Biomedical subjects
Publications and source records attributed to J L Rodicio.
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OBJECTIVE: To compare the effects of standard therapy (diuretic, beta-blocker or both) with those of angiotensin converting enzyme (ACE) inhibition with quinapril on renal function and urinary albumin excretion in patients with essential hypertension. METHODS: A 1-year, placebo-controlled, randomly allocated study was conducted in a group of 40 patients with essential hypertension. Before beginning the active treatment phase, all patients were given a matched placebo for quinapril for at least 14 days. At baseline and after 1, 3, 6 and 12 months of treatment, blood pressure, heart rate, body weight, renal plasma flow, glomerular filtration rate, plasma renin activity, plasma aldosterone and urinary albumin excretion were measured. RESULTS: Both the standard therapy and quinapril produced similar decreases in blood pressure, but only quinapril produced a significant decrease in micro-albuminuria, from 68.5 +/- 16.7 to 47.2 +/- 14.9 mg/24 h (P < 0.05). The renal plasma flow remained constant in both study groups while the glomerular filtration rate and filtration fraction decreased significantly (P < 0.05) in the quinapril group. CONCLUSIONS: The results of this study indicate that long-term therapy for essential hypertension with ACE inhibition has a more favorable effect on micro-albuminuria than standard therapy for an equal level of blood pressure control.
Established essential hypertension is characterized by normal equilibrium between the intake and renal excretion of sodium. Urinary sodium excretion is interrelated with that of other ions, such as potassium and calcium, and that the response of blood pressure to salt ingestion can be conditioned by the simultaneous intake of varying levels of those ions. The authors address three aspects: the correlations between urinary excretion of sodium and calcium and sodium and potassium in a population of untreated essential hypertensive persons, the response of blood pressure during the escape induced by exogenous mineralocorticoid administration in mild essential hypertension, and the effect of intravenous calcium gluconate infusion on sodium excretion and renal function. The first part shows that sodium excretion is closely correlated with that of other ions in essential hypertension, and the second part shows that, to escape from the sodium-retaining effect of a mineralocorticoid, mild hypertensive subjects must have increased blood pressure within or near the cutoff point that defines salt sensitivity. Of interest, the elevation in blood pressure takes place while sympathetic nervous activity is blunted. The third part provides evidence to explain one of the mechanisms by which calcium influences renal function and enhances renal sodium excretion. The intrarenal effects of low doses of calcium are dependent on the renal production of prostaglandins.
AIM: To review the renal benefits of calcium antagonists. METHODS: Review of published studies. RESULTS: Both experimental and clinical studies have indicated that, apart from being highly potent antihypertensive agents, calcium antagonists may also provide tissue protection and preservation. In three well defined clinical situations, the use of calcium antagonists has proved to be of value. First, in acute renal failure we and others have shown that the administration of dihydropyridine or diltiazem can, by preventing an intracellular calcium overload, avoid the renal damage induced by the use of a radiographic contrast agent. Second, in chronic renal failure, the administration of a calcium antagonist has been shown to be safe and at least similar in efficacy to other commonly used antihypertensive drug classes. Third, in renal transplant patients, calcium antagonists have been shown to prevent both acute and chronic cyclosporin nephrotoxicity. Calcium antagonists have a clear advantage in the case of acute toxicity because they allow faster renal function recovery and a shorter hospitalization time. The mechanisms by which this class reduces cyclosporin toxicity may be related to a reduction in the calcium influx into cells during ischaemic and reperfusion periods, which would reduce the generation of oxygen-free radicals and perhaps reduce thromboxane production. CONCLUSIONS: Calcium antagonists have potential renal protective effects that favour their use in many clinical situations where renal function is impaired.
Proteinuria (protein excretion > 300 mg/d) is an independent risk factor for the development of cardiovascular disease and renal failure. The finding of persistent proteinuria in otherwise asymptomatic patients often precedes the development of arterial hypertension and renal failure. When proteinuria is accompanied by arterial hypertension, blood pressure control can decrease the quantity of protein excretion but not the incidence of proteinuria. In this sense, converting enzyme inhibitors seem to possess a higher capacity to reduce proteinuria. Nevertheless, the effects of reducing proteinuria on renal function and cardiovascular risk remain to be elucidated. Microalbuminuria (urine albumin excretion oscillating between 30 and 300 mg/d) seems to be a predictor of cardiovascular disease in diabetic and nondiabetic subjects and has been established as a predictor for the development of diabetic nephropathy. Blood pressure levels and urinary albumin excretion correlate positively, and antihypertensive therapy of any kind decreases the quantity of albumin present in the urine. The role of increased albumin excretion in essential hypertension and in renal failure remains to be elucidated.
