Biomedical subjects
Publications and source records attributed to E B Pedersen.
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Studies on plasma aldosterone, total serum protein, electrolytes, osmolal concentrations in serum and urine, creatinine, lithium and osmolal clearances were carried out on 14 patients suffering from lithium intoxication. The determinations were done on samples obtained on admission and during the following twelve days of treatment with hemodialysis, sodium chloride loading, or forced diuresis. Plasma aldosterone and total serum protein were increased; serum sodium concentrations and creatinine clearances were decreased on admission. Serum osmolality was normal; urine osmolal concentration was just above that in plasma. The results showed that the lithium intoxicated patients were moderately depleted of sodium and water on admission. Plasma aldosterone, total serum protein and serum sodium were normalized during treatment. Creatinine clearance increased but did not normalize in all patients. Renal concentrating tests were performed in five patients three to four weeks after lithium intoxication. The renal concentrating ability was reduced in all. The elevated plasma aldosterone seen in lithium intoxication might have been a result of sodium and water depletion. It is suggested that impaired renal concentrating ability induced by lithium may make some patients more susceptible to conditions which can lead to sodium and water loss, and thereby to lithium intoxication.
Total exchangeable body potassium (KE) was determined in fifteen patients with essential hypertension, and total exchangeable body sodium (NaE) in ten, before and after propranolol administration for 2-3 months. Blood pressure was reduced; serum potassium increased, but KE was unchanged. Serum sodium and NaE were unaffected during therapy. It is concluded that the increase in serum potassium during propranolol treatment could not be attributed to potassium retention, but is possibly due to a displacement from the intra- to the extracellular fluid compartment. The antihypertensive effect of propranolol could not be related to changes in NaE.
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Albumin, beta2-microglobulin and free light chains were determined in urine in nine manic-depressive patients before and at intervals during three months of lithium treatment (longitudinal study). The same determinations were carried out in twenty-seven manic-depressive patients who had been treated with lithium for 3 months to 20 years and also in a control group (transversal study). There were no statistically significant changes in urinary excretions of albumin, beta2-microglobulin and free light chains during the longitudinal study. In one patient albumin excretion gradually increased during the study and remained elevated on reexamination 1 year later. No significant differences were found between the lithium treated patients and control subjects in the transversal study in either albumin, beta2-microglobulin or free light chain excretion. It is not clear whether the increased and sustained albumin excretion in one of the patients was due to lithium or was conincidental. The study shows that in most patients lithium treatment does not affect renal protein excretion.
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The present report describes a case of potassium-wasting nephropathy with the physiological and endocrinological findings that are typical for Bartter's syndrome (BS). However, the renal juxtaglomerular apparatus showed no hyperplasia at two renal biopsies two years apart. The short-term (9 days) effect of indomethacin in combination with spironolactone was a suppression of hyperreninemia and hyperaldosteronism and an increase in vascular sensitivity to angiotensin II associated with potassium and sodium retention. Subsequently, on indomethacin alone, potassium balance was obtained on a lower level with persistent hypokalemia and persistent renal potassium leakage. Hypokalemia persisted during long-term (9 months) treatment with indomethacin despite normalization of the activity of the renin-aldosterone system. The results indicate that indomethacin as long-term treatment may be ineffective in maintaining a normal potassium balance in BS.
Plasma renin concentration was determined in patients given lithium treatment. In longitudinal study plasma renin concentration was determined in nine patients before the start of lithium treatment and at intervals during 3 months of treatment. In a transversal study, 18 patients given lithium treatment for 2--20 years were compared with 11 control persons. In the longitudinal study, plasma renin concentrations did not, during lithium treatment, deviate significantly from pre-treatment values. In the transversal study, values in the lithium treated patients did not differ significantly from values in the control group. There were no correlations, in the transversal study, between serum lithium concentrations and plasma renin concentrations. Our study indicates that the plasma renin concentration remains unaffected by lithium administered in nontoxic doses.
In a selected material of 228 patients with chronic inflammatory bowel disease (CIBD) the incidence of urolithiasis was 15% (95% confidence limit 11-21). The tendency to urolithiasis is significantly correlated to small-bowel resection and its extent and to obstruction in the urinary tract. On the other hand, there is no definite correlation to the duration or extent of the bowel disease. The significant correlation between urolithiasis and ileal resection is in agreement with the hyperabsorption of oxalate as an important cause of stone formation demonstrated by others. That local factors too play an essential role in the formation of urinary calculi is apparent from the increased incidence of urolithiasis in obstruction of the urinary tract. The incidence of urolithiasis was particularly high (22-25%) among patients with ileostomies. The few and negligible symptoms of and sequelae to, urolithiasis in CIBD encourage a conservative attitude.
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Plasma renin concentration (PRC) was measured in 46 patients with essential hypertension before and after treatment for 4 weeks with alprenolol 600-1200 mg daily. In 27 of these patients PRC was measured after 4 weeks of combined treatment with alprenolol and hydralizine. During alprenolol treatment PRC and blood pressure were reduced, but the changes were not correlated. Alprenolol treatment caused similar blood pressure reductions in patients with high and low PRC, and the antihypertensive efficacy of beta-adrenergic blocking agents could not be predicted from the pretreatment PRC. When beta-adrenergic blockade was supplemented with hydralazine, blood pressure was further reduced, but PRC remained unchanged. Although a causal relationship between blood pressure reduction and suppression of renin, production might exist at low doses of beta-adrenergic blocking agents, the present study did not indicate such a relationship when higher doses were used. It was shown that alprenolol inhibited the increase in PRC usually induced by hydralazine, but it is not known whether this was important for the effectiveness of the fall in blood pressure produced by hydralazine.
