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Biomedical subjects

L M Ruilope

Publications and source records attributed to L M Ruilope.

At least 163 records · Page 9Linked to original sources
PubMed1991

Nephrotic proteinuria without hypoalbuminemia: clinical characteristics and response to angiotensin-converting enzyme inhibition.

Although hypoalbuminemia is a fundamental characteristic of nephrotic syndrome (NS), there are many patients with massive proteinuria that do not develop hypoalbuminemia. We have studied the clinical and biochemical characteristics of 19 patients with persistent massive proteinuria (greater than 5 g/d) and normal serum albumin (group I) in comparison with 16 patients with similar proteinuria excretion, but persistent hypoalbuminemia (group II). Most of group I patients had diagnoses suggesting glomerular hyperfiltration (focal glomerulosclerosis [FGS] associated with vesicoureteral reflux [VUR], reduction of renal mass, proteinuria associated with obesity, sclerotic phase of idiopathic crescentic glomerulonephritis [GN] in contrast with those of group II, in which membranous GN was the most frequent diagnosis. We prospectively investigated differences in the antiproteinuric effect of captopril, an antiotensin-converting enzyme inhibitor (ACEI); after 6 months of treatment, proteinuria decreased clearly in group I (7.1 +/- 1.7 to 3.7 +/- 1.7 g/d; P less than 0.001), whereas no significant changes were observed in group II (8.1 +/- 2.4 to 8.8 +/- 4 g/d). Serum creatinine (Scr) remained stable during captopril treatment in group I, whereas three patients in group II showed a worsening of renal function.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1991

A single mechanism to explain the effect of calcium on renal function.

It is known that calcium induces the formation of potent vasodilators in endothelial cells and vasoconstriction in smooth muscle cells, whereas in the renal parenchyma, it modulates sodium excretion through vascular and tubular mechanisms. Consequently, an increased concentration of calcium in renal circulation may induce a sequence of contrasting hemodynamics and excretory effects depending on the threshold of a particular mechanism that is first being stimulated. In order to identify this sequence of responses and their respective thresholds, we infused into the renal artery of anesthetized dogs progressively increasing doses of calcium gluconate that ranged from 1 to 400 micrograms/kg/min. The administration of 1, 10, and 100 micrograms/kg/min of calcium gluconate was followed by a significant increase in urinary excretion of PGE2 and 6-keto-PGF1 alpha and by a marked diuresis and natriuresis without altering renal blood flow (RBF) or glomerular filtration rate (GFR). Renin release was increased by 80% only during the infusion of the 10 micrograms/kg/min dose. The intrarenal infusion of a 400 micrograms/kg/min dose of calcium produced marked decreases in RBF and GFR, while urine sodium excretion (UNaV), UPGE2V, and U6-keto-PGF1 alpha V continued and were markedly elevated. During all these maneuvers, mean arterial pressure remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Tolerance to nitrendipine in patients with arterial hypertension accompanying chronic renal failure.

To test the tolerance to nitrendipine in arterial hypertension secondary to chronic renal parenchymatous disease, a group of 10 patients so diagnosed and adequately controlled with a diuretic alone or with a beta-blocker were switched to nitrendipine at a dose to insure similarly adequate control of blood pressure. Patients were followed for 1 year at monthly intervals during which blood pressure measurement and the determination of a biochemical profile were performed. During the follow-up, nitrendipine adequately controlled blood pressure and a significant fall was observed in hematocrit (p less than 0.05) and serum uric acid (p less than 0.01) values. Meanwhile, the glomerular filtration rate, determined by the creatinine clearance, did not exhibit significant changes nor did the 24-h urinary excretion of proteins. The tolerance of the drug was adequate, with two patients presenting minimal ankle edema. These results seem to indicate that nitrendipine can be safely used in patients with arterial hypertension secondary to chronic renal parenchymatous disease.

Adult↗
PubMed1991

Renal effects of nitrendipine.

Calcium-entry blockers exert several characteristic effects on the kidney that potentiate their antihypertensive effect. Long-term therapy with nitrendipine, a dihydropyridine derivative, lowers blood pressure while maintaining renal hemodynamics within limits similar to pretreatment values in essential hypertension with normal renal function. This is accompanied by a persistent natriuretic effect that probably facilitates its antihypertensive action and is not followed by changes of the renin-angiotensin-aldosterone system. Preliminary data also seem to indicate that nitrendipine could be safely used in patients with arterial hypertension and chronic renal failure.

Blood Pressure↗
PubMed1990

Long-term diuretic therapy and renal function in essential arterial hypertension.

