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Biomedical subjects

E J Mees

Publications and source records attributed to E J Mees.

At least 19 recordsLinked to original sources
PubMed2004

[Diabetic nephropathy: the role of blood pressure and extra-cellular volume in its pathogenesis and treatment].

Hypertension is an important risk factor for the development of cardiovascular disease and for the progression of renal insufficiency. In the pathophysiology of hypertension in diabetes mellitus, expansion of the extracellular fluid volume has a pivotal role. Coinciding derangements are probably responsible for this expansion: increased proximal tubular reabsorption, inadequate activation of the renin-angiotensin system and impaired renal autoregulation. Together, these lead to glomerular hypertension and resultant glomerular damage. Many clinical trials emphasise the importance of the renin-angiotensin system in the treatment of diabetics with hypertension. There are strong indications that correction of the excess volume is pivotal in the treatment of hypertension in patients with diabetic nephropathy. However, many recent studies have omitted consideration of the role of extracellular fluid-volume expansion. Many questions remain unanswered about the pathophysiology of hypertension in diabetes mellitus. More insight into the pathophysiology could well result in improved treatment of the hypertension and thus help to delay the progression of diabetic nephropathy.

Blood Pressure↗
PubMed1999

[Epidemic of cardiovascular diseases in patients undergoing chronic hemodialysis; closer attention needs to be paid to volume expansion].

The very high mortality of patients on chronic haemodialysis treatment is mainly due to cardiovascular complications. Despite the fact that some dialysis centres report much better survival by adhering to the long-known principle of volume control, investigators and advisory committees all over the world define 'adequate dialysis' exclusively in terms of removal of 'toxic factors'. Volume expansion leads to hypertension, cardiac dilatation and cardiac failure through a clear pathophysiological sequence. By giving more responsibility to dialysis nurses patients may be helped to regain their 'dry weight'.

Cardiovascular Diseases↗
PubMed1999

Treatment of hypertension in dialysis patients by ultrafiltration: role of cardiac dilatation and time factor.

We retrospectively analyzed the blood pressure (BP) and cardiothoracic index (CTi) of 67 hemodialysis patients with hypertension who could be followed up for at least 8 months. A new treatment policy was adopted, aimed at strict volume control. Dietary salt restriction was strongly emphasized. Ultrafiltration (UF) was applied during regular dialysis sessions and sometimes in additional sessions, as long as BP and CTi remained at greater than normal values. All antihypertensive drugs were discontinued at the beginning of treatment. Average BP decreased from 173 +/- 17/102 +/- 9 to 139 +/- 18/86 +/- 11 mm Hg after 6 months and to 118 +/- 12/73 +/- 6 mm Hg after 36 months. Corresponding values for CTi were 52% +/- 4%, 47% +/- 3%, and 42% +/- 4%, respectively. Conventional relatively short dialysis (three times weekly for at least 4 hours) can achieve normal BPs with prolonged effort in most patients, whereas improvement in heart condition facilitates this.

Adolescent↗
PubMed1995

Comparison of the effects of enalapril and theophylline on polycythemia after renal transplantation.

Posttransplant erythrocytosis (PTE) is a potentially serious complication for which (apart from phlebotomy) two alternative treatments have been proposed: theophylline (Theo) and angiotensin-converting enzyme inhibitors. We investigated 28 patients with PTE, who were assigned to 3 matched groups. Group 1 (10 patients) received 10 mg of Enalapril (Ena)/day. After 2 months, mean hematocrit (Ht) had dropped from 0.57 (range 0.52-0.62) to 0.45 (0.34-0.49). Ena was stopped and, after a period of 3.8 +/- 0.3 months, Ht had risen again to baseline values (0.56, range 0.52-0.61) in 8 of them. These 8 patients were then given 5 mg/day Ena. Ht decreased more slowly, and after 3 months reached a mean of 0.49 (0.44-0.54). Group 2 (9 patients) received 600 mg/day Theo in 2 doses. After 2 months, Ht had decreased from 0.56 (0.52-0.61) to 0.52 (0.46-0.63), but in 5 patients, Ht remained above 0.51. After 1 month discontinuation of treatment, PTE persisted in 7 patients. These patients were given 10 mg/day Ena, whereupon Ht decreased from 0.55 (0.52-0.64) to 0.46 (0.40-0.53) after 2 months and to 0.41 (0.33-0.47) after 3 months. Group 3 did not receive medical treatment. After 3 months, PTE persisted in 8 out of the 9 patients and remained unchanged during the following 3 months. Mean values for Ht were: baseline, 0.55 (0.52-0.58); after 3 months, 0.56 (0.53-0.59); and after 6 months, 0.55 (0.52-0.60). We conclude that Ena is superior to Theo in the treatment of PTE. There were no resistant patients, but individual sensitivity differs. Its effect is dose dependent, reversible, and reproducible. Excessive Ht decrease may occur; thus, doses should be titrated individually.

