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Biomedical subjects

S C Textor

Publications and source records attributed to S C Textor.

At least 73 records · Page 4Linked to original sources
PubMed1987

Renal, volume, and hormonal changes during therapeutic administration of recombinant interleukin-2 in man.

Changes in blood pressure, renal function, and fluid balance were studied in 12 patients receiving intravenous recombinant interleukin-2 (IL-2) (100,000 units/kg every eight hours) over five days for treatment of metastatic melanoma and renal and colorectal cancers. The IL-2 regimen produced progressive hypotension, azotemia, and sodium avidity (fractional excretion of sodium = 0.20 +/- 0.07 percent) despite massive fluid administration (mean: 18.4 liter per five days) and weight gain (mean: 4.0 kg). Plasma renin activity rose. Hypoalbuminemia developed rapidly (3.6 +/- 0.1 g/dl to 2.2 +/- 0.1 g/dl, p less than 0.01) with widespread edema formation despite normal central venous pressures. Hematocrit did not change during the IL-2 period, consistent with a "capillary-leak." Hemodynamic and renal functional changes reversed after the IL-2 regimen was discontinued, but hypoalbuminemia and elevated urinary n-acetyl-glucosaminidase levels persisted after six days. These studies demonstrate widespread hemodynamic and vascular effects of IL-2 administration that limit its safe use and suggest a possible role for the lymphokine in mediating cardiovascular instability under other circumstances, such as endotoxic shock.

Adult↗
PubMed1987

Localization of autonomic nervous system dysfunction in dialysis patients.

Autonomic nervous system dysfunction has been described frequently in uremic patients. The purpose of this study is to determine the localization of this abnormality and to study the possible relationship between autonomic dysfunction and the occurrence of dialysis hypotension. Sixteen consecutive patients participated in the study, 5 of whom had a history of dialysis-induced hypotension. These 5 patients were compared to the other 11 as regards the cardiovascular response to isoproterenol infusion, tilt test and arteriovenous (AV) fistula occlusion. None of the responses to the above mentioned stimuli was significantly different between the 2 groups. In the whole study population, an index of parasympathetic control of heart rate (variation of heart period, VHP) was reduced (31 +/- 5 vs. 59 +/- 9 ms in age-matched controls; p less than 0.025). Heart rate and diastolic blood pressure response to isoproterenol infusion was normal (+23 +/- 2 beats/min and -9 +/- 3 mm Hg; p less than 0.005 for both), indicating normal response of effector organs to beta-adrenergic agonist stimulation. Similarly, plasma norepinephrine increased significantly (+294 +/- 51 pg/ml; p = NS from normal laboratory values) in response to head-up tilt, and heart rate increased simultaneously in all but 5 patients. Blood pressure response was within normal after 10 min of head-up tilt at 60 degrees in all but 3 patients; only 1 of these 3 patients was in the group of dialysis hypotension. However, during AV fistula occlusion, heart rate did not change markedly, despite the significant increase in systolic blood pressure, suggesting an altered sensitivity of baroreceptor reflex arc.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Renal hemodynamics in hypertension.

The relationships between systemic arterial pressures, renal blood flow, filtration, and sodium homeostasis are complex. Considerable evidence has accrued indicating that changes in renal sodium handling as a function of perfusion pressure participate in the pathogenesis of hypertension. Central to this viewpoint is the normalization of BP after transplantation of a normal kidney to a hypertensive host, both in animals and humans. Renal blood flow varies inversely with the severity and duration of hypertension. Studies of regional hemodynamics underscore the importance of independent regulation of different vascular beds. Some observations suggest that abnormal renal vascular reactivity may be among the earliest changes in essential hypertension. The degree to which these represent structural changes as opposed to functional responses to endocrine or neurogenic stimuli may vary under different circumstances and merits further study. Although antihypertensive therapy generally has been well tolerated by the kidney, deterioration of renal function has been encountered during pharmacological BP reduction. In the presence of preglomerular arterial disease, blood flow and filtration may become sensitive to hemodynamic fluctuations, which leads to the designation of "critical perfusion pressure." Awareness of the mechanisms by which changes in systemic hemodynamics impinge upon renal function may lead to more rational use of specific antihypertensive agents.

Animals↗
PubMed1986

Nitrendipine, a calcium-entry blocker. Renal and humoral effects in human arterial hypertension.

