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K W Hansen

Publications and source records attributed to K W Hansen.

54 records · Page 3Linked to original sources
PubMed1992

Effects of ACE inhibition supplementary to beta blockers and diuretics in early diabetic nephropathy.

Angiotensin converting enzyme (ACE) inhibition has shown promising results in diabetic nephropathy, but long-term results on survival are not available. In a cohort of patients receiving antihypertensive treatment predominantly consisting of beta blockers in combination with diuretics, support for an improved survival has been presented. Addition of ACE inhibition to such a combination treatment may be favorable both due to the suggested renoprotective effects of ACE inhibitors and because diuretics activate the renin-angiotensin system. In 10 insulin-dependent diabetic patients with early diabetic nephropathy [urinary albumin excretion rate (UAE) less than 100o micrograms/min], who were receiving continuous therapy with metoprolol and bendroflumethiazide, a double-blind crossover study with four months addition of ramipril 5 mg (Ramace) and placebo was conducted. UAE (radioimmunoassay) and fractional albumin excretion were significantly reduced after the four months of ramipril administration [UAE: 114.1 x/divided by 1.3 (geometric mean x/divided by confidence factor] versus 174.6 x/divided by 1.2 micrograms/min, 2P less than 0.005). Renal plasma flow (clearance of 131I-hippuran) tended to increase [497 +/- 25 (mean +/- SE) vs. 464 +/- 28 ml/min/1.73 m2, 2P = 0.08], while GFR (125I-iothalamate) stayed unchanged (121 +/- 8 vs. 120 +/- 9 ml/min/1.73 m2). Mean arterial pressure during clearance studies fell moderately (95 +/- 3 vs. 101 +/- 1 mm Hg, 2P less than 0.05) and renal resistance was decreased (2P less than 0.03). ACE activity was suppressed in all patients. Twenty-four-hour ambulatory blood pressure measurements were not significantly different after the two periods (daytime averages: 91 +/- 2 vs. 93 +/- 2, nighttime 80 +/- 2 vs. 84 +/- 3 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1992

Micro-albuminuria and the organ-damage concept in antihypertensive therapy for patients with insulin-dependent diabetes mellitus.

OBJECT OF TREATMENT: Antihypertensive treatment in hypertensive patients with insulin-dependent diabetes mellitus is intended to prevent long-term complications, particularly diabetic nephropathy. DIABETIC HYPERTENSIVES WITH ABNORMAL ALBUMINURIA: Antihypertensive therapy, particularly with angiotensin converting enzyme (ACE) inhibitors, typically produces a permanent reduction in the decline of the glomerular filtration rate (GFR) in diabetic patients with abnormal albuminuria. The rate of decline in the GFR during antihypertensive treatment is a well accepted end-point in diabetic renal disease. DIABETIC HYPERTENSIVES WITHOUT ABNORMAL ALBUMINURIA: In insulin-dependent diabetic patients with essential hypertension but with normal urinary albumin excretion there is no reduction in the GFR. Longitudinal studies have shown a fall in the GFR only in the presence of significantly increased urinary albumin excretion. ABNORMAL ALBUMINURIA AS A MARKER OF INCIPIENT NEPHROPATHY: Micro-albuminuria and proteinuria may be pathogenetic factors in the development of nephropathy, leading eventually to end-stage renal failure in diabetic patients. Measurements of micro-albuminuria and proteinuria, in addition to blood pressure recordings, might therefore be used as indications for initiating antihypertensive treatment. NEED TO MONITOR PATIENTS FOR ABNORMAL ALBUMINURIA: Transglomerular macromolecular traffic may produce mesangial damage, with subsequent glomerulopathy and diabetic nephropathy. Thus, close monitoring for micro-albuminuria and proteinuria is desirable in the management of diabetic hypertensive patients.

Albuminuria↗
PubMed1992

A plea for consistent reliability in ambulatory blood pressure monitors: a reminder.

