Conflicting results between glomerular filtration rate and serum creatinine measurements in chronic renal failure.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Aurell.
Explore the source record for details and available documents.
The influence on urinary excretion of sodium (NNa . V) of intrapelvic pressure, urinary flow, and mean arterial blood pressure during forced diuresis was evaluated in 12 patients with unilateral hydronephrosis. Total and divided renal functions were measured using 51Cr-EDTA clearance and isotope renography. The amount of sodium, excreted by the obstructed kidney, decreased with higher maximum intrapelvic pressure and increased with higher differences between the mean arterial blood pressure and maximum intrapelvic pressure. The higher the concentrating ability, the lower the amount of sodium excreted by the obstructed kidney. There was a highly significant negative correlation between maximum intrapelvic pressure and urinary flow, but no correlation between mean arterial blood pressure and maximum intrapelvic pressure. Thus, obstructed kidneys with normal concentrating ability have the same excretion of sodium as the nonobstructed contralateral kidney during forced diuresis. Obstructed kidneys with decreased concentrating ability on the other hand excrete comparatively more sodium. This is probably due to a defect in sodium resorption.
Plasma renin activity (PRA) and noradrenaline concentration (NA) were measured in the renal veins (V) and arterial blood (A) in 30 patients investigated for renin-mediated hypertension. Both PRA and NA concentrations in arterial blood were above our reference limits and they were positively correlated. In 18 of the patients renin secretion was unilateral from the diseased side. Their renal vein NA concentration was always higher on that side, compared to the contralateral one, but there were V-A gradients for NA on both sides in all but two cases. In 15 of the patients with such lateralisation of renin secretion the changes of PRA and NA V-A gradients were determined 30-60 min after an i.v. injection of dihydralazine. Both PRA and NA increased more markedly in the renal vein on the affected side where the estimated renal plasma flow was lower than on the contralateral side. The NA gradients increased less than the PRA gradients when changes on the renin secreting side were compared in patients with proven increase of renin secretion. We conclude that patients with renal hypertension have a high sympathetic nervous activity as evidenced by increased plasma NA concentrations and (V-A) gradients for NA on both sides. The release of NA into the renal circulation in renin mediated hypertension is thus not invariably accompanied by renin release. The higher renal vein NA concentration on the involved renin secreting side is explained by reduced RPF on this side.
Desmopressin tests to measure renal concentrating capacity, preceded by two different fluid regimens, have been compared in 19 adult subjects. The results show that peak osmolality in urine after 40 micrograms desmopressin intranasally is higher after fluid restriction. This observation confirms the need of a standardised fluid restriction before the desmopressin test.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Thirty middle-aged, moderately obese men with untreated mild hypertension were allocated to two groups of 15 men each. Both groups were placed on energy-reduced diets (5.1 MJ/day) for 9-11 weeks which resulted in similar losses of body mass (8.5 kg). In group I the low energy diet was supplemented with sodium chloride leading to no change in urinary sodium excretion. During dieting there were significant reductions of plasma renin activity (PRA) and urinary excretion of noradrenaline and aldosterone. Heart rate but not mean arterial pressure (MAP) decreased significantly. Then followed a period of sodium restriction which resulted in a significant decrease in MAP and an increase in aldosterone excretion. In group II there was a reduction of sodium intake by about 80 mmol as judged from determinations of urinary sodium excretion. In this group the energy restriction was not accompanied by any changes in PRA or urinary excretion of aldosterone, whereas urinary noradrenaline excretion, heart rate and MAP decreased significantly. Urinary adrenaline excretion remained unchanged. It is concluded that the hypotensive response to moderate energy and sodium reduction cannot be explained by changes in the renin-aldosterone. system.
Infusion of prostacyclin during cardiopulmonary bypass (CPB) reduces platelet activation, diminishes postoperative blood loss and decreases arterial blood pressure. In spite of continuous prostacyclin infusion, there is a delayed gradual rise in arterial pressure and resistance from low initial levels. We measured epinephrine (E), norepinephrine (NE), serotonin (5-HT), angiotensin II (ATII) and arginine-vasopressin (AVP) in plasma and carried out hemodynamic studies in 19 patients operated for coronary vascular disease. Eight patients served as a control group and were subjected to routine CPB. Eleven patients received prostacyclin 50 ng/kg/min during CPB. E and NE increased four- to sixfold during CPB from about 0.5 ng/ml (P less than 0.001). There was no difference between the groups. During CPB AVP increased sixfold from about 20 pg/ml in both groups (P less than 0.001), decreased early after CPB and increased again to high levels 3 h after CPB. The combined action of E, NE and AVP is of likely importance for the rise in systemic vascular resistance and/or need of vasodilation during CPB in the control group. ATII did not increase in the control group, but increased fourfold to about 20 pg/ml (P less than 0.01) during CPB in the prostacyclin group. The addition of AT II to E, NE and AVP seems responsible for the gradual return of arterial pressure and resistance during prostacyclin infusion. Postoperative hypertension and/or need of vasodilation 3 h after CPB was associated with high AVP levels in both groups. Hypotension caused by prostacyclin infusion did not increase E, NE or AVP above levels produced by CPB and moderate hypotension alone.
Explore the source record for details and available documents.
