PubMed Health⌕ Search

Biomedical subjects

C K Christensen

Publications and source records attributed to C K Christensen.

At least 55 records · Page 3Linked to original sources
PubMed1985

Increased myocardial contractility in short-term type 1 diabetic patients: an echocardiographic study.

Cardiac function was investigated by echocardiography in 24 short-term Type 1 diabetic patients with a mean diabetes duration of 7 years (range 4-14 years) during conditions of ordinary metabolic control. Compared to 24 age and sex matched normal control subjects, measurements of myocardial contractility as left ventricular fractional shortening and mean circumferential shortening velocity were increased by 12% and 20% respectively. Another 8 Type 1 diabetic patients were examined during conditions of poor (hyperglycaemia and ketosis) and good metabolic control. Following improved glycaemic control, left ventricular fractional shortening and mean circumferential shortening velocity decreased by 16% and 24% respectively. Our findings show that short-term Type 1 diabetes is associated with increased myocardial contractility. Furthermore, this condition is related to the state of metabolic control.

Adult↗
PubMed1985

The course of incipient diabetic nephropathy: studies of albumin excretion and blood pressure.

With the aim of defining the transitional phase from normal or near normal albumin excretion to overt diabetic nephropathy, 23 male diabetics of more than 7 years' duration, below 40 years of age and a baseline urinary albumin excretion above 15 micrograms/min but without clinical proteinuria (incipient diabetic nephropathy) were studied. For comparison 18 normals, 23 diabetics with normal albumin excretion and 10 patients with overt nephropathy were also examined. Diastolic blood pressure (DBP) was elevated to 88 +/- 9 mmHg (mean +/- S.D.) compared to patients with normal urinary albumin excretion: 80 +/- 7 (S.D.) (2p = 0.13%) but was below pressures in patients with overt diabetic nephropathy 109 +/- 15 (2p = 0.002%). Glomerular filtration rate (GFR) was elevated to 142 +/- 21 ml/min (mean +/- S.D.) compared to 132 +/- 9 in patients with normal urinary albumin excretion (2p = 4.3%). Renal plasma flow (RPF) was not altered. Renal vascular resistance (RVR) was increased (0.200 +/- 0.035) compared to that of patients with normal urinary albumin excretion (0.180 +/- 0.025) (2p = 3.8%). In a longitudinal study of 10 of the patients with incipient nephropathy, followed for 4.9 (Mean) years, urinary albumin excretion increased significantly during the observation period, the yearly increase rate being 19 +/- 22% (mean +/- S.D.). DBP increased from 84 +/- 9 to 93 +/- 13 (2p = 3.8%) in 6 patients followed for more than 4 years.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Predicting diabetic nephropathy in insulin-dependent patients.

We studied whether microalbuminuria (urinary albumin excretion rates of 15 to 150 micrograms per minute) would predict the development of increased proteinuria in Type I diabetes. We also studied the influence of glomerular filtration rate, renal blood flow, and blood pressure on the later development of proteinuria. Forty-four patients who had had Type I diabetes for at least seven years and who had albumin excretion rates below 150 micrograms per minute were studied from 1969 to 1976, and 43 were restudied in 1983. Of the 14 who initially had albumin excretion rates at or above 15 micrograms per minute, 12 had clinically detectable proteinuria (over 500 mg of protein per 24 hours) or an albumin excretion rate above 150 micrograms per minute at the later examination. Of the 29 who initially had albumin excretion rates below 15 micrograms per minute, none had clinically detectable proteinuria at the later examination, although four had microalbuminuria. Those whose condition progressed to clinically overt proteinuria had elevated glomerular filtration rates and higher blood pressures at the initial examination than did those in whom proteinuria did not develop. Renal blood flow was not elevated in these patients. We conclude that microalbuminuria predicts the development of diabetic nephropathy and that elevated glomerular filtration rates and increased blood pressure may also contribute to this progression.

Adolescent↗
PubMed1984

Abnormal albuminuria and blood pressure rise in incipient diabetic nephropathy induced by exercise.