Accidental hypothermia is defined as a spontaneous decrease in core temperature to 35 degrees C or below. Several techniques of active core rewarming have been described. We present the case of a 34-year-old man with severe hypothermia (27 degrees C) caused by cold environment exposure and barbiturate intoxication treated with general supportive measures and active core rewarming with hemodialysis. Core temperature increased by 2.15 degrees C/h with hemodialysis and became normal in 4 h. The clinical situation clearly improved during the hemodialysis session and the patient recovered without any defect. Hemodialysis is a rapid and effective treatment for accidental hypothermia.
A 66-year-old woman presented a spastic quadriparesis due to compression of the cervical cord 6 years after the beginning of chronic hemodialysis. Five years later, she developed a second episode of compressive myelopathy affecting the lumbar spine. On both occasions, surgical laminectomy with removal of fibroligamentous rings that compressed the cord led to a total recovery of the patient. Histological study demonstrated the presence of massive amyloid deposits in the surgically excised material.
Angiotensin-converting enzyme inhibitors are nowadays widely employed for the treatment of arterial hypertension. They exhibit comparable levels of efficacy and better tolerability when compared with the other antihypertensive agents. In mild arterial hypertension they have been shown to be more efficacious than nonpharmacological therapy that is recommended as the first-step therapeutic approach for most cases of this type of hypertension. Potential advantages for the control of associated metabolic risk factors and specific renal and cardiac effects make these drugs suitable for the first step pharmacological therapy on mild hypertension.
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AIM: To review cyclosporin nephrotoxicity and its prevention by calcium antagonists. METHOD: Review of published and unpublished studies. RESULTS: Cyclosporin A nephrotoxicity is the most important side effect of this potent immunosuppressive drug. Several mechanisms have been implicated in the production of this adverse effect but elevated endothelin release is perhaps the most frequently cited cause. Calcium antagonists have demonstrated a beneficial effect in preventing cyclosporin A nephrotoxicity in renal cadaveric transplants, during both short- and long-term follow-up. Lacidipine, a lipophilic dihydropyridine calcium antagonist, prevents the reductions in the glomerular filtration rate and renal plasma flow that are often seen after cyclosporin A administration. This effect is not related to endothelin suppression. CONCLUSIONS: Calcium antagonists can provide renal protection in patients who undergo renal cadaveric transplantation and are treated with cyclosporin.
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Angiotensin-converting enzyme inhibitors (ACEI) can reduce proteinuria in diabetic and nondiabetic nephropathy. However, no studies have determined whether this antiproteinuric effect modifies the progression of renal insufficiency. We studied the evolution of 46 nondiabetic patients with nephrotic proteinuria treated with captopril for a minimum of 12 months. The follow-up period before captopril treatment was 12 to 18 months. At the end of follow-up, after captopril introduction (24.4 +/- 7.6 months), proteinuria had decreased from 6.3 +/- 2.5 to 3.9 +/- 3.1 g/24 h (P less than 0.001), with a mean decrease of 45% +/- 28%. The proteinuria decrease was higher in patients with reflux nephropathy, proteinuria associated with reduction of renal mass, inactive crescentic glomerulonephritis, nephroangiosclerosis, and IgA nephropathy, whereas patients with membranous glomerulonephritis and idiopathic focal glomerulosclerosis showed a poorer response. Patients were separated according to a proteinuria reduction greater (group A, 23 patients) or lower (group B, 23 patients) than 45% of the initial value. At the end of follow-up, renal function had not significantly changed in group A with respect to values at the start of treatment: serum creatinine (SCr) was 229 +/- 167 mumol/L (2.6 +/- 1.9 mg/dL) versus 203 +/- 97 mumol/L (2.3 +/- 1.1 mg/dL), and creatinine clearance (CrCl) was 0.80 +/- 0.52 mL/s (48 +/- 31 mL/min) versus 0.87 +/- 0.47 mL/s (52 +/- 28 mL/min). The slope of the reciprocal of Scr (1/SCr) showed a significantly beneficial change after captopril introduction.(ABSTRACT TRUNCATED AT 250 WORDS)
