PubMed Health⌕ Search

Biomedical subjects

J L Rodicio

Publications and source records attributed to J L Rodicio.

At least 73 records · Page 4Linked to original sources
PubMed1996

Cyclosporine nephrotoxicity and rejection crisis: diagnosis by urinary enzyme excretion.

The urinary enzymes alanine aminopeptidase (AAP; EC 3.4.11.2) and N-acetyl-B-D-glucosaminidase (NAG; EC 3.2.1.30) were measured daily in 35 renal transplant recipients during the early postoperative period. Each peak value of fractional excretion was corrected for its baseline value (CFE). CFE values above normal for both NAG and AAP were more frequently found in episodes of acute rejection than in cyclosporine acute nephrotoxicity episodes (76 vs. 0%; p < 0.001). Consequently, a rise in CFE levels for both NAG and AAP is strongly suggestive of acute rejection crisis.

Acetylglucosaminidase↗
PubMed1996

Aging abolishes the renal response to L-arginine infusion in essential hypertension.

A defect in the endothelium-dependent vasorelaxation could contribute to the development of arterial hypertension through the facilitation of renal vasoconstriction and sodium retention. In this study, we tested the hypothesis that aging impairs kidney function in essential hypertension through a derangement of nitric oxide-dependent renal mechanisms. To this end, we compared the renal response to an intravenous infusion of the precursor of nitric oxide synthesis, L-arginine, in young and aged essential hypertensives. In young hypertensives, L-arginine induced a significant increase in renal plasma flow, glomerular filtration rate, natriuresis and kaliuresis, without changes in filtration fraction. These effects were not observed in aged hypertensives. Neither PRA nor PA were affected by L-arginine infusion in any group. These results indicate that aging produces a derangement of endothelial function in essential hypertension.

Adult↗
PubMed1996

Hypertension, atherosclerosis and microalbuminuria in ELSA. European Lacidipine Study of Atherosclerosis.

Microalbuminuria constitutes a good predictor of cardiovascular risk in general population and also in hypertensive and diabetic patients. This reason led us to consider of interest the measurement of urinary albumin excretion, initially and during the follow-up, in a subset of patients of the ELSA Study. By doing so we will be able to know which is the prevalence of microalbuminuria in the type of patients entering the ELSA Study. The evolution of microalbuminuria with the two different therapies and its correlation with the changes observed by ultrasonography in the carotid wall will also be investigated.

Albuminuria↗
PubMed1996

Renal effects of calcium antagonists with special reference to manidipine hydrochloride.

OBJECTIVE: The aim of this study was to review the effect of the calcium antagonists in general and manidipine hydrochloride in particular on the different renal haemodynamic parameters in experimental animals and human beings. DESIGN: The paper includes data from experimental and human studies performed between 1978 and 1995. RESULTS: As far as renal blood flow and glomerular filtration rate are concerned in experimental animals and in men, manidipine, a long-lasting dihydropyridine calcium antagonist, demonstrated its action not only on the afferent arteriole, as other dihydropyridines, but also on the efferent one. This action, which avoids producing any increase in intra-glomerular pressure and renal damage, would be similar to that of angiotensin converting enzyme inhibitors. The direct natriuretic effect of manidipine, observed also with other dihydropyridines, has been demonstrated by two studies performed in both spontaneously hypertensive and normotensive rats, indicating a direct renal tubular effect. In 5/6 nephrectomized rats treated with manidipine, blood pressure, proteinuria, serum creatinine and glomerular lesions, observed after histological examination, were significantly reduced with respect to control untreated 5/6 nephrectomized rats. Calcium antagonists have demonstrated a clear beneficial effect on renal vasoconstriction induced by cyclosporine therapy in renal transplant patients and in the prevention of acute renal failure secondary to the administration of radiocontrast agents, amphotoricin B, cisplatin and aminoglycosides. CONCLUSIONS: Calcium antagonists are effective drugs for controlling blood pressure and for inducing renal vasodilatation. Manidipine hydrochloride increases renal blood flow and glomerular filtration rate with vasodilation of afferent as well as efferent arterioles, reducing intraglomerular pressure. According to experimental and human studies on renal haemodynamics, manidipine could be used in diabetic nephropathy, glomerular lesions, microalbuminuria and proteinuria.