The aim of the study was to evaluate the influence of light to moderate dynamic work (450 kpm/min followed by 600 kpm/min during 20 min each) on the blood pressure and renal protein handling in insulin-dependent diabetic patients with incipient nephropathy (D3) (elevated baseline albumin excretion but without clinical proteinuria). Fifteen male diabetic patients (D3) with a mean age of 26.5 +/- 4.8 years (SD) and a diabetes duration of 15.6 +/- 3.4 years (SD), 11 comparable diabetic patients with normal urinary albumin excretion (D2), and ten non-diabetic subjects (C) were studied. In D3 baseline diastolic blood pressure was elevated [92.1 mm Hg +/- 6.0 (mean +/- SD)] compared to D2 (80.9 mm Hg +/- 4.8, 2P = 0.003%) and C (79.5 mm Hg +/- 12.4, 2P = 1.2%). Baseline systolic blood pressure was not significantly different in the three groups, but systolic blood pressure was more elevated at 600 kpm/min in D3 (193.0 mm Hg +/- 23.0) compared to D2 (170.5 +/- 17.3, 2P = 1.2%) and C (157.5 mm Hg +/- 20.9, 2P = 0.07%). Baseline albumin excretion in D3 was 82.6 micrograms/min X/ divided by 2.5 (geometric mean X/ divided by tolerance factor) and during exercise the maximal albumin excretion rose to 195.0 micrograms/min X/ divided by 2.6 (2P = 0.01%). In D2 albumin excretion rose from 3.3 micrograms/min X/ divided by 1.9 to 7.9 micrograms/min X/ divided by 1.5 (2P = 0.02%). The albumin excretion in C did not change during exercise. A highly significant correlation between maximal exercise induced systolic blood pressure and maximal exercise induced albumin excretion was demonstrable in D3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

The stages in diabetic renal disease. With emphasis on the stage of incipient diabetic nephropathy.

Alterations in renal function and structure are found even at the onset of diabetes mellitus. Studies performed over the last decade now allow definition of a series of stages in the development of renal changes in diabetes. Such a classification may be useful both in clinical work and in research activities. Stage 1 is characterized by early hyperfunction and hypertrophy. These changes are found at diagnosis, before insulin treatment. Increased urinary albumin excretion, aggravated during physical exercise, is also a characteristic finding. Changes are at least partly reversible by insulin treatment. Stage 2 develops silently over many years and is characterized by morphologic lesions without signs of clinical disease. However, kidney function tests and morphometry on biopsy specimens reveal changes. The function is characterized by increased GFR. During good diabetes control, albumin excretion is normal; however, physical exercise unmasks changes in albuminuria not demonstrable in the resting situation. During poor diabetes control albumin excretion goes up both at rest and during exercise. A number of patients continue in stage 2 throughout their lives. Stage 3, incipient diabetic nephropathy, is the forerunner of overt diabetic nephropathy. Its main manifestation is abnormally elevated urinary albumin excretion, as measured by radioimmunoassay. A level higher than the values found in normal subjects but lower than in clinical disease is the main characteristic of this stage, which appeared to be between 15 and 300 micrograms/min in the baseline situation. A slow, gradual increase over the years is a prominent feature in this very decisive phase of renal disease in diabetes when blood pressure is rising. The increased rate in albumin excretion is higher in patients with increased blood pressure. GFR is still supranormal and antihypertensive treatment in this phase is under investigation, using the physical exercise test. Stage 4 is overt diabetic nephropathy, the classic entity characterized by persistent proteinuria (greater than 0.5 g/24 h). When the associated high blood pressure is left untreated, renal function (GFR) declines, the mean fall rate being around 1 ml/min/mo. Long-term antihypertensive treatment reduces the fall rate by about 60% and thus postpones uremia considerably. Stage 5 is end-stage renal failure with uremia due to diabetic nephropathy. As many as 25% of the population presently entering the end-stage renal failure programs in the United States are diabetic. Diabetic nephropathy and diabetic vasculopathy constitute a major medical problem in society today.

Albuminuria↗
PubMed1983

Rapidly reversible albumin and beta 2-microglobulin hyperexcretion in recent severe essential hypertension.

Seven young patients with newly diagnosed severe hypertension were studied for one week. The mean age was 34.9 years (range 28-44). The mean initial values +/- s.d. for systolic and diastolic pressures were 223 +/- 27 and 141 +/- 8 mmHg, respectively. Secondary hypertension was excluded by conventional methods and serum creatinine was normal. A pronounced but quite variably elevated albumin excretion 440 +/- 448 micrograms/min (mean +/- s.d.) and a moderately increased beta 2-microglobulin excretion 3.06 +/- 3.29 micrograms/min was noted before treatment. The abnormal albumin excretion with ensuing fall in blood pressure was rapidly and almost completely reversible in all but one patient during conventional treatment and the increased beta 2-microglobulin excretion was totally reversible in all but one patient. Both albumin and beta 2-microglobulin excretion rate were positively correlated to arterial pressures in all patients. Thus glomerular and to some extent tubular protein handling were both affected in untreated patients, but rapidly reversible during initial antihypertensive treatment. The data indicate that the beta 2-microglobulin hyperexcretion is secondary to enhanced filtration of plasma protein saturating the tubular reabsorption capacity, while the hyperexcretion of albumin is mainly due to the increased filtration pressure per se, though other factors may be partly responsible.