One of the main objectives of antihypertensive therapy is to preserve renal function from the deleterious effects of elevated blood pressure. Diuretics alone or in combination are effective for the treatment of arterial hypertension. Nevertheless, their use is accompanied by unwanted biochemical side effects, which have been attributed to their renal effects. During the last 10 years a group of 211 patients, diagnosed as having essential hypertension, were followed up. During the follow-up, they received a stepped-care therapeutic regimen consisting of nonpharmacologic measures (group 1), hydrochlorothiazide and amiloride (group 2), propranolol (group 3) and, if necessary, hydralazine (group 4). During the study, blood pressure remained within comparable, well-controlled levels in the 4 groups of patients. A progressive elevation of the levels of total serum cholesterol and glucose was observed in every group. The elevation attained statistical significance (p less than 0.01) after 4 years of therapy in those groups receiving the diuretic alone or in combination. Nevertheless, after 8 years of follow-up, the increment observed in these 2 parameters did not differ when patients in group 1 were compared with those in the remaining groups, indicating that thiazide diuretics could contribute to the earlier appearance of forthcoming events. Serum potassium levels were significantly lower (p less than 0.01) in groups 2 and 3 than in group 1. At the same time, we have observed the progressive appearance of clinically relevant proteinuria in 15.2% of patients, and the range of protein excretion ranged from 350 to 3,700 mg/24 hours. The appearance of proteinuria did not depend on the lack of control of blood pressure, nor on the different therapeutic requirements but was accompanied by a progressive decrease in creatinine clearance. The consequences of the renal effects of diuretics are of great importance during long-term therapy. The present results indicate that diuretics preempt the appearance of a forthcoming increase in serum glucose and cholesterol, and lessen the clinical relevance of these events.(ABSTRACT TRUNCATED AT 250 WORDS)

Diuretics↗
PubMed1990

Renal effects of calcium entry blockers.

Calcium entry blockers exert several characteristic effects on renal function that contribute to their blood-pressure lowering capacity. They are able to dilate renal vasculature and, in certain circumstances, can increase the glomerular filtration rate, both effects being dependent on the preexisting vascular tone. Calcium blockers are also able to increase renal sodium excretion, mainly through a direct tubular effect that remains during the chronic administration of these drugs. These effects clearly differentiate calcium entry blockers from nonspecific vasodilators and contribute to their effectiveness when they are used as first-step drugs in the therapy of arterial hypertension.

Calcium Channel Blockers↗
PubMed1990

Does an adequate control of blood pressure protect the kidney in essential hypertension?

We analyzed the clinical course of 120 patients who were diagnosed as having primary hypertension and subsequently given standard stepped-care therapy (diuretic, beta-blocker and vasodilator) for 9 years. At the end of the follow-up period, 21 patients (17.5%) had developed overt proteinuria. The initial study showed no difference in systolic blood pressure, age, sex, serum creatinine and its clearance, glucose, cholesterol and triglycerides between these patients and those who had not become proteinuric, but uric acid levels and diastolic blood pressure were higher (both P less than 0.01). An adequate control of blood pressure was obtained and maintained in all patients, who had similar therapeutic needs. During the follow-up period, uric acid levels remained significantly elevated (P less than 0.01) in the proteinuric patients, while changes in serum glucose, cholesterol and triglycerides were similar in all patients. These results indicate that long-term treatment of primary hypertensives does not fully protect kidney function and that initially elevated uric acid levels could be a predictor of a poor prognosis.

Adrenergic beta-Antagonists↗
PubMed1990

[Differential diagnosis of secondary arterial hypertension].

The adequate performance of the differential diagnosis will permit us to classify any increase in blood pressure as due to primary or secondary causes. The data obtained in the clinical history and physical examination as well as those obtained through the minimal laboratory tests to be performed are the clues to identify secondary causes of arterial hypertension.

Blood Pressure↗
PubMed1989

[Treatment of arterial hypertension in the aged].

The response to different therapeutic schedules in arterial hypertension in the elderly is studied and compared with response to treatment in younger patients. Blood pressure in the elderly was best controlled with non pharmacologic measures and low doses of diuretics; there were no differences between both groups with respect to complications and side effects. The response to angiotensin-converting enzyme inhibitors is also evaluated, presenting good results on blood pressure control without side effects in the elderly, although efficaciousness was higher in younger patients. The possible therapeutic schedules in arterial hypertension in the aged are discussed.

Age Factors↗
PubMed1989

Converting enzyme inhibition in chronic renal failure.

Ten patients with chronic renal failure whose hypertension was controlled with triple drug therapy consisting of propranolol-hydralazine-furosemide were switched to the angiotensin-converting enzyme (ACE) inhibitor captopril for a period of 12 months. Control of hypertension was similar with both antihypertensive regimens. Clearance of inulin and of paraaminohippuric acid increased during the first 3 months of captopril therapy and remained stable thereafter. Moreover, the decline in the reciprocal of serum creatinine over time observed during triple drug therapy was arrested during therapy with the ACE inhibitor. If the salutary effects of captopril are sustained, the results obtained in the current studies would suggest that control of hypertension by ACE inhibition may be effective in slowing progression of renal failure. Future studies to answer this important question are necessary.

Adult↗