Animals↗
PubMed1995

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis.

Very few patients with familial hypomagnesemia, hypercalciuria and nephrocalcinosis have been described. Information about clinical course, familial studies or evolution after renal transplantation is very scant. We have studied eight patients with this syndrome who belong to five different families. The mean age at diagnosis was 15 +/- 7 years (5 to 25 years). The primary clinical data were polyuria-polydipsia (8 cases), ocular abnormalities (5), recurrent urinary tract infections (5) and recurrent renal colics with stone passage (2). Bilateral nephrocalcinosis was observed in all cases. Every patient showed hypomagnesemia (1.1 +/- 0.2 mg/dl) with inappropriately high urinary magnesium (Mg) excretions (70 +/- 17 mg/day), Mg clearances (4.4 +/- 1.2 ml/m) and Mg fractional excretions (16.2 +/- 7.1%). Hypercalciuria was present in every case except in those with advanced renal insufficiency. Serum parathormone levels were abnormally high. Serum calcium (Ca), phosphorus and potassium, and urinary excretions of uric acid and oxalate were normal. Neither chronic oral Mg administration nor thiazide diuretics normalized serum Mg levels or urinary Ca excretions, respectively. Follow-up was 6 +/- 4.5 years. Renal function worsened in every case with six patients starting on chronic dialysis after 4.3 +/- 3.8 years. The progression rate of renal insufficiency correlated with the severity of nephrocalcinosis. Five patients have received a kidney graft, and their serum Mg and urinary Ca have always been within normal values after transplantation. Twenty-six members of four of the affected families were studied: none of them showed hypomagnesemia, renal insufficiency or nephrocalcinosis. However, eleven cases (42%) had hypercalciuria and four of them presented with recurrent renal stones. Two family members had medullary sponge kidneys. In conclusion, progression to renal insufficiency is common in this syndrome; oral Mg and thiazide diuretics are ineffective to correct abnormalities. After kidney graft, tubular handling of Mg and Ca was normal. A striking incidence (42%) of hypercalciuria was found in the familial study.

Adolescent↗
PubMed1995

Assessing renal effects and renal protection.

ASSESSMENT OF RENAL FUNCTION: There are a number of methods of evaluating renal function, including measurements of glomerular filtration, renal plasma flow, tubular function, micro- and macroalbuminuria and urinary sediment. Of these, microalbuminuria, glomerular filtration and renal plasma flow are the most appropriate. RENAL EFFECTS OF CALCIUM ANTAGONISTS: Calcium antagonists have important effects on renal function, including a reduction in renal vasoconstriction, increased renal blood flow and, in some circumstances, reduced protein excretion. In particular, these agents can reverse the mild renal vasoconstriction that is seen in the offspring of hypertensive patients. The renal effects of calcium antagonists have been studied in animal models, where radioimaging techniques have shown a biphasic haemodynamic response. RENAL PROTECTION WITH CALCIUM ANTAGONISTS: Two important beneficial effects of calcium antagonists are prevention of acute renal failure and protection against cyclosporin nephrotoxicity. Calcium antagonists have thus been used therapeutically in renal transplant patients and in patients with acute renal failure secondary to the effects of nephrotoxic agents.

Albuminuria↗
PubMed1995

Effects of body-weight loss and captopril treatment on proteinuria associated with obesity.

