of the TAG+ animal was markedly elevated and plasma creatinine level was in the normal range, indicating prerenal azotemia without renal failure. These findings are consistent with impaired renal perfusion with secondary volume expansion probably as the result of vascular hyperplasia. These transgenic animals provide a unique genetic model for studying the physiology of primarily renal vascular hyperplasia as well as blood pressure control in a low renin state.
Hypertension 1991 Jun
PMID:Renin promoter SV40 T-antigen transgenic mouse. A model of primary renal vascular hyperplasia. 204 62

Thrombotic thrombocytopenic purpura (TTP) is a syndrome that occurs mainly in adults with multiorgan microvascular thrombosis consisting of thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, renal involvement, and fever. The female to male ratio is 3:2, and peak incidence occurs in the 3rd decade of life. Clinical signs are the consequence of hyaline thrombosis and occlusion of capillaries and arterioles. Renal ailment manifests itself in hematuria and proteinuria with azotemia and even overt renal failure. In severe disease, azotemia is typical of hemolytic uremic syndrome (HUS). TTP was first described in 1925 by Moschcowitz. The clinical picture of TTP consists of a prodromal phase, a viruslike disease occurring in up to 40% of patients. 60% have neurologic disturbances, 90% have purpura initially, and fever occurs in all. Anemia is often severe with hemoglobin values of 7-9 gm/dl, renal involvement in 90%, and renal failure in 40-80% of patients. Clinical variants include the acute and fulminant variety mortality, the chronic form, and the relapsing form. Predisposing factors and triggering agents are autosomal recessive inherited traits in acute idiopathic TTP, systemic diseases, tumor antigens, pregnancy and puerperium, viruses (endotoxins for HUS), and possibly oral contraceptives and hypertension. Therapy includes corticosteroids (prednisone 100-400 mg/day); heparin for postpartum HUS; and antiplatelet agents (Dextran 70, aspirin, and dipyridamole in high doses). The infusion of PGI2 is controversial; splenectomy is also questionable; and vincristine, azathioprine, and cyclophosphamide have unproven efficacy. Fresh-frozen plasma exchange is the method of choice as it produces survival in 90%. Others are iv immunoglobulins, vitamin E, and dialysis and renal transplant. Platelet transfusions are contraindicated because of sudden death and decreased survival.
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PMID:Thrombotic thrombocytopenic purpura and related disorders. 210 74

Autosomal dominant polycystic kidney disease (ADPKD) is the commonest hereditary nephropathy. We collected 92 cases in VGH. Diagnosis was confirmed by intravenous pyelogram, renal sonogram, or renal CAT scan. The incidence of having positive family history was just only 28.3%. Patients were diagnosed at the mean age of 54 +/- 11 years (26-74 years). The common clinical findings were hypertension (73.9%), abdominal mass, proteinuria, anemia, azotemia, abdominal or back pain and pyuria in orders. Hypertension might present in the early stage with normal renal function (near 40%). Polycystic liver was the major extrarenal lesion (57.6%), but the incidence of abnormal liver function was only 10.1%. Enlarged kidneys were not always palpable, even at end stage of renal function (mean age 56 +/- 9 years, 89.4% kidney palpable). Patient's urine amount was usually nonoliguric, even in uremic stage (82.9%). Sepsis was the first cause of death. Cardiovascular disease and uremia were followed in sequence. Their expired mean age was 61 +/- 7 years (53-74 years).
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PMID:[Autosomal dominant polycystic kidney disease clinical analysis in VGH--Taipei]. 217 45

Angiotensin-converting enzyme inhibitory therapy is widely used to treat hypertension. With long-term use, it is now being shown to have a beneficial effect on renal function and proteinuria in patients with renal insufficiency. When hypertensive patients with renal insufficiency are treated with enalapril, glomerular filtration rate is maintained, effective renal plasma flow is increased, and microalbuminuria and gross proteinuria are reduced. These beneficial renal changes with enalapril therapy differ from those of most other conventional antihypertensive medications. Clinical awareness of potential problems with hyperkalemia and increasing azotemia, particularly in the setting of salt/volume depletion, is important to assure optimal patient management. When these problems occur, they are nearly always reversible by correcting salt/volume status and/or interrupting enalapril therapy.
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PMID:Long-term renal effects of enalapril therapy in patients with renal insufficiency. 218 74

Causes of congestive heart failure include hypertension, coronary artery disease, alcohol abuse and valvular heart disease. Two-dimensional echocardiography with Doppler examination is excellent for identifying valvular heart disease. While noninvasive screening for coronary artery disease may seem cost-effective, the consequences of a missed diagnosis are such that coronary angiography should be strongly considered if there is any suggestion of ischemic heart disease. Medical management primarily consists of vasodilators, diuretics and inotropic agents. Vasodilator therapy may prolong the patient's life. Digoxin and diuretics improve symptoms and hemodynamic abnormalities. With advanced heart failure, adequate control of fluid retention and dyspnea may require diuretic doses associated with azotemia, and systolic blood pressure may have to be maintained at less than 100 mm Hg in spite of postural hypotension.
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PMID:Congestive heart failure. 220 40

