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Biomedical subjects

A Elli

Publications and source records attributed to A Elli.

At least 37 records · Page 2Linked to original sources
PubMed1993

Effect of cyclosporin A on renal cortical resistances measured by color Doppler flowmetry on renal grafts.

Doppler spectra were recorded at different cyclosporin A (CSA) levels (trough and peak) in 30 stable renal-transplanted outpatients: 15 with unimpaired renal function (plasma creatinine < 150 mumol/l) and 15 with renal impairment (plasma creatinine 150-350 mumol/l). Pulsatility (PI) and resistive indexes (RI) have been measured in the renal artery at the hilum and in the renal cortex. RI and PI were markedly increased (p < 0.0001) in the cortex at peak time while in the renal artery no significant changes were observed. These variations were statistically related with CSA blood levels (PI = p < 0.02; r = 0.54, RI = p < 0.05; r = 0.45). These effects were also found in the presence of renal damage. CSA dose-dependently reduces cortical blood flow, causing a persistent arteriolar vasoconstriction and a reduction in diastolic flow. This effect can be measured in man in a noninvasive and repeatable way using color Doppler sonograms.

Adult↗
PubMed1992

Cyclosporine renal cortical vasoconstriction measured by colour Doppler imaging in kidney transplantation.

Important side-effects limit the use of cyclosporine A (CSA), the most insidious of which is nephrotoxicity, which manifests as a preglomerular arteriolar vasoconstriction causing a reduction in glomerular filtration rate (GFR) and renal plasma flow (RPF). This condition is initially purely functional, but with time can become anatomic and irreversible. In clinical practice we lack suitable methods for evaluating CSA vasoconstriction. Our present knowledge is based on indirect information obtained from repeated measurerments of plasma creatinine levels and from blood concentrations of the drug. Sometimes more complex and non-routine tests, such as the evaluation of GFR and RPF, or invasive methods, such as renal biopsy, are also employed. In this study we used the colour-Doppler technique to measure directly the vascular effects of CSA in patients with transplanted kidneys, evaluating changes in blood flow at the hilus and on the cortex of the kidney when the drug was at trough or peak levels.

Adult↗
PubMed1991

Mechanisms of cyclosporine-induced hypertension.

The mechanisms of cyclosporine A (Cs A) nephrotoxicity are not clear, but may be associated with high blood pressure and high serum uric acid levels even when kidney function is still normal. To evaluate proximal tubular resorption and its relationship with erythrocyte cation transport systems that are known to be abnormal in essential hypertension, we measured fractional excretion of endogenous uric acid (FE Ur%) and exogenous lithium (FE Li%), erythrocyte sodium concentration, Na-K pump, Na-K cotransport and Li-Na countertransport in two groups of kidney transplant recipients with normal kidney function (creatinine less than 1.6 mg/dL), one treated with Cs A and steroid (Cs A group) and the other with azathioprine and steroid (Aza group). Patients were matched for sex, body mass index, and age. Antihypertensive treatment was measured using arbitrary scores. Erythrocyte sodium transport systems were similar in the two groups. Despite normal kidney function, the Cs A group had higher blood pressure (mean blood pressure 108.6 +/- 3.1 mmHg vs 98.3 +/- 2.4, p less than 0.01), although taking more antihypertensive treatment, and increased proximal tubular resorption (FE Li%: 12.8 +/- 1.5 vs 20.5 +/- 1.7, p less than 0.001) and global proximal tubular resorption (FE Ur%: 5.2 +/- 0.48 vs 7.09 +/- 0.41, p less than 0.05). These findings may explain the greater prevalence of hypertension in the Cs A group. Increased urate resorption may be involved in interstitial abnormalities, which are the earliest signs of Cs A toxicity. Cs A did not modify erythrocyte ion transport systems.

Absorption↗
PubMed1988

Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria.