OBJECTIVE: To compare three different software versions [read-only memory (ROM) versions 1.22, 1.24 and 1.28] of the SpaceLabs model 90202 ambulatory blood pressure monitor. DESIGN: Simultaneous measurements in a two-arm crossover design. METHODS: Ten measurements each in 14 normotensive persons were performed to compare each pair of monitors. The results were corrected according to the deviation from a mercury column. The systolic (SBP), diastolic (DBP) and mean arterial blood pressure (MAP) was noted and the factor K = (MAP - DBP)/(SBP - DBP) was calculated. RESULTS: The K factor in the two older ROM versions was close to 0.25, with no statistically significant difference. In contrast the K factor was higher in the most recent ROM version than in one of the previous versions. This could be explained by a 5.4 mmHg increase in MAP found by the new version. A significant difference in blood pressure was observed even between two monitors with the same ROM version. CONCLUSION: Unnotified changes in the software version in the SpaceLabs 90202 monitor operating by an oscillometric technique seriously affect the reliability of MAP measurements. Whenever possible in clinical trials the same monitor should be used for the same patient on each occasion. The industry should inform clinicians of the consequences of updating apparently identical monitors.

Blood Pressure↗
PubMed1992

Normoalbuminuria ensures no reduction of renal function in type 1 (insulin-dependent) diabetic patients.

Recent reports have suggested that impaired renal function in type 1 diabetic patients may be present despite normal urinary albumin excretion (UAE). We have studied kidney function by means of a constant-infusion technique in normoalbuminuric type 1 diabetic patients without antihypertensive medication (UAE less than 20 micrograms min-1, n = 134), in microalbuminuric patients (20 greater than or equal to UAE less than 200 micrograms min-1, n = 50) and in 27 non-diabetic control subjects. Mean UAE was 4.5 micrograms min-1 (range 1.0-19.3 micrograms min-1) in normoalbuminuric patients, 53.1 micrograms min-1 (range 20.8-147.5 micrograms min-1) in microalbuminuric patients, and 4.0 micrograms min-1 (range 2.1-17.9 micrograms min-1) in controls. Glycosylated haemoglobin A1c was significantly higher in microalbuminuric patients (8.9%, range 5.9-12.6%) than in normoalbuminuric patients (7.9%, range 5.5-11.5%) (P less than 0.0001). Glomerular filtration rate in normoalbuminuric patients (135 ml min-1, range 97-198 ml min-1) was significantly higher than in controls (118 ml min-1, range 94-139 ml min-1) (P less than 1 x 10(-6), and significantly lower than in microalbuminuric patients (142 ml min-1, range 100-186 ml min-1) (P less than 0.05). Mean arterial blood pressure was lower in normoalbuminuric patients (91 mmHg, range 78-108 mmHg) than in microalbuminuric patients (98 mmHg, range 82-131 mmHg) (P less than 1 x 10(-6), but not significantly different from that of controls (89 mmHg, range 73-103 mmHg). We conclude that normal UAE is a reliable indicator of well-preserved renal function. Glomerular hyperfiltration, elevated blood pressure and poor metabolic control are characteristic features of microalbuminuric patients.

Adolescent↗
PubMed1992

Blood pressure elevation versus abnormal albuminuria in the genesis and prediction of renal disease in diabetes.

A number of risk factors associated with the development of diabetic nephropathy has been described, such as elevated blood pressure, poor metabolic control, hyperlipidemia, and smoking. Abnormal albuminuria also is associated with progression of renal disease, but has until recently been considered principally a marker of disease activity rather than a risk factor. This article discusses the role of elevated blood pressure versus abnormal albuminuria in a genesis and prediction of renal disease in diabetes. Controversy exists regarding parental disposition to hypertension and early blood pressure elevation in the course of diabetes, but all studies agree that elevated blood pressure--in the presence of abnormal albuminuria--constitutes a risk factor. Because abnormal albuminuria is associated with progression disease, it may itself be a risk factor because increased macromolecular traffic over the glomerular membrane may produce glomerulopathy. Problems related to blood pressure measurement are important, and 24-h recordings of blood pressure may be recommended in some situations. Regarding renal structure, preliminary results suggest that structural lesions precede blood pressure elevation. The solid end point for evaluation of renal disease progression is the fall rate of GFR, with abnormal albuminuria as an intermediate end point, also in drug trials. Abnormal albuminuria may constitute a new indication for antihypertensive treatment, being, as it is, a clear indicator of organ damage, whereas elevated blood pressure with normal AER may not increase risk substantially.

Albuminuria↗
PubMed1991

Ambulatory blood pressure measurement in type 2 diabetic patients: methodological aspects.