Adult↗
PubMed1995

'Paradoxical' rise in blood pressure during ultrafiltration in dialysis patients.

In some hypertensive haemodialysis (HD) patients, blood pressure rises further during ultrafiltration (UF). We investigated seven such patients, who were not responsive to hypotensive drugs, including converting enzyme inhibitors. All had marked cardiac dilatation, but most were non-oedematous. They were treated with repeated intense UF while monitoring cardiac function by echocardiography. After a variable time period they all became (near) normotensive without medication. Mean systolic and diastolic blood pressure decreased by 46 +/- 18 and 22 +/- 9 mmHg respectively while bodyweight decreased by a mean of 6.7 +/- 3.0 kg. Plasma volume decreased by 22%, and mean albumin increased from 3.9 +/- 0.3 to 4.2 +/- 0.3 g/dl. Cardiothoracic index decreased from a 0.56 +/- 0.02 to 0.45 +/- 0.03. Mitral and tricuspid insufficiency was present in four patients and improved or disappeared in all of them. Diameters of the inferior vena cava, left atrium, and end systolic and diastolic left ventricle markedly decreased in all patients. Ejection fraction increased, but remained subnormal in some patients, while cardiac output increased in five and decreased in two patients. We conclude that paradoxical blood pressure rise with UF usually occurs in the presence overhydration and cardiac dilatation and should be treated by intensified UF. The explanation of this phenomenon remains speculative.

Adult↗
PubMed1988

Suppressed diluting segment reabsorption in Bartter's syndrome: studies in 1 patient and synthesis of literature data.

We analyzed renal sodium handling in a patient with Bartter's syndrome after equilibration on diets containing 200 and 700 mmol NaCl/day. No potassium supplements were given. Clearance studies were performed during maximal water diuresis, maximal free water clearance was taken as measure of diluting segment sodium reabsorption. A normal reference frame of diluting segment NaCl reabsorption at varying delivery rates to that segment was drawn from data collected in similarly studied normal subjects after equilibration on low (20 and 200 mmol/day) or very high (916-1,224 mmol/day) sodium intakes. The results were compatible with a defect in diluting segment reabsorption in the patient, which appeared more pronounced during the high sodium intake. Recent reports do not agree with the existence of such a defect in Bartter's syndrome. One of the reasons of this difference may be the lack of a proper reference frame in previously published studies. We, therefore, compared clearance data in adults with Bartter's syndrome published by others with our studies in normals. Our analysis showed that in Bartter's syndrome (1) a moderate diluting segment NaCl reabsorption defect is often present, and (2) the proximal reabsorption is frequently elevated relative to sodium intake. Severely suppressed diluting segment reabsorption and relatively low proximal reabsorption may also occur, particularly in association with salt loading or reduced glomerular filtration. It seems, therefore, that much of the continuing controversy on renal sodium handling in Bartter's syndrome may be solved by using the proper frame of reference.

Adult↗
PubMed1988

Enalapril attenuates natriuresis of atrial natriuretic factor in humans.

We studied the effect of converting enzyme inhibition with enalapril on the natriuresis observed after administration of atrial natriuretic factor (human ANF-[99-126], given as a 100-micrograms bolus i.v. injection) in eight healthy humans consuming a 100 mmol sodium diet. Without enalapril, sodium excretion rose from 127 +/- 19 (mean +/- SE) to 437 +/- 103 mumol/min in the first 20 minutes after ANF was administered. Clearance studies performed during maximal water diuresis indicated a rise in glomerular filtration rate (inulin clearance), free water clearance, phosphate, lithium, uric acid, and magnesium excretion. Four days of enalapril (20 mg b.i.d.) increased effective renal plasma flow (p-aminohippurate clearance) and reduced blood pressure (from 114/71 +/- 2/2 to 105/60 +/- 2/1 mm Hg). Under these conditions baseline sodium excretion was not different from the control study, but it rose less after ANF (from 117 +/- 22 to 242 +/- 63 mumol/min), and the increments in glomerular filtration rate, free water clearance, phosphate, lithium, uric acid, and magnesium were all blunted and nonsignificant. In addition, effective renal plasma flow tended to fall; this effect was not observed when ANF was given without enalapril. These results support the notion that the effects of ANF on renal hemodynamics and on tubular sodium handling depend on renal angiotensin II and that blood pressure reduction may interfere with the ANF-induced natriuresis.

Adult↗
PubMed1987

Effects of indomethacin on renal response to atrial natriuretic peptide.