Idiopathic hypercalciuria is a common disorder whose inheritance suggests an enzyme abnormality in calcium transport. We measured calcium-magnesium-ATPase activity in erythrocytes from 38 patients (mean age [+/- SEM], 40 +/- 2.1 years) with idiopathic hypercalciuria (24-hour urinary calcium excretion greater than or equal to 0.1 mmol per kilogram of body weight) and a history of multiple calcium oxalate kidney stones. As compared with 41 healthy controls, the patients with hypercalciuria had increased erythrocyte-membrane calcium-magnesium-ATPase activity (64.2 +/- 2.19 vs. 51.6 +/- 1.91 nmol of ATP split per milligram per minute; P less than 0.01) and increased sodium-potassium pump activity (6866 +/- 233 vs. 6096 +/- 228 mumol of sodium per liter of red cells per hour; P less than 0.05). No significant difference between the two groups was found in erythrocyte sodium-potassium cotransport, sodium-lithium countertransport, or potassium content. In 66 patients with kidney stones (38 with hypercalciuria and 28 with normal calcium excretion), 24-hour urinary calcium excretion correlated with calcium-magnesium-ATPase activity (r = 0.46, P less than 0.001). Erythrocyte calcium-magnesium-ATPase activity remained unchanged in eight subjects studied after four months on a low-calcium diet. A study of 30 healthy families found significant correlations between mean values in parents and those in offspring for calcium-magnesium-ATPase (r = 0.68, P less than 0.001) and urinary calcium excretion (r = 0.45, P less than 0.02), with no significant correlations between parents with respect to these measures (r = 0.27 and r = 0.08, respectively). We conclude that abnormalities in erythrocyte calcium-magnesium-ATPase activity may represent an inherited defect in calcium transport related to the cause of idiopathic hypercalciuria.

Adult↗
PubMed1986

High plasma ionized calcium with normal PTH and total calcium levels in normal-function kidney transplant recipients.

Hypercalcemia is a postrenal transplant complication. We found a high frequency of elevated plasma ionized calcium values (65.8%) in 41 normal-function renal graft recipients. In 8 patients increased free calcium was associated with high PTH levels, whereas in 19 PTH was not increased but free calcium was high. In the other 14 patients both free calcium and PTH were in the normal range. The mean transplant duration was different in the three groups: shorter in high PTH patients, longer in normal free calcium patients, intermediate in normal PTH and high free calcium patients. Our findings confirm that a condition of hyperparathyroidism persists in the first post-transplant period, and suggest that this complication evolves towards normalization of the blood chemistry values, passing through a condition of inappropriate PTH secretion with elevated plasma free calcium which in this period is the only marker of parathyroid hyperfunction.

Adult↗
PubMed1986

Cell membrane abnormalities and genetic hypertension.

Evidence indicates that an alteration in kidney function has a causal role in the pathogenesis of hypertension in the Milan hypertensive strain (MHS) rat. At the prehypertensive stage, these animals have increased glomerular filtration rate and 24-hour urinary output, whereas plasma renin activity and urinary kallikrein are lower. After transplantation, the MHS kidney increases the blood pressure of a normotensive recipient. Micropuncture experiments, where single nephron filtration rate, tubuloglomerular feedback, proximal tubular reabsorption, micro-pressures in tubuli, and interstitium and interstitial oncotic pressure were measured, suggest that the intrinsic ability of MHS proximal tubular epithelium to reabsorb solute and water is greater in prehypertensive MHS rats than in Milan normotensive strain (MNS) rats. Also rheogenic Na transport across the brush-border vesicles isolated from proximal tubular cells is faster. When erythrocytes and proximal tubular cells of MHS rats are compared to those of MNS rats, the former have smaller volume and Na content, whereas the Na transport is faster and the Ca ATPase at Vmax is lower. This indicates that the genetic cellular abnormality responsible for the renal functional abnormality and hypertension is also present in erythrocytes. Moreover, MHS erythrocyte abnormalities are genetically determined within the stem cells and are genetically associated with hypertension. Because a correlation was also found in human hypertension between erythrocyte Na transport abnormality and renal function, it is proposed that the erythrocyte may be used for studying the genetic molecular mechanisms of hypertension.

Animals↗
PubMed1986

Effects of captopril and of other antihypertensive drugs on cell membrane ion transport--a preliminary report.

We measured red blood cell Na+-K+ pump, Na+-Li+ countertransport and Na+-K+ cotransport activities, together with intraerythrocyte sodium content before and after 3 months therapy with captopril and two other antihypertensive drugs (atenolol and canrenoate potassium) in subjects suffering from essential hypertension. All patients discontinued any previous treatment at least 3 months before the basal evaluation of cell membrane activities. All three drugs significantly lowered blood pressure but only captopril and canrenoate potassium induced significant modifications in red blood cell parameters. After three months of captopril therapy intraerythrocyte Na+ content was significantly decreased (P less than 0.01) without any detectable change in cation transport system activity. After 3 months of canrenoate potassium therapy we also observed a significant decrease in internal Na content (P less than 0.01), together with a significant increase in Na+-K+ pump (P less than 0.02) and Na+-Li+ countertransport (P less than 0.05) activities.

Adolescent↗