Thirteen patients with hypertension and normal renal function received nitrendipine, a calcium entry blocker. Nitrendipine did not modify renal blood flow (RBF) or glomerular filtration rate (GFR), decreased mean arterial pressure (MAP) and total peripheral resistance, and did not significantly change cardiac output. Individual RBF changes did not correlate with MAP or cardiac output modifications. Mean arterial pressure changes were inversely correlated with basal renin levels and directly associated with age. Plasma catecholamines and plasma renin activity increased, but plasma aldosterone and plasma volume did not change significantly. However, the greater decrements of MAP tended to be associated with the greater increases in plasma volume. Data show that long-term calcium entry blockade by nitrendipine does not modify RBF or GFR despite the decreased renal perfusion pressure. Further, nitrendipine may be more effective in older patients and the presence of low renin.

Adult↗
PubMed1985

Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease.

We studied renal plasma flow and glomerular filtration rate during graded blood pressure reduction induced with sodium nitroprusside infusion in 16 hypertensive patients with atherosclerotic renovascular disease. Eight patients with unilateral disease tolerated pressure reduction from 205 +/- 9 (SE)/103 +/- 2 mm Hg to 146 +/- 6/84 +/- 3 mm Hg (p less than 0.01) with no change in total renal function. In 8 other patients with bilateral renal arterial stenosis (all arteries 70% or more stenosed), similar pressure reduction produced marked but reversible decrements in plasma flow (152 +/- 28 mL/min to 66 +/- 13 mL/min; p less than 0.01) and glomerular filtration rate (38 +/- 8 mL/min to 16 +/- mL/min; p less than 0.01). In 4 patients restudied after revascularization, sensitivity of renal function to pressure changes was no longer present. These data indicate that vascular stenosis to the entire renal mass may limit function and provide a means for evaluating patients at risk for loss of renal function during antihypertensive therapy.

Aged↗
PubMed1984

Regulation of renal hemodynamics and glomerular filtration in patients with renovascular hypertension during converting enzyme inhibition with captopril.

Changes in regional hemodynamics and function of the kidney during inhibition of angiotensin converting enzyme were studied in 25 patients with renovascular hypertension. A variety of patterns were observed depending upon (1) the activity of the renin-angiotensin system and concomitant administration of diuretics, and (2) the presence of bilateral renal artery stenosis. Increase in blood flow, glomerular filtration rate and sodium excretion during angiotensin blockade, in some instances, indicated tonic renal vasoconstriction before therapy. Release of the kidney from these effects may explain, in part, the sustained effectiveness of converting enzyme inhibition in chronic congestive heart failure. When compared with blood pressure reduction due to nitroprusside administration, initial captopril therapy in patients with unilateral stenosis produced a selective decrease in glomerular filtration, despite well-preserved renal blood flow. These results confirm the importance of efferent arteriolar vasoconstriction due to angiotensin II in man. Experimental studies demonstrate that angiotensin may become critical to sustaining glomerular filtration rate in the presence of stenosis during vasodilation. In patients with bilateral stenosis, this effect produces a syndrome of functional renal insufficiency. Taken together, these data demonstrate an intrarenal action of angiotensin II in human renovascular hypertension and underscore the importance of evaluating the functional impact of changes in regional hemodynamics.

Adult↗
PubMed1984

Pathophysiology of renovascular hypertension.

Studies of the renin-angiotension system and the effects of pharmacologic blockade have enhanced our understanding of renovascular hypertension. A critical degree of arterial stenosis produces kidney ischemia sufficient to activate this hormonal system, whose actions include vasoconstriction and sodium retention. Accurate clinical evaluation may depend upon recognizing the differences in pathophysiology between "one-kidney" and "two-kidney" forms and the dynamic nature of this condition.

Angiotensin II↗
PubMed1984

Clinical and systemic hemodynamic effects of nitrendipine.

The antihypertensive effects of nitrendipine were evaluated in 12 subjects with hypertension, one of whom could not tolerate the drug for more than 3 days; hence hemodynamics were studied in the 11 subjects who were treated for 2 wk. In one patient taking 40 mg twice a day, blood pressure reduction was associated with a hemodynamic pattern of hyperkinetic circulation. Of the other 10 subjects, all of whom were taking 20 mg twice a day, two did not respond, but 8 had significant reduction in mean arterial pressure (136 +/- 4.3 to 106 +/- 3.2 mm Hg) resulting from a decrease in total peripheral resistance (52 +/- 3.7 to 35 +/- 2.6 U X m2). Changes in cardiac output, heart rate, and cardiopulmonary volume varied widely among subjects, such that average changes did not attain significance. Heart rate and cardiopulmonary volume, however, changed in the same direction, which suggests that the alterations in both were related to the degree of reflex sympathetic stimulation induced by nitrendipine. Plasma renin activity (PRA) increased during treatment (2.6 +/- 1.0 to 9.3 +/- 4.1 ng/ml/hr), whereas the increase in plasma aldosterone (PA) levels did not attain significance (13.7 +/- 1.6 to 21.5 +/- 4.5 ng/dl). As a result, PA/PRA decreased (16.1 +/- 4.9 to 9.4 +/- 2.6). These results suggest that calcium entry blockade might have interfered with steroidogenesis, thus blunting the effect of increased PRA. Finally, blood pressure response to nitrendipine in the whole group correlated inversely with pretreatment PRA (r = -0.88), suggesting greater activity of the drug in low-renin hypertension.

