The aim of the present investigation was to discover whether disturbed left ventricular (LV) function limits renal replacement therapy in patients with juvenile onset diabetes mellitus. Seventeen patients given functioning kidney grafts were studied non-invasively (M-mode echocardiography, apexcardiography, phonocardiography) before renal transplant and an average of six, 13 and 44 months after transplant. The main pretransplant findings were pronounced LV hypertrophy with impaired diastolic LV function (prolonged relaxation time + signs of decreased LV distensibility) and a hyperdynamic circulation. Most of these abnormalities were significantly less severe after successful kidney transplantation. LV mass decreased by 37% 44 months after transplant (p less than 0.01) and LV diastolic and systolic volumes decreased with a subsequent increase in ejection fraction from 0.65 to 0.78 (p less than 0.01). The LV distensibility and filling pattern improved significantly while the prolonged relaxation time was unchanged. These findings imply that pretransplant disturbances in LV function are related more to factors such as hypertension, volume overload and uraemia than to diabetes per se because no pronounced improvement in the metabolic disorder resulting from diabetes can be expected, even after the most successful transplant. Disturbed LV function should not, therefore, exclude uraemic diabetics from renal replacement.
Low basal and stimulated plasma renin activity (PRA) levels have been reported in patients witn diabetic nephropathy (DN). We have measured PRA before and after stimulation with captopril in 28 patients with DN and in 25 control patients. Renal function impairment was similar in both groups. Most patients were treated with furosemide. In 19 patients with DN the PRA-response to dihydralazine was also studied. PRA before and after captopril were higher in the DN than in the control group (P < 0.001). PRA increased from 4.6 ± 3.6 to 6.3 ± 5.3 in the DN, and from 1.8 ± 2.7 to 2.7 ± 3.4 in the control patients. The increases in PRA, caused by decreased angiotensin II feed-back inhibition, were comparable. PRA did not increase after dihydralazine despite a pronounced blood-pressure reduction. The difference in response to these stimuli indicate selective lesions involving both the sympathetic innervation and the renal baroreceptor function in DN. Overhydration is a plausible explanation to the low PRA earlier reported in DN. The results thus indicate that a preserved renin secretion capacity is present in DN. Differences in PRA between the both groups can only partly be explained by other factors than DN. Our findings indicate a role for the reninangiotensin-system in hypertension in DN.
Strokes occurring among persons between 15 and 65 years of age (population 300 000) have been registered since 1970 in Göteborg, Sweden. Control of the validity showed that less than 10% of all cases of stroke were undetected. During the period Nov. 15, 1970–May 14, 1975, 986 stroke events occurred in 941 patients, giving an annual average incidence rate of 73 (89 for men and 58 for women) per 100 000 individuals 15–65 years of age. The incidence for all ages was estimated to be about 200/100 000. The rates were higher for men than for women in all age groups. There was a female preponderance for subarachnoid haemorrhage but a male preponderance for other types of stroke. Incidence rates increased with age, most rapidly for brain infarcts and unspecified stroke. Fatality rates levelled out 3 weeks after onset of stroke; they were high for subarachnoid and intracerebral haemorrhage and low for cerebral infarction and unspecified stroke. Incidence rates were lower than those found in two similar studies from Denmark and Finland, and even greater variations were found with respect to types of stroke. Fatality rates were similar to those reported by other authors.
The antihypertensive effect and sideeffects during 12 months' treatment with bendrotlumethiazide and propranolol have been compared in two randomly selected, equally large groups (n= 53) of previously untreated male hypertensives. Systolic BP above 170 or diastolic BP above 105 mmHg on two occasions were defined as hypertension. The
ABSTRACT. Body fat, body cell mass, fasting blood sugar, glucose tolerance and fasting insulin have been determined in 106 hypertensive males aged 47–54 years and in 41 normotensive 50‐year‐old males. Both groups were derived from screening examinations in random population samples. The hypertensive subjects were more often obese and had more often an impaired glucose tolerance and a higher fasting insulin compared with the normotensive subjects. The metabolic differences were not explained simply by the higher degree of obesity in the hypertensive subjects, as the differences remained when the hypertensive subjects were matched for body fat with normotensive controls. The impaired glucose metabolism demonstrated quantitatively in an unselected group of hypertensive subjects, might be one of the factors explaining the variable prognosis in hypertensive subjects.
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