Ambulatory blood pressure was measured over 24 h on two occasions in 29 Type 2 diabetic patients age 65 (range 52-74) years, and the reproducibility compared with that of ordinary clinic measurements recorded by Hawskley's random zero sphygmomanometer. The variability of the difference between blood pressure measurements on the two occasions was twice as large for clinic measurement as for ambulatory measurement (2p less than 0.01). If applied to clinical trials this would allow a fourfold reduction of patient numbers without losing test power. In the group of patients treated with antihypertensive medication (n = 16) the spontaneous decline in blood pressure after leaving the hospital proved to be most prominent in those patients with the highest clinic blood pressure, a phenomenon with importance for the management of hypertension. The individual difference between clinic measurements and ambulatory day-time measurements from the same day was unpredictable. Ambulatory blood pressure measurement in the outpatient clinic may be a practicable approach for optimizing antihypertensive treatment in Type 2 diabetic patients.

Aged↗
PubMed1991

Expansion of extracellular volume and suppression of atrial natriuretic peptide after growth hormone administration in normal man.

Sodium retention and symptoms and signs of fluid retention are commonly recorded during GH administration in both GH-deficient patients and normal subjects. Most reports have however, been casuistic or uncontrolled. In a randomized double blind placebo-controlled cross-over study we therefore examined the effect of 14-day GH administration (12 IU sc at 2000 h) on plasma volume, extracellular volume (ECV), atrial natriuretic peptide (ANP), arginine vasopressin, and the renin angiotensin system in eight healthy adult men. A significant GH induced increase in serum insulin growth factor I was observed. GH caused a significant increase in ECV (L): 20.45 +/- 0.45 (GH), 19.53 +/- 0.48 (placebo) (P less than 0.01), whereas plasma volume (L) remained unchanged 3.92 +/- 0.16 (GH), 4.02 +/- 0.13 (placebo). A significant decrease in plasma ANP (pmol/L) after GH administration was observed: 2.28 +/- 0.54 (GH), 3.16 +/- 0.53 (placebo) P less than 0.01. Plasma aldosterone (pmol/L): 129 +/- 14 (GH), 89 +/- 17 (placebo), P = 0.08, and plasma angiotensin II (pmol/L) levels: 18 +/- 12 (GH), 14 +/- 7 (placebo), P = 0.21, were not significantly elevated. No changes in plasma arginine vasopressin occurred (1.86 +/- 0.05 pmol/L vs. 1.90 +/- 0.05, P = 0.33). Serum sodium and blood pressure remained unaffected. Moderate complaints, which could be ascribed to water retention, were recorded in four subjects [periorbital edema (n = 3), acral paraesthesia (n = 2) and light articular pain (n = 1)]. The symptoms were most pronounced after 2-3 days of treatment and diminished at the end of the period. In summary, 14 days of high dose GH administration caused a significant increase in ECV and a significant suppression of ANP.

Adult↗
PubMed1991

Renal factors influencing blood pressure threshold and choice of treatment for hypertension in IDDM.

In this article, we analyze the blood pressure (BP) threshold for the start of antihypertensive treatment in insulin-dependent diabetes mellitus (IDDM) patients, with particular emphasis on those with persistent microalbuminuria or proteinuria (incipient and overt nephropathy, respectively). In such individuals, there is a clear increase in the prevalence of hypertension and in actual measured BP values that is not observed in normoalbuminuric patients. In 94 young healthy adults (less than 45 yr of age), average mean +/- SD arterial pressure (MAP; diastolic + 1/3 pulse pressure) was approximately 90.0 +/- 8.1 mmHg, closely corresponding to large population studies. In microalbuminuric IDDM patients, MAP values between approximately 105 and approximately 95 mmHg have been found in different studies, and the level has progressively decreased in various studies between 1984 and 1990 with similar BP-measuring techniques. Somewhat higher values are seen in patients with proteinuria, who are also consistently characterized by reduced glomerular filtration rate (GFR). A clear correlation is found between MAP plotted against the increased rate of microalbuminuria (%/yr) in incipient nephropathy and against fall rate of GFR (ml.min-1.mo-1) in proteinuric patients. In the natural history of renal disease, different cutoff points in MAP for start of progression are observed: greater than 95 mmHg for the start of progression of microalbuminuria and greater than 105 mmHg for the decrease in GFR. During antihypertensive treatment, there is reduction or no progression in microalbuminuria with MAP of approximately 90-95 mmHg and only a limited fall in GFR with MAP of approximately 100 mmHg. However, certain antihypertensive drugs (angiotensin-converting enzyme inhibitors) may have specific renoprotective actions, reducing microalbuminuria at rather low BP levels or even independent of BP reduction. The optimal way of monitoring BP may be by 24-h ambulatory recording.

