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)

ACTION OF CALCIUM ANTAGONISTS: In patients with chronic renal failure, controlling hypertension is an integral part of the therapeutic scheme aimed at preventing further degradation of renal function. Hypertension accelerates such degradation and inversely the renal disease aggravates hypertension. Normal blood pressure is thus crucial. Several studies have elucidated the action of calcium antagonists in these patients. KIDNEY TRANSPLANT RECIPIENTS: Calcium antagonists have several highly favorable effects on the transplanted kidney. These effects are explained by the attenuation of the ischemic effects of cyclosporin on the kidney. These patients should be given a calcium antagonist which does not raise the serum level of cyclosporin. DIABETIC NEPHROPATHY: In acute regimens, all calcium antagonists do not appear to have the same effect in patients with diabetic nephropathy. With the notable exception of nifedipine, calcium antagonists can lower acute proteinuria in these patients. Three controlled sudies conducted for more than 6 months have shown that the proteinuria lowering effect of calcium antagonists is equivalent to that of CEIs. Combined CEI and a calcium antagonist is probably the prescription of choice for these patients. Besides the antihypertensive synergism, this combination reduces the side effects of each class prescribed alone. In addition, there is experimental evidence supported by several clinical trials showing an improved nephroprotector effect compared with single prescription of each drug class alone. MECHANISMS OF NEPHROPROTECTION: Chronic renal failure results form intricated hemodynamic and cellular mechanisms. A lower intraglomerular hydrostatic pressure is a crucial element in nephroprotection. All the intrarenal effects of calcium antagonists have not been identified. Certain effects concern preglomerular vasodilatation alone while others have pre- and post-glomerular effects and thus have a potentially greater nephroprotector effect.
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PMID:[Nephro-protective effect of calcium antagonists]. 1054 2

We report a case of a renin secreting tumor, which is a very rare cause of secondary high blood pressure. A 22-year-old woman was hospitalised for exploration of high blood pressure (160/110 mmHg) with severe hypokaliemia (2,7 mmol/l) and secondary hyperaldosteronism. Physical examination was normal except the high blood pressure. Bioassays show increased kaliuresis (66 mmol/24h), plasma renin (89 pg/ml in clinostastism--108 pg/ml in orthostatism), pro-renin (1207 pg/ml in clinostastism--1412 pg/ml in orthostatism) and aldosterone (210 pg/ml in clinostastism--566 pg/ml in orthostatism). The rest of the endocrine tests were normal (cortisol and ACTH at 8:00 am, urinary free cortisol, overnight 1 mg dexamethasone suppression test). Doppler ultrasound method, performed by an experienced radiologist, did not show renal artery stenosis. Abdominal computerized tomography showed a nodular formation at the upper pole of the right kidney, isodense to renal medullary. The size tumor was 15 mm. The renal vein sampling shows high values of renin on both sides whereas, for the pro-renin, the values were higher on the tumor side. In spite of treatment with CEI (Converting Enzyme Inhibitors) and calcium antagonists, the blood pressure was not controlled. Hypokaliemia persisted (3 mmol/l) in spite of high daily potassium intake (64 mmol/l of potassium chloride). After tumor resection, reninoma was diagnosed by the pathology examination and blood pressure, plasma rennin, plasma aldosterone level returned to normal.
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PMID:[Reninoma: a rare but curable cause of high blood pressure, a case report]. 1291 61

Diabetic nephropathy (DN) is the most common cause of chronic renal failure (CRF), in Mexico prevalence of diabetes is higher than other countries. Genetic susceptibility, arterial hypertension, proteinuria and initial hyperfiltration are risk factors for CRF. Renal injury is mediated by protein glycation, proteinuria and hemodynamics alterations induced by arterial hypertension and impaired renal autoregulation. Angiotensin II is directly involved in renal injury through its hemodynamic effects, oxidative stress, induction of proinflammatory and profibrotic factors and cellular proliferative effect. Prospective, well controlled clinical trials in patients with type 1 and type 2 DM have shown that interrupting the renin angiotensin system with CEI or ARA effectively prevent progression of DN. Combination of both drugs may provide further nephroprotection. Antihypertensive therapy in patients with DN must include CEI or ARA and to reduce BP below 130/85 mmHg and if proteinuria is present, under 120/75.
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PMID:[Arterial hypertension and diabetic nephropathy. Evidence based therapy]. 1296 48


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