Absorption↗
PubMed1982

Long-term therapy of arterial hypertension with nifedipine given alone or in combination with a beta-adrenoceptor blocking agent.

The antihypertensive effect of nifedipine during long-term therapy was investigated in 5 patients receiving nifedipine as the sole drug and in 10 patients who had nifedipine in combination with a beta-adrenoceptor blocking drug. Nifedipine monotherapy was problematic because of side-effects and development of resistance to therapy after a few months. In patients who received the combined therapy significant and stable blood pressure reductions were maintained during the whole observation period (12-33 months). However, the occurrence of peripheral oedema in 4 of the patients necessitated the addition of a thiazide diuretic. It is concluded that nifedipine is not a first choice drug for the long-term treatment of arterial hypertension. When given in addition to a beta-blocker it is well tolerated and powerful but fluid retention may occur and if not counteracted by a diuretic it will limit the antihypertensive potential of the drug.

Adrenergic beta-Antagonists↗
PubMed1982

Renal effects of acute calcium blockade with nifedipine in hypertensive patients receiving beta-adrenoceptor-blocking drugs.

The effects on blood pressure and renal function of a single 20-mg sublingual dose of nifedipine were investigated in 10 patients with mild to moderate arterial hypertension insufficiently treated on beta-blocker monotherapy. Nifedipine induced a prompt and marked reduction of both systolic and diastolic blood pressure (average maximal reduction 30/22 mm Hg, P less than 0.001). Despite the beta blockade, heart rate rose 25%. Only insignificant increments of glomerular filtration (RVR) was markedly reduced (P less than 0.001). Urinary excretion rate of albumin and beta-2 microglobulin rose after nifedipine, reflecting changes in glomerular as well as tubular function. Mean blood pressure seemed to be a major determinant of the excretion of proteins. There was a marked increase in the excretion of sodium after nifedipine and urine volume rose from a mean of 8.2 +/- 1.3 to 12.5 +/- 1.8 ml/min (P less than 0.01). The changes in sodium excretion rate correlated with the renal hemodynamic changes. Uric acid excretion rate rose remarkably after nifedipine and the magnitude of the changes seemed intimately related to the basal level of RVR. The results indicate that nifedipine therapy may be advantageous in patients whose hypertension is insufficiently controlled with beta blockers alone. Renal blood flow is maintained and there is a desirable diuretic action and enhancement of uric acid excretion.

Adult↗
PubMed1982

The individual variation in pharmacokinetics and pharmacodynamics of furosemide in young normal male subjects.

Following a 24 h control period in the ward 80 mg furosemide was injected intravenously to ten young healthy, male volunteers. The serum clearance of furosemide (Cls) was between 140 and 201 ml min-1 and on the average the renal clearance was 60% of Cls. During the initial 30 min period a maximum additional excretion rate of sodium of 3.3 mmol min-1 was reached at an excretion rate of 0.8 mg furosemide min-1. A marked initial drop in creatinine clearance (Clcr) was noted and Clcr(24 h) showed an average decrease of 12% after the drug administration. The serum concentration of potassium was decreased at 1 and 2 h after the injection and of sodium from 2 h and on. The concentration of albumin in serum increased by 3% (P less than 0.05) already after 5 min. After 2 h a maximum increase of 14% was reached. After 8 min diastolic blood pressure was increased by 13% (P less than 0.05), whereas systolic blood pressure reached a significant decrease gradually (7% after 3 h).

Adult↗
PubMed1982

Urinary excretion of albumin in normal man: the effect of water loading.

The urinary excretion of albumin and beta 2-microglobulin in response to two different types of oral water load was studied in 18 healthy subjects. Both acute water loading (1 litre of tap water given over 10 min) and chronic water loading (250 ml of water given every 20 min for the 4-h duration of the test) produced a short-lived but significant increase in the urinary excretion of albumin, but not in beta 2-microglobulin. Albumin excretion returned promptly to basal values in spite of high and sustained urine flow. The decrease in haematocrit, plasma osmolality, plasma sodium concentration and pulse rate and the increase in creatinine clearance suggest that the elevation in albumin excretion might be the result of a transient volume expansion associated with an increase in glomerular filtration rate and in filtration of albumin. However, a washout of proteins from the tubular lumen with preferential reabsorption of small molecular weight proteins (i.e. beta 2-microglobulin) during high tubular flow cannot be excluded. Studies investigating changes in urinary albumin excretion should be performed after baseline conditions of stable urinary excretion of albumin have been established.