Blood Pressure↗
PubMed1991

ACE-inhibition and renoprotection in early diabetic nephropathy. Response to enalapril acutely and in long-term combination with conventional antihypertensive treatment.

Early antihypertensive treatment with beta1 blockers and diuretics has proved to delay progression in diabetic nephropathy. Application of angiotensin converting enzyme inhibitors (ACE-I) may also be relevant. To elucidate possible differences in acute renal response to ACE-I and beta-blockers, kidney function was investigated before and after enalaprilat (10 mg) and metoprolol (10 mg) i.v. in 8 microalbuminuric insulin-dependent diabetic patients on no antihypertensive therapy (Study A). Glomerular filtration rate (clearance of 125I-iothalamate) was unchanged with both agents. ACE-I gave rise to efferent renal vasodilation: renal resistance and filtration fraction fell, renal plasma flow (RPF; 131I-hippuran) tended to rise (2p = 0.07) and blood pressure and urinary albumin excretion rate (UAE; radioimmunoassay) were reduced. In contrast, metoprolol caused a decline in RPF, an increase in renal resistance and filtration fraction, and no change in blood pressure or UAE. In 10 diabetic, nephropathic patients undergoing treatment with metoprolol and thiazide (Study B), the acute response to enalaprilat corresponded closely to that observed in Study A, including a decrease in UAE and blood pressure. Over 6 months the addition of enalapril (20 mg/d) to metoprolol and thiazide produced a more pronounced UAE-reduction, although no significant decrease in blood pressure was observed. The present findings support that ACE-I may process specific renoprotective effects. A combination therapy with beta1 blockers, ACE-I, and diuretics is suggested.

Adult↗
PubMed1982

Possible regulatory role of histamine in human platelet function examined by thrombin-induced serotonin release.

The influence of histamine on human platelet function was studied by thrombin-induced serotonin release. The thrombin-induced 3H-serotonin release was confirmed to be a rapid process which does not require external calcium. Histamine was found to reduce the release of serotonin and the inhibition was abolished when H1-plus H2-antagonists were added together with histamine. H1- and H2-receptor stimulation was examined in two ways, by a combination of histamine with cimetidine or diphenhydramine and by the selective agonists 2-(2-pyridyl)-ethylamine and impromidine. In both instances H1- and H2-stimulation was found to reduce the platelet serotonin release. These results suggest a regulatory role of histamine in the platelet function by stimulation of platelet H1- and H2-receptors.

Blood Platelets↗
PubMed1980

Histamine H2 receptor-mediated cyclic AMP formation in human platelets.

The influence of histamine on the level of cyclic AMP was studied in human platelets. A dose-related accumulation of cyclic AMP was obtained, culminating at about 10 microM of histamine. The response was blocked by the H2 antagonist cimetidine, but neither by H1 antagonists nor by alpha- or beta-adrenergic antagonists. The results suggest that histamine causes an accumulation of cyclic AMP in human platelets by stimulation of H2 receptors. Cyclic AMP accumulation is supposed to be associated with a depression of the platelet function, and a reduced platelet release reaction was actually demonstrated by our results.

Blood Platelets↗
PubMedDate not supplied

24-h blood pressure recordings in type I diabetic patients.

Ambulatory blood pressure (AMBP) is of particular interest in diabetes because of the close association between elevated BP and diabetic nephropathy and the attenuated night drop in some diabetic subgroups: (1) Normoalbuminuric patients: If standardized for type of day (work or day off), coefficient of variation (CV) for 24 h AMBP is 2%-3% and 5%-6% for night/day ratio. The male-female difference in AMBP seen in healthy subjects is reduced in diabetes. Smoking did not significantly affect AMBP. AMBP is increased in patents with high normal urinary albumin excretion (UAE). Night/day ratio of AMBP and night heart rate is higher in long than short term diabetic patients. This difference in night/day ratio is not significant if the slightly higher UAE in long-term patients is accounted for. (2) Microalbuminuric patients: Diastolic night/day ratio is increased compared with healthy controls, with the value for normoalbuminuric patients in between. A large overlap between groups is evident. Thus the prognostic value of a single abnormal night/day ratio is doubtful. If divided into dippers and nondippers, no difference in extracellular- or plasma volume is found, but nondippers have a lower plasma aldosterone and arginine vasopressin level, possibly to counteract volume expansion. (3) Patients with overt nephropathy: A marked increased in AMBP and a clear reduction of the nocturnal blood pressure fall is seen. In conclusion, AMBP (but not night/day ratio) is highly reproducible. The association between elevated AMBP, elevated night/day ratio, and pathological UAE is detectable even in normoalbuminuric patients. The prognostic importance of abnormal circadian variation of BP is unsettled.