The hypothesis that converting enzyme inhibition and a protein-restricted diet could have additive antiproteinuric effects has been tested. A group of 17 patients with proteinuria in excess of 3 g/24 h per 1.73 m2 of body surface area were submitted to a 3-wk period of study, after a 4-wk wash-out period during which protein intake was 1.0 g/kg per day and in the absence of any medication. During the first and second weeks of the study, protein intake was lowered to 0.3 g/kg per day, and in the third week, it returned to 1.0 g/kg per day. Enalapril (20 mg daily) was administered during the second and third weeks of the study. Initially and at the end of each week thereafter, we determined blood pressure, GFR (inulin clearance), RPF (para-aminohippurate clearance), plasma sodium and potassium, PRA and aldosterone, and the 24-h urine excretion of sodium potassium, protein, and urea. The low protein intake during the first week induced a significant fall of proteinuria (P < 0.01), GFR (P < 0.01), and RPF (P < 0.01) in the absence of changes in filtration fraction. The addition of enalapril induced a further decrease of proteinuria (P < 0.01) and a fall in filtration fraction (P < 0.05), whereas plasma potassium, PRA, GFR, and RPF values increased (P < 0.01). The rise in protein intake during the last week of the study induced a significant rise in proteinuria, GFR, and RPF (P < 0.01), although the first of these parameters attained values significantly lower (P < 0.05) than those observed initially.(ABSTRACT TRUNCATED AT 250 WORDS)
Information is limited regarding the efficacy of antihypertensive drugs in patients with hypertension associated with renal insufficiency. To address this question, a group of 14 outpatients with essential hypertension and mild renal insufficiency received slow release verapamil 240 mg/day for 14 days after a 4-week washout period. Patients were randomly assigned to a low (4 g/day) or high (11 g/day) salt diet, and crossed over to the alternative diet after 7 days. 24-Hour blood pressure monitoring was performed at the end of the washout period and after 7 and 14 days during verapamil treatment. Verapamil induced a significant fall in mean 24-hour blood pressure that was similar for patients on both diets (p < 0.01). As expected, natriuresis increased significantly during high sodium intake (p < 0.01), and bodyweight fell significantly when sodium intake was reduced (p < 0.05). Meanwhile, serum creatinine and creatinine clearance remained stable. These results indicate that the antihypertensive effect of verapamil is independent of sodium intake even in the presence of mild renal insufficiency.
The calcium antagonist verapamil has been demonstrated to be effective in reducing hypertension in patients in whom sodium intake was not restricted. The present study evaluated the effect of verapamil in reducing hypertension in patients with chronic renal failure on low or high sodium diets. Also, the present study evaluated the effect of verapamil on proteinuria in chronic renal failure patients who were administered a normal and low protein diet. The results reveal that verapamil-SR 240 mg daily is effective in reducing hypertension in patients with chronic renal failure and the effect of verapamil is equal in patients on a high or low sodium intake. In addition, verapamil-SR 240 mg daily is effective in maintaining reduced proteinuria in chronic renal failure patients on low protein diet and may prevent proteinuria in such patients on a normal protein diet. Therefore, verapamil-SR 240 mg daily appears to be an excellent choice for the treatment of hypertensive chronic renal failure patients.
AIM: To seek ways of improving the prognosis for renal function in the presence of arterial hypertension. BACKGROUND: Nephrosclerosis is a term used to define the renal damage induced by arterial hypertension. The renal vasculature can participate in the genesis of essential hypertension and can suffer the consequences of elevated blood pressure. There is no doubt that antihypertensive therapy has dramatically improved the prognosis for renal function in the presence of arterial hypertension. RESULTS OF LITERATURE REVIEW: There appears to be a need for a further improvement in the prognosis for renal hypertension. At present, the prevalence of nephrosclerosis as a cause of terminal renal failure may be increasing and a progressive fall in renal function in treated hypertensive patients compared to normotensives has been described. CONCLUSIONS: It is not yet clear whether improvements in renal hypertension depend merely on the effectiveness of antihypertensive therapy in reducing arterial blood pressure or whether it will be necessary to improve the metabolic disturbances that accompany hypertension or the renal hemodynamic effects of different drugs before the prognosis for nephrosclerosis can be improved.