Adult↗
PubMed1984

Transient renal dysfunction during initial inhibition of converting enzyme in congestive heart failure.

Treatment with captopril in resistant normotensive congestive heart failure is associated with a pronounced reduction in blood pressure, particularly after the first dose. The effects of this reduction on renal function were assessed in 10 patients at the beginning of and during chronic treatment (at one week and three months). Renal plasma flow and glomerular filtration rates were measured by isotope clearance during water diuresis. The first dose of captopril (25 mg) led to a pronounced fall in renal plasma flow and glomerular filtration rates together with a decrease in mean arterial pressure; this fall correlated with baseline plasma renin activity. These changes were paralleled by decreases in water and sodium excretion. In contrast, by the end of the first week of treatment a similar fall in mean arterial pressure occurred together with a pronounced increase in renal plasma flow; the glomerular filtration rate was maintained and there was no decrease in water and sodium excretion. This new response pattern recurred after three months of treatment. The difference in response at different stages of treatment may reflect the balance between the different mechanisms influencing kidney dynamics in heart failure and their alteration by converting enzyme inhibition. The sustained increase in renal plasma flow during chronic treatment with captopril may account for the continued control of heart failure in these patients.

Adult↗
PubMed1984

Analysis of relative change and initial value in biological studies.

In analyzing longitudinal data, the relationship between initial value (x1) and change in response to a maneuver or over time is often of interest. This relationship is often determined by the Pearson correlation between x1 and subsequent change (x2 - x1), but a correlation will often be obtained by mathematical necessity even when x1 and x2 are uncorrelated. It has been suggested that use of relative change, or (x2 - x1)/x1, avoids these mathematical artifacts. By reference to early work by Pearson (Proc. R. Soc. London 60: 489-498, 1897) on an approximation to the correlation between ratios and by computer simulations, this paper shows that this solution is frequently not valid. An alternative approach to the analysis of the relationship between x1 and relative change is presented and is illustrated by a study of renal blood flow.

Antihypertensive Agents↗
PubMed1984

Revascularization to preserve renal function in patients with atherosclerotic renovascular disease.

There are a significant number of patients with advanced atherosclerotic renovascular disease whose blood pressure is well controlled with medical therapy but in whom such vascular disease poses a grave risk to overall renal function. This article reviews current concepts regarding screening, evaluation, and selection of patients with this disease for revascularization to preserve renal function. The underlying rationale for this approach is an increasing awareness that, in selected patients, atherosclerotic renovascular disease represents a surgically correctable cause of progressive renal failure.

Arteriosclerosis↗
PubMed1983

The changing clinical spectrum of primary aldosteronism.

In a prospective study of 80 patients with primary aldosteronism (70 with adenoma and 10 with hyperplasia), "refractory" hypertension, hyperkinetic circulation, and hypovolemia were frequent occurrences. We found that measurements of serum potassium concentration and plasma renin activity were inadequate screening tests because of high rates of false-positive and false-negative results. The demonstration of excessive aldosterone production after three days of salt loading provided the best sensitivity (96 percent) and specificity (93 percent) in identifying patients with primary aldosteronism. Severe, persistent hypokalemia, increased plasma 18-hydroxycorticosterone values, and an anomalous postural decrease in the plasma aldosterone concentration, when present, provided the best indicators of the presence of an adenoma. Of three localizing procedures (selective adrenal venography, adrenal computed tomographic scan, and adrenal venous sampling for plasma aldosterone concentration) the measurement of adrenal venous plasma aldosterone concentration yielded 100 percent accuracy. These results indicate a wider clinical spectrum in primary aldosteronism than previously described. They also show that nonsuppressible aldosterone production is its most important diagnostic hallmark and the single best diagnostic screening procedure, and that adrenal venous sampling for plasma aldosterone concentration remains the most precise technique for identification and localization of tumors.

Adenoma↗
PubMed1983

Membranous glomerulopathy associated with captopril therapy.

Two cases of nephrotic syndrome and biopsy-proved membranous glomerulopathy (membranous glomerulonephritis) were encountered during captopril treatment of 53 hypertensive subjects in our institution. Both patients had impaired renal function before treatment and were treated with 600 mg per day. Discontinuation of captopril led to transient partial remission of proteinuria but was followed by a recurrent, fluctuating course over one year later. Repeat biopsies, eight and 12 months after discontinuation of the drug, demonstrated persistent subepithelial deposits in the glomerular basement membrane. There has been a decline in glomerular filtration rate since discontinuation of the drug, apparently due to arterionephrosclerosis. These studies suggest that glomerular basement membrane deposits in captopril-associated membranous glomerulonephritis are not readily reversible and may be associated with persistent proteinuria, contrary to some previous reports.