Percutaneous transluminal renal angioplasty (PTRA) is a low risk, cost-effective procedure with a high degree of technical and therapeutic success in most categories of renovascular hypertension (RVH) when performed at experienced centers. The role of radiology in screening and diagnosis is discussed with special attention to renal vein sampling for renin assay (RVR) and digital subtraction angiography (DSA). The results of PTRA are compared with surgery. At New York Hospital, PTRA is the procedure of first choice in fibromuscular dysplasia, unilateral nonostial atheroma, arteritis, renal transplantation, and pediatrics. In patients with bilateral and ostial atherosclerotic disease and/or azotemia, the choice between surgery or PTRA depends on the surgical risk category of the patient.
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PMID:Radiologic diagnosis of renovascular hypertension and percutaneous transluminal renal angioplasty. 252 72

Reduction of renal mass (11/12) in rats leads to progressive azotemia, proteinuria, and hypertension. Less extensive renal ablation resulting from uninephrectomy also accelerates the progression of focal glomerulosclerosis (FGS) induced by experimental diabetes, renal irradiation, aminonucleoside nephrosis, or aging. The consequence of the absence of one kidney in man are examined in three different clinical situations. Unilateral renal agenesis seems to predispose to the development of FGS, but most reports include isolated cases and the true incidence of FGS is not known. The solitary kidney following uninephrectomy for acquired unilateral disease undergoes a compensatory rise in glomerular filtration rate (GFR) that remains stable for several decades. Finally, kidney donors followed for over 2 decades show unimpaired GFR, elevated at 70% to 80% of the normal (two-kidney) GFR. Some donors develop mild, nonprogressive proteinuria. Their incidence of hypertension matches that in the control population. Thus, hyperfiltration secondary to 50% reduction of renal mass in humans does not lead to loss of function of the remaining parenchyma.
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PMID:The solitary kidney: a model of chronic hyperfiltration in humans. 277 30

Fifty to sixty percent of clinical hypertension is sensitive to sodium (Na) intake: known causes, primary aldosteronism, bilateral renal artery stenosis, mild azotemia, acromegaly, and low-renin hypertension account for only a fraction. We have identified a group of normal-renin hypertensives characterized by inability to modulate normally their renal vascular and adrenal responsiveness to angiotensin II. These patients handle shifts in Na intake abnormally, show more positive balance on a high-salt diet, and raise their blood pressure when shifted to a high-salt diet. Renal blood flow does not shift with Na intake, but does respond strikingly to converting enzyme inhibition, which also corrects altered renal and adrenal responsiveness, ability to handle a sodium load, and hypertension. These patients have a striking family history of hypertension; 50% of the offspring of hypertensives show similar features, including a renal vasodilator response to converting enzyme inhibitors or calcium channel blocking agents. Accumulating evidence suggests that the abnormality is inherited and may be the most common form of hypertension.
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PMID:Sodium-sensitive hypertension. Implications of pathogenesis for therapy. 267 76

Fifty-six patients with acute glomerulonephritis were studied prospectively during 1984. Their ages ranged from 10 months to 14 years old with the peak age range between 5 to 9 years. Most of them had edema, hypertension, hematuria with or without proteinuria and had low serum complement. Azotemia was found in 45 per cent of the cases. Serologic evidence for streptococcal infection was positive in 68 per cent and only 6 per cent had positive culture. Edema and hypertension were all resolved within 2 weeks. All patients that were followed up had normal serum complement by the 6th week, normal BUN, Scr by one year. The hematuria disappeared by 6 months and proteinuria by 2 months in 50 per cent of the cases. By the 4th year only one patient had microscopic hematuria and mild proteinuria with normal serum creatinine, normotension and no edema. In conclusion, in Thailand AGN is still a common kidney disease in children but with prompt and proper treatment its prognosis is still very good.
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PMID:Acute glomerulonephritis in children: a prospective study. 273 44

The chemistry, pharmacology, pharmacokinetics, clinical use, adverse effects, and dosage of lisinopril are reviewed. Lisinopril, a new nonsulfhydryl angiotensin-converting-enzyme (ACE) inhibitor, is absorbed in its active form. Like the other ACE inhibitors, it lowers peripheral vascular resistance, with a resultant decrease in blood pressure. Approximately 29% of lisinopril is absorbed after oral administration. No measurable metabolism occurs, and excretion is primarily renal. Accumulation of lisinopril occurs in patients with renal dysfunction; however, dosage adjustment is necessary only when the creatinine clearance is less than 30 mL/min. Lisinopril has been shown to be an effective antihypertensive agent at doses of 10 to 80 mg given once daily in patients with essential and secondary hypertension caused by renal artery stenosis. The effectiveness of lisinopril is comparable to that with diuretics, beta blockers, and calcium-channel antagonists. In patients who are unresponsive to maximal doses of lisinopril alone, addition of another antihypertensive agent may be beneficial. Limited information suggests that lisinopril may be comparable to captopril for the treatment of congestive heart failure. Adverse effects associated with lisinopril are relatively minor and are comparable to those associated with enalapril. Hematological abnormalities have not been reported with lisinopril. Class-related adverse effects include cough, azotemia, angioedema, hypotension, and hyperkalemia. Lisinopril appears to be comparable to other ACE inhibitors for the treatment of hypertension and may be as effective as its predecessors for the treatment of congestive heart failure. Further study is needed to better define a therapeutic niche for lisinopril.
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PMID:Lisinopril: a nonsulfhydryl angiotensin-converting enzyme inhibitor. 285 60


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