The new calcium antagonist felodipine with a pronounced arteriolar dilating capacity was used to treat 11 patients with severe hypertension resistant to treatment (4 with essential hypertension, 5 with renoparechymatous hypertension, 2 with renovascular hypertension). Mean glomerular filtration rate for 10 patients was 34 +/- 27 ml/min/1.73 m2 body surface area (51Cr-EDTA clearance) before felodipine. One patient was on haemodialysis treatment. Mean arterial blood pressure in the outpatient clinic was 206 +/- 39/119 +/- 18 mm Hg in spite of treatment with 3 or more antihypertensive drugs. All but 2 patients had been given an angiotensin converting-enzyme inhibitor without success. All vasodilating agents were discontinued and the following morning 5 to 10 mg felodipine was given orally. This resulted in a reduction of average supine blood pressure from 190/110 mm Hg to 150/90 mm Hg during the first hour. The antihypertensive effect was unchanged during 6 hours and the drug was subsequently administered twice or three times a day. Mean systolic and diastolic blood pressure after 1 month was 155 +/- 19/91 +/- 12 mm Hg. Eight patients showed a favourable long term response with a mean systolic and diastolic blood pressure of 154 +/- 17/89 +/- 6mm Hg after 6 months. One patient died from his underlying disease after 2 months and 1 patient discontinued treatment because of ankle oedema after 6 weeks. In the long term treated patients with glomerular filtration rates greater than 15 ml/min/1.73m2 all but 1 showed an improved renal function by 26 +/- 19% (n = 5) after initiation of felodipine therapy. In 2 cases with very low glomerular filtration rate (6 to 7 ml/min/1.73m2) the deterioration of renal function continued after felodipine, but at a slower rate. It is concluded that felodipine decreased blood pressure dramatically in patients with severe hypertension where a majority of the cases had been resistant to a previous therapy. The drug appeared safe also in advanced renal insufficiency.
Ten to eighteen years after donor uninephrectomy (UN) the compensatory increase in renal function is maintained. Albuminuria was slightly increased in a few donors compared to the controls. We found no evidence for donor uninephrectomy to carry a risk for progressive renal failure. Further studies 2-3 decades after UN will provide additional insight in how UN affects the development of proteinuria and renal function.
Ten to eighteen years after donor uninephrectomy (UN) there was no evidence for deterioration of renal function. The mean urinary albumin excretion was slightly increased. There was a positive correlation between the assessed protein intake at investigation and the glomerular filtration rate (GFR).
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Seventy-four patients from four short-term studies of captopril in mild-moderate essential hypertension continued in a cooperative long-term efficacy and tolerance program. The duration of observation is 2- greater than 4 years, the total treatment time being 2434 months. No development of resistance to therapy was observed. The total daily dose of captopril has been gradually decreased and in 20 patients changed from t.i.d. to b.i.d. regime. The drug has been well tolerated and only few and mild side-effects have been observed after the initial titration period. The drop-outs (n = 19) were mostly due to non-medical causes (n = 14). Except for one case of proteinuria, no laboratory abnormalities were detected and there were no signs of long-term toxicity.
Blockade of the actions of the renin-angiotensin-aldosterone axis by inhibition of the angiotensin-converting enzyme with captopril is a new tool in the field of hypertension. As treatment with captopril makes pressure control volume-dependent, the addition of a saluretic is considered the best choice if an additional hypotensive agent is needed. The reason for and experience of the use of captopril in combination with saluretics for treatment of severe hypertension is reviewed. Published results indicate that captopril alone is insufficient, but as many as a third of the patients with previously uncontrollable hypertension manage well when a saluretic is added. Only one in six remains uncontrolled despite the addition of several other hypotensive agents. These observations apply to both essential and secondary forms of hypertension.
Captopril, an angiotensin-converting enzyme inhibitor, was used to treat 14 patients with lupus nephritis and severe hypertension. All patients had reduced renal function and were on regular immunosuppressive therapy with corticosteroids and azathioprine. The initial dosage of captopril was reduced according to the level of renal impairment. 11 patients were treated for more than 6 months. Excellent blood pressure control was achieved with captopril, from a mean of 178 +/- 7/110 +/- 4 to 145 +/- 5/92 +/- 3 mm Hg at 6 months, usually in combination with a diuretic only. In 5 cases, a beta-blocker was added. In 3 patients, captopril therapy was discontinued within the 1st month of treatment. 1 patient did not respond to captopril at all; 1 patient had a rejection crisis and required dialysis; in 1 case, a general exanthema developed within 3 weeks and captopril medication was stopped. In addition to blood pressure control, renal function improved in 7 of the long-term-treated patients (mean increase in glomerular filtration rate 73 +/- 34%). In 3 patients, a continued slow deterioration renal function occurred, and in 1 patient, renal function remained unchanged. It is concluded that captopril is an effective antihypertensive drug in patients with systemic lupus erythematosus (SLE). Captopril treatment increased renal function in 64% of patients on long-term therapy. Not only optimal blood pressure control but other factors may also contribute to this beneficial effect, such as drug-induced prostaglandin release potentiating immunosuppressive treatment. Captopril may in fact be the drug of choice for the treatment of SLE patients with severe hypertension.
Explore the source record for details and available documents.