Albuminuria↗
PubMedDate not supplied

Blood pressure by 24 h ambulatory recordings in type 2 (non-insulin dependent) diabetics. Relationship to urinary albumin excretion.

The relationship between blood pressure and microalbuminuria, both associated with cardiovascular disease and death, is sparsely studied in Type 2 (non-insulin-dependent) diabetes, and results may be interfered by the phenomenon of "white-coat-hypertension". We therefore investigated blood pressure by 24h ambulatory recordings (oscillometry) and examined whether blood pressure related to the level of urinary albumin excretion rate (UAER) by synchronous 24h collections. Seventeen diabetics (50-75 years of age) with microalbuminuria (15 less than UAER less than 200 micrograms/min) (DM), 15 with normal urinary albumin excretion (DN) and 10 healthy controls (C) participated. All groups were of comparable sex, age degree of obesity and had normal serum creatinine, and the groups of diabetics were of similar known duration, glycemic control and frequency of antihypertensive treatment. Blood pressures measured at the clinic were significantly higher (p less than 0.01) than 24h recordings. An average systolic pressure of 142 +/- 11 mmHg in DN was increased (p less than 0.01) as compared to C: 130 +/- 10 mmHg, but no further increase was seen in DM: 146 +/- 19 mmHg. Diastolic pressures were not different among the groups (C: 77 +/- 8 mmHg, DN: 80 +/- 11 mmHg, DM: 79 +/- 9 mmHg). Average 24h systolic pressure correlated to the UAER r = 0.61, p = 0.009 in DM, whereas not in DN. By the present method we found isolated systolic hypertension in Type 2 diabetes which may express "vascular stiffness". There was, however, no further rise in blood pressure in patients with microalbuminuria, but in these patients albuminuria may be pressure dependent and/or expressive of vascular pathology.

Aged↗
PubMedDate not supplied

Effects of captopril on ambulatory blood pressure, renal and cardiac function in microalbuminuric type 1 diabetic patients.

OBJECTIVE: To study the effect of Captopril on ambulatory blood pressure, renal and cardiac function and extracellular volume in microalbuminuric Type 1 diabetic patients. DESIGN: Randomized, double blind placebo controlled study of two years duration. SETTING: University clinic. PATIENTS: Twenty-two patients without hypertension. INTERVENTION: Patients received 50 mg Captopril or placebo twice a day. MEASUREMENTS: Ambulatory blood pressure, renal function, extracellular volume, and echocardiographic indices of cardiac function and dimensions were assessed annually. Clinic blood pressure and urinary albumin excretion were measured every 3 months. RESULTS: Twenty-four hour mean arterial blood pressure was unchanged in the Captopril group (mean +/- SD) (baseline 93 +/- 4 and follow up 91 +/- 8 mmHg) and in the placebo group (96 +/- 7 and 97 +/- 10 mmHg, NS). Night/day ratio of blood pressure was unaffected. Glomerular filtration rate was unchanged and renal plasma flow increased in the Captopril (557 +/- 97 and 600 +/- 112 ml min-1) versus the placebo group (574 +/- 85 and 535 ml min-1, p = 0.05). Filtration fraction was reduced in the Captopril versus the placebo group (p < 0.05). Extracellular volume and echocardiographically derived parameters were unaffected. The relative change in day time mean arterial blood pressure in the Captopril group correlated with changes in urinary albumin excretion (Spearmans r = 0.85, p < 0.05) unlike clinic mean arterial blood pressure (r = 0.33, p = 0.35). CONCLUSION: Diurnal rhythm of blood pressure was unaffected by long term administration of Captopril. Renal plasma flow was increased and filtration fraction reduced. A significant association between changes in urinary albumin excretion and blood pressure after Captopril was revealed only by the implementation of ambulatory blood pressure measurements.

Adult↗