We studied the effect of alpha-human natriuretic peptide (ANP, 100 micrograms iv) on renal sodium handling in eight healthy subjects before and after 7 days of indomethacin (50 mg 3 times a day). Sodium intake was 100 mmol/day. Prior to indomethacin, ANP caused a fourfold rise in sodium excretion over the first 20 min and a threefold rise in fractional sodium excretion. The clearance studies, performed during maximal water diuresis, showed increased fractional free water clearance and lithium clearance. Indomethacin caused marked sodium retention. Complete escape did not occur until the sixth day, when cumulative balance was 244 mmol (range 176-337). By this time renin and aldosterone were suppressed and fractional lithium and free water clearance reduced. The natriuretic effect of ANP was not attenuated, and the fractional excretion of sodium and chloride rose even more than without indomethacin. The reduction in lithium and free water clearance under indomethacin tended to be reversed by ANP. These data suggest that the natriuretic effect of ANP is not mediated by or dependent on renal prostaglandins. Indomethacin and ANP appear to have opposite effects on sodium excretion, maximal free water clearance, and lithium clearance.

Adult↗
PubMed1987

Renovascular hypertension identified by captopril-induced changes in the renogram.

Radioisotope renography was performed in 21 patients with hypertension and unilateral renal artery stenosis with and without premedication with 25 mg of captopril, and the results were compared with the effect of percutaneous transluminal angioplasty on the blood pressure, assessed 6 weeks after angioplasty. Angioplasty caused a considerable decrease in blood pressure in 15 of the 21 patients. In 12 of these 15 patients, captopril induced changes in the time-activity curves of the affected kidney only, suggesting deterioration of the excretory function of that kidney, while the function of the contralateral kidney remained normal. After angioplasty the asymmetry in the time-activity curves diminished despite identical pretreatment with captopril. Such captopril-induced unilateral impairment of the renal function was not seen in the six patients with unilateral renal artery stenosis whose blood pressure did not change after percutaneous transluminal angioplasty or in 13 patients with hypertension and normal renal arteries. The functional impairment of the affected kidneys was characterized by a decrease of 99mTc-diethylenetriamine pentaacetic acid uptake and a delay of 131I-hippurate excretion, while the 131I-hippurate uptake remained unaffected. These data are in agreement with a reduced glomerular filtration rate and diuresis during preservation of the renal blood flow, changes that can be expected after converting enzyme inhibition in a kidney with low perfusion and an active, renin-mediated autoregulation of the glomerular filtration rate. These data suggest that functional captopril-induced unilateral changes, shown by split renal function studies with noninvasive gamma camera scintigraphy, can be used as a diagnostic test for renovascular hypertension caused by unilateral renal artery stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Comparison of enalapril and propranolol in essential hypertension.

In 40 patients with essential hypertension, enalapril was compared with propranolol as an antihypertensive agent in a double-blind study. The patients were randomly given either enalapril 5-10-20 mg bid or propranolol 40-80-120 mg bid in a treatment consisting of step-by-step increases in dosage. When the diastolic blood pressure remained greater than 90 mm Hg on the highest dosage, hydrochlorothiazide was added. Both enalapril and propranolol reduced blood pressure, although the patients tended to achieve lower blood pressures while on enalapril. More patients on propranolol required additional diuretic therapy than patients on enalapril. Propranolol reduced heart rate; with enalapril there were no changes in heart rate. Both drugs increased serum potassium and urea. Plasma renin substrate was reduced by enalapril, but raised by propranolol. Enalapril increased plasma renin activity and angiotensin I, while propranolol reduced both. Converting enzyme activity was lowered with enalapril but was unchanged with propranolol. Both drugs reduced angiotensin II. Plasma aldosterone concentration was more suppressed with propranolol than with enalapril.

Adult↗
PubMed1986

Changes in blood pressure and body fluid volumes during diuretic therapy in patients with essential hypertension who receive enalapril.

We evaluated the effect of additional chlorthalidone therapy on blood pressure and body fluid volumes in 10 patients with essential hypertension who did not respond to chronic converting enzyme inhibition with enalapril. Values assessed after 3 days and 6 weeks of combined enalapril and chlorthalidone therapy were compared with initial values during enalapril monotherapy. After 3 days the mean arterial pressure (MAP), plasma volume (PV), blood volume (BV), and extracellular fluid volume (ECFV) decreased. There was a positive correlation between the percentage decreases in MAP and BV. After 6 weeks the MAP decreased further, but the decreases in PV, BV, and ECFV were less pronounced. At this time there was a positive correlation between the percentage decreases in MAP and ECFV. Our results support the hypothesis that contraction of the ECFV is an antihypertensive mechanism of diuretics. The antihypertensive effect of diuretics is enhanced during converting enzyme inhibition, while the body remains protected against volume deficits, possibly by the lower blood pressure itself.

Aged↗