Basement Membrane↗
PubMed1983

Predictive value of angiotensin II blockade with (sarcosine-1, threonine-8) angiotensin II in renovascular hypertension.

Administration of an angiotensin II antagonist, (sarcosine-1, threonine-8) angiotensin II, was used to diagnose renovascular hypertension in 22 patients before renal revascularization or nephrectomy. Positive and negative responses to infusion occurred in 12 and 10 patients, respectively. Postoperatively, hypertension was cured in 13 patients, improved in 6 and unchanged in 3. The over-all accuracy of the infusion test in predicting the outcome of surgical therapy was 59 per cent, the false positive rate was 8.3 per cent and the false negative rate was 80 per cent. A similar high incidence of false negative results has been observed with differential renal vein plasma renin assays. The most accurate prediction of the blood pressure response to surgical therapy is obtained by considering multiple factors rather than a single test.

Adolescent↗
PubMed1983

Renal failure limiting antihypertensive therapy as an indication for renal revascularization. A case report.

Although surgical repair of renal artery stenosis occasionally improves renal function, it is not yet known when revascularization is indicated for that reason. We report the results observed in a patient with renovascular hypertension and additional stenosis in the contralateral kidney whose renal function deteriorated on repeated occasions during antihypertensive therapy. Renal hemodynamic studies during sodium nitroprusside infusion showed severely impaired autoregulation of blood flow, and glomerular filtration rate was corrected after revascularization of the contralateral kidney alone. After surgery, normal BPs were tolerated without loss of function. These findings demonstrate a specific clinical indication for renal revascularization to preserve kidney function.

Antihypertensive Agents↗
PubMed1982

Hyperkalemia in azotemic patients during angiotensin-converting enzyme inhibition and aldosterone reduction with captopril.

Thirty-three hypertensive patients with a wide range of renal function were studied during initiation of angiotensin-converting enzyme inhibition with captopril to evaluate changes in potassium levels concomitant with reduction of aldosterone excretion. Ten patients (Group I) with low levels of plasma renin activity had no change in either aldosterone excretion or potassium during the first week of therapy. Twenty-three other patients (Group II) had decreased aldosterone excretion of an average of 63 percent, often reversing secondary hyperaldosteronism. This was associated with a rise in serum potassium from 3.6 +/- 0.1 to 4.4 +/- 0.1 mEq/liter (p less than 0.001). Serum potassium levels during captopril therapy were inversely related to glomerular filtration rate (creatinine clearance) and transiently exceeded 6.0 mEq/liter in markedly azotemic subjects. Despite rising potassium levels, nine patients had reduced aldosterone excretion to subnormal levels, sometimes for many months. During initiation of converting-enzyme inhibition, potassium-sparing agents and supplements should be discontinued and serum potassium levels should be monitored closely, particularly in patients with imparied renal function.

Adolescent↗
PubMed1981

Evidence for bradykinin potentiation by angiotensin congeners in conscious rats.

It has become increasingly clear that the potent vasoactive peptides bradykinin and angiotensin share a common point of metabolism, i.e., angiotensin-converting enzyme or kininase II, and may interact with prostaglandins to regulate regional blood flow. To establish whether the sensitivity to exogenous bradykinin was affected by the presence of angiotensin, vasodepressor dose-response curves to injected bradykinin were performed in conscious rats before and during a 1-h infusion of angiotensin I (30 ng/min), angiotensin II (30 and 300 mg/min), and [Sar2,Ala8]angiotensin II (5 micrograms/min). All of these induced a parallel leftward shift of the bradykinin dose-response curve of approximately threefold. No similar changes were observed during control infusions of dextrose, similar pressor doses of lysine vasopressin, or norepinephrine. Sensitivity to bradykinin was enhanced by saralasin in normal and nephrectomized rats, suggesting that the antagonist itself was responsible. Similar potentiation was present during both acute (1 h) and chronic infusions (9 days) of angiotensin II and attenuated the effect of a converting-enzyme inhibitor on bradykinin sensitivity. Accordingly, these results suggest a competitive interaction in vivo between angiotensin congeners and bradykinin at a point of bradykinin degradation, probably angiotensin-converting enzyme or kininase II. This is a potential additional mechanism by which these systems may interact to affect regional blood flow and must be considered in the interpretation of results obtained during saralasin infusion.

Angiotensin I↗