Adolescent↗
PubMed1981

Reduced 2,25-dihydroxyvitamin D and 24,25-dihydroxyvitamin D in epileptic patients receiving chronic combined anticonvulsant therapy.

Thirty-one adult epileptic outpatients on chronic combined anticonvulsant therapy were investigated. Eleven patients took vitamin D2 supplementation 400-1200 IU/day as multivitamin tablets. Mean serum calcium and renal calcium excretion were reduced. Serum alkaline phosphatase and urinary hydroxyproline excretion were increased. Forearm bone mineral content was reduced. Serum concentrations of 25-hydroxyvitamin D (25-OHD), 24-25-dihydroxyvitamin D (24,25-(OH)2D) and 1,25-dihydroxyvitamin D (1,25-(OH)2D) were reduced (p less than 0.001). A positive correlation was found between the serum 25-OHD and 24,25-(OH)2D concentrations (p less than 0.05) with the highest levels in those receiving vitamin D2 supplementation (p less than 0.01). Serum 1,25-(OH)2D correlated positively with renal calcium excretion (r = 0.65, p less than 0.001) suggesting that the intestinal calcium absorption in epileptic patients depends on 1,25-(OH)2D levels.

24,25-Dihydroxyvitamin D 3↗
PubMed1981

Antihypertensive effect of atenolol (100 mg once a day) and methyldopa (250 mg thrice a day). A double-blind cross-over multicentre study.

In a double-blind cross-over multicentre study lasting for 16 weeks, the antihypertensive effect of atenolol (100 mg once a day) was compared with that of methyldopa (250 mg thrice a day) in 48 patients with mild to moderately severe hypertension. At the end of the trial, atenolol was superior to methyldopa in achieving clinically relevant BP levels, less than 150/95 mmHg (p less than 0.001), and in respect to patients' drug preference (p less than 0.04). The BP levels after the first 2 weeks of treatment with either drug were identical but, in contrast to methyldopa, atenolol caused further significant reduction in BP during the following 4 weeks. This finding implies that one should hesitate to start additional therapy until after at least six weeks of atenolol treatment, whereas no further reduction in BP can be expected after the first 2 weeks of treatment with methyldopa. Two patients had to be withdrawn from the study during treatment with atenolol, as they developed severe bradycardia and dyspnoea, respectively. Other side-effects were few and of minor clinical importance.

Adult↗
PubMed1981

The use of HPLC to elucidate the metabolism and urinary excretion of furosemide and its metabolic products.

Three principles for the use of HPLC with spectrophotometric detection to determine the concentration of furosemide and of 4-chloro-5-sulfamoyl anthranilic acid (CSA) were studied. A reversed phase microbondapack C18 column was used for the separation of either unchanged furosemide (I), CSA (II) or the diazo product of CSA (III). The sensitivity of the methods for the determination of furosemide added to serum in vitro were for I 0.05, for II 0.020 and for III 0.01 microgram/ml. The methods I and II were used to study the excretion pattern in the urine of furosemide and CSA after intravenous injection of 80 mg to 10 normal subjects. An average of 48.1 +/- 9.8% (S.D.) of the furosemide was excreted during the first hour as unchanged furosemide. Simultaneously 1.9 +/- 0.8% of the dose was excreted as CSA. Only very low concentrations of CSA were found in serum and that metabolite apparently was excreted with a higher renal clearance than furosemide during the period 30-60 min. after the administration (30.3 +/- 145 ml/min. for CSA and 88 +/- 23 ml/min. for furosemide). During the 24 hour period following the administration 52.6 +/- 8.1 mg was excreted as unchanged furosemide and 11.4 +/- 5.2 mg as a glucuronidated product.

Adult↗
PubMed1981

Renal function and cimetidine. Urinary albumin and beta 2-microglobulin excretion and creatine clearance during cimetidine treatment.

Urinary albumin and beta 2-microglobulin excretion and creatinine clearance were measured during 8 weeks' conventional cimetidine treatment in 13 ulcer patients without signs of renal disease. No changes were found in albumin or in beta 2-microglobulin excretion, indicating no changes in glomerular permeability and tubular reabsorption of proteins in the kidney. Creatinine clearance fell about 28 ml/min (26%) during cimetidine treatment but normalized after termination of medication. Concomitantly, serum creatinine increased by 22% during treatment and fell again after termination of treatment. The mechanism behind the changes in renal handling of creatinine during cimetidine was not clarified in the present study. It is concluded that the conventional 8 weeks' cimetidine treatment seems safe from the renal point of view, at least in patients without signs of renal disease.

Adult↗