The renal excretion of calcium was determined in ten subjects before and at intervals during 3 months of lithium treatment. The calcium excretion fell by more than 40% within the first week of treatment and remained low throughout the treatment period. The reduction in urinary calcium excretion could be accounted for by an increase in fractional tubular reabsorption of calcium. There were no changes in serum calcium or inorganic phosphate, nor in urinary inorganic phosphate. The results indicate that lithium interferes with the regulation of calcium metabolism.
1. The effect of intravenous loading with 500 ml of sodium chloride solution (50 g/l) on plasma renin concentration, plasma aldosterone concentration, urinary sodium excretion and mean blood pressure was studied in 15 young patients with mild essential hypertension and 10 healthy normotensive control subjects. 2. Plasma renin concentration and plasma aldosterone concentration were suppressed to the same degree during loading in both the hypertensive and normotensive groups. Urinary sodium excretion was significantly higher in the hypertensive patients than in the normotensive subjects. Mean blood pressure increased slightly in both groups. 3. Plasma renin concentration and plasma aldosterone concentration were significantly correlated in both groups before sodium loading. The increase in urinary sodium excretion was significantly correlated to the suppression of plasma aldosterone concentration in the hypertensive, but not in the normotensive, group. No correlation was found between changes in urinary sodium excretion and changes in plasma renin concentration or mean blood pressure. 4. The results indicate that the suppressibility of the renin-aldosterone system by hyperosmotic sodium chloride solution is normal in young patients with mild essential hypertension. It is suggested that the changes in plasma aldosterone concentration induced by sodium loading might be involved in the regulation of exaggerated natriuresis in essential hypertension.
The effects on renal plasma flow (RPF) and glomerular filtration rate (GFR) of an i.v. sodium load and exercise have been measured in 14 young patients with essential hypertension before and after 3-4 months' treatment with propranolol as well as in 10 normotensive control subjects. In the untreated hypertensive patients, RPF and GFR were significantly reduced during sodium loading and exercise. After propranolol treatment, RPF and GFR were unaffected by sodium loading but decreased during exercise. In the normotensive control group, GFR and RPF were unchanged during sodium loading; RPF decreased during exercise, wherease GFR was not significantly reduced. RPF was significantly lower in the untreated hypertensive patients than in the normotensive control subjects during sodium loading and exercise. Propranolol treatment induced a significant reduction of BP and heart rate. RPF and GFR were not altered by propranolol treatment during sodium loading. During exercise, however, RPF was significantly lower after treatment than before. Urinary sodium excretion during sodium loading was significantly higher in the hypertensive patients than in the control subjects and decreased significantly during propranolol treatment. The reason for the abnormal reduction in renal haemodynamics during sodium loading in patients with essential hypertension is not clarified, but may possibly be related to functional or structural alterations in the renal vascular bed. The lower RPF during exercise after treatment with propranolol is most likely caused by an inhibition of the cardiac output induced by beta-adrenergic blockade. It is conceivable that the reduced urinary sodium excretion during propranolol treatment is attributable to the reduction of BP.
Blood pressure (BP), plasma renin concentration (PRC), plasma aldosterone concentration (PAC) and exchangeable sodium (ES) were studied in 19 kidney recipients on different fixed levels of sodium intake after successful kidney transplantation. The following groups of kidney recipients were investigated: group 1: 7 normotensives, group 2:7 hypertensives without transplant renal artery stenosis (TRAS), group 3:5 hypertensives with angiographically verified TRAS. Hypertension in the recipients without TRAS (group 2) was characterized by a positive correlation between BP and ES and a normal response of PRC and PAC to a fixed low (10 mEQ/day) and high (150 mEq/day) sodium intake. In contrast, hypertension in the recipients with TRAS (group 3) was characterized by a normal or varyingly increased PRC on a liberal sodium intake and a reduced response of PRC to sodium restriction, whereas PAC did not differ from the other groups of recipients. In one recipient in group 3 who underwent surgical correction for TRAS, PRC and PAC decreased before operation during sodium restriction, but BP remained high until after operation, when it normalized simultaneously with a decrease in ES. The results indicate that sodium retention is involved in the pathogenesis of posttransplant hypertension and suggest that an increased activity of the renin--angiotensin system is counterbalanced by an accumulation of sodium in TRAS.
Plasma prolactin was determined in a longitudinal study, where -9 manic-depressive patients were examined before lithium treatment and at various times during the treatment with the aim of unravelling a possible association between initial changes in water and sodium balance during lithium treatment and changes in plasma prolactin level. No significant changes were found, nor could any correlation between serum lithium and plasma prolactin be established. Some reports have indicated association between breast cancer and prolonged elevated plasma prolactin, such as is seen during treatment with phenothiazines and reserpine. In a transversal study, determination of plasma prolactin during long-term lithium treatment in 26 patients did not reveal any elevation compared with 16 controls. Lithium is accordingly not among the drugs which produce prolonged elevation of plasma prolactin.