We have identified 17 obese patients (body mass index, BMI, 37.9 +/- 4.1) with proteinuria > 1 g/day (1.3-6.4 g/24 h, mean 3.1 +/- 1.7). Their age was 34-70 years (48.3 +/- 10); 11 were females and 6 males. Six patients had only one functioning kidney and a sleep apnea syndrome had been diagnosed in 5. Renal biopsies, obtained in 5 cases, showed focal glomerulosclerosis in 2 cases, minimal changes in 2 and mesangial proliferation in 1. Nine patients (group 1) were treated with hypocaloric diets; body weight significantly decreased (BMI 37.1 +/- 3, 34 +/- 3.5 and 32.6 +/- 3.2 at 0, 6 and 12 months, respectively) as well as proteinuria (2.9 +/- 1.7, 1.2 +/- 1 and 0.4 +/- 0.6 g/24 h). There was a significant correlation between body weight loss and decrease in proteinuria (r = 0.69, p < 0.05). Eight patients (group 2) were treated with captopril, without dietary changes. BMI remained stable but proteinuria showed a dramatic decrease, similar to that in group 1 (3.4 +/- 1.7, 1.2 +/- 0.9 and 0.7 +/- 1 g/24 h, respectively). Renal function remained stable in both groups. In summary, both body weight loss and captopril treatment can induce a sharp decrease in obesity-related proteinuria.

Adult↗
PubMed1994

Evaluation of the renal effects of calcium antagonists.

Calcium antagonists exert renal effects consisting mainly of renal vasodilation and facilitation of renal excretion of sodium through a direct action on renal tubules. These effects facilitate the antihypertensive action of this class of drugs and make them suitable for therapy of different forms of human hypertension, including that accompanying chronic renal failure. At the same time, renal vasodilation and enhanced natriuresis could also be of value for correcting the renal defect that initiates essential hypertension. Renal effects of calcium antagonists have also fostered the concept of a renoprotective effect of these drugs in different situations. A demonstration of this concept has been shown in cyclosporine-related nephrotoxicity. Calcium antagonists can improve the short- and long-term prognosis for renal function in human transplantation through their effects in avoiding cyclosporine-induced renal vasoconstriction and in facilitating renal sodium output.

Antihypertensive Agents↗
PubMed1994

Are renal hemodynamics a key factor in the development and maintenance of arterial hypertension in humans?

The kidney plays a key role in the control of body fluids and blood pressure. Evidence has shown that impairment of renal function can lead to the development of arterial hypertension. The regulation of renal blood flow appears to be a key element in the pathophysiology of the hypertensive process, because multiple evidence suggests the existence of a functional enhancement of renal vascular tone in this disorder. The existence of renal vasoconstriction and of an inherited defect in the regulation of renal blood flow has been proposed in the prehypertensive stage. The mechanisms responsible for this alteration include a lack of modulation of the renal vasculature to angiotensin II, increased sympathetic activity, or suppressed renal dopaminergic activity. Established hypertension is characterized by elevated renal vascular resistance, decreased renal blood flow, sustained glomerular filtration rate, and increased filtration fraction. The increase in renal vascular resistance is initially due to elevations in renal vascular tone and is reversible, whereas later it becomes irreversible because of structural changes involved in nephrosclerosis. Antihypertensive drugs are able to decrease blood pressure and to prevent the development of further renal vascular damage independently of variable effects on renal hemodynamics.

Antihypertensive Agents↗
PubMed1994

Relationship between blood pressure and renal function.

RENAL DAMAGE CAUSED BY HYPERTENSION: Renal vasoconstriction seems to be a key factor in the origin of arterial hypertension and accounts for the decrease in renal blood flow commonly observed in patients with hypertension. An inverse correlation has been found between renal blood flow and clinic blood pressure levels in established hypertension. Other features of renal damage attributable to high blood pressure have also been correlated with clinic blood pressure levels. Microalbuminuria is a good example of an alteration in renal function that depends in part on blood pressure levels. EFFECTS OF ANTIHYPERTENSIVE AGENTS: Antihypertensive agents can prevent or ameliorate renal vascular damage secondary to arterial hypertension, including renal failure. Ambulatory blood pressure monitoring is an excellent method of studying blood pressure levels in relation to end-organ damage and the blood pressure response to antihypertensive agents. Preliminary studies using this technique indicate that changes in renal function are closely correlated with the average daily blood pressure in arterial hypertension. CONCLUSIONS: Further studies are needed on the mechanisms of renal deterioration and on how to preserve renal function in arterial hypertension.

Antihypertensive Agents↗