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H H Parving

Publications and source records attributed to H H Parving.

At least 127 records · Page 7Linked to original sources
PubMed1996

Fish oil in diabetic nephropathy.

OBJECTIVE: Recent studies in nondiabetic kidney diseases suggest that dietary supplementation with n-3 polyunsaturated fatty acids (fish oil) may have beneficial effects on albuminuria, kidney function, arterial blood pressure, and dyslipidemia. Therefore, we evaluated the long-term effect of fish oil in diabetic nephropathy. RESEARCH DESIGN AND METHODS: A 1-year double-blind randomized controlled study comparing fish oil (4.6 g n-3 fatty acids/day) with placebo (olive oil) was performed in an outpatient clinic in a tertiary referral center. Thirty-six normotensive IDDM patients with diabetic nephropathy were included; 18 were treated with fish oil. Seven patients dropped out (four received fish oil), and results for the remaining 29 are presented. Albuminuria (enzyme immunoassay), glomerular filtration rate (51Cr-labeled EDTA plasma clearance), 24-h ambulatory blood pressure, and lipid profile were determined every 6 months. RESULTS: Albuminuria increased by 22% (1-46%) (mean [95% CI]) in the fish oil group vs. 15% (-11-49%) in the placebo group (NS). Glomerular filtration rate decreased from 116 +/- 7 to 105 +/- 7 ml.min-1.1.73 m-2 (mean +/- SE) vs. from 108 +/- 6 to 103 +/- 7, fish oil and placebo, respectively (NS). No significant changes occurred in 24-h ambulatory blood pressure: from 141 +/- 4/82 +/- 2 mmHg to 142 +/- 5/83 +/- 2 vs. from 140 +/- 4/78 +/- 2 to 144 +/- 4/80 +/- 3, fish oil and placebo, respectively (NS). In the fish oil group, serum triglycerides (median [range]) decreased from 0.97 (0.5-4.0) mmol/l to 0.8 (0.4-3.0) vs. from 1.01 (0.4-2.0) to 1.09 (0.4-2.0) in the placebo group (P < 0.05) and VLDL cholesterol decreased from 0.45 (0.23-1.88) to 0.37 (0.21-1.43) mmol/l vs. from 0.44 (0.21-0.94) to 0.41 (0.17-1.94) (P < 0.05), but total and LDL cholesterol rose in the fish oil compared with the placebo group. CONCLUSIONS: Our study does not suggest that fish oil has beneficial effects on albuminuria, kidney function, blood pressure, and dyslipidemia in normotensive IDDM patients suffering from diabetic nephropathy.

Adult↗
PubMed1996

Increased plasma apolipoprotein (a) levels in IDDM patients with diabetic nephropathy.

OBJECTIVE: The relative mortality from cardiovascular disease (CVD) is increased 40-fold in IDDM patients suffering from diabetic nephropathy as compared with nondiabetic subjects on average. We assessed the potential contribution of dyslipidemia in general and elevated serum apolipoprotein (a) [apo(a)] in particular to CVD in nephropathic patients with IDDM. RESEARCH DESIGN AND METHODS: We investigated 199 IDDM patients with diabetic nephropathy and 192 normoalbuminuric IDDM patients matched for sex, age, diabetes duration, and BMI. RESULTS: The prevalence of CVD was 30 and 12% in patients with and without nephropathy, respectively (P < 0.001). The level of apo(a) was significantly higher in patients with nephropathy, 189 (20-2,350) U/l as compared with the normoalbuminuric group, 103 (20-1,940) U/l (P < 0.005). The prevalence of plasma apo(a) > 300 U/l (at-risk level for cardiovascular pathogenicity) was 38% (31-45) vs. 22% (16-28) in patients with and without nephropathy, respectively (P < 0.0005). In nephropathic patients, the prevalence of plasma apo(a) > 300 U/l was raised in patients with CVD (48%, 36-61%) as compared with patients without (34%, 26-42%) (P = 0.05). Furthermore, the serum concentrations of the following apolipoproteins and lipids were higher in patients with nephropathy as compared with normoalbuminuric patients: apoB 1.33 +/- 0.37 vs. 1.06 +/- 0.26 g/l; total cholesterol 5.6 +/- 1.2 vs. 4.8 +/- 0.9 mmol/l; and triglycerides 1.22 (0.31-9.87) vs. 0.77 (0.28-3.05) mmol/l, P < 0.0001. Multiple logistic regression analysis of cardiovascular risk factors revealed that plasma apo(a) concentration > 300 U/l is an independent risk factor for coronary heart disease, odds ratio 1.86 (1.03-3.36) (P < 0.05). CONCLUSIONS: Dyslipidemia and raised plasma concentrations of apo(a), particularly > 300 U/l, may contribute to the enhanced morbidity and mortality from CVD characteristically observed in IDDM patients with diabetic nephropathy.

Adult↗
PubMed1996

Raised serum sialic acid concentration in NIDDM patients with and without diabetic nephropathy.

OBJECTIVE: Raised serum sialic acid concentration is a strong predictor of cardiovascular mortality in the general white population. A progressive increase in cardiovascular morbidity and mortality takes place in relation to increasing albuminuria in NIDDM patients. Therefore, we investigated the potential association between serum sialic acid and micro- and macroangiopathy in NIDDM patients. RESEARCH DESIGN AND METHODS: We studied a prevalence cohort of all white NIDDM patients < 76 years of age attending a diabetic clinic during 1 year. Of the patients, 319 had normoalbuminuria, 148 had microalbuminuria, and 75 had macroalbuminuria (diabetic nephropathy was in 47 of 75 patients); 66 nondiabetic age- and sex-matched subjects acted as a control group. Blood samples were taken for measurements of sialic acid, lipids, creatinine, and HbA1C. Retinopathy was assessed by funduscopy. The prevalence of cardiovascular disease was based on Minnesota-coded electrocardiograms and the World Health Organization cardiovascular questionnaire. RESULTS: A progressive raise in serum sialic acid was demonstrated with an increasing urinary albumin excretion rate: [median (range)] 2.02 (1.55-2.63); 2.42 (1.47-6.48); 2.67 (1.57-5.86), and 2.95 (1.52-7.86) mmol/l in nondiabetic subjects, NIDDM patients with normoalbuminuria, microalbuminuria, and diabetic nephropathy, respectively (P < 0.05 or less for differences between groups). Multiple linear regression analysis showed that serum cholesterol concentration, serum HDL cholesterol concentration, BMI, albuminuria, smoking, and cardiovascular disease correlate independently with logarithmic (10) serum sialic acid concentration. CONCLUSIONS: Our study revealed a progressive raise in serum sialic acid with increasing urinary albumin excretion rate in NIDDM patients. Furthermore, several modifiable cardiovascular risk factors were associated with serum sialic acid.

Aged↗
PubMed1996

The acute effect of smoking on systemic haemodynamics, kidney and endothelial functions in insulin-dependent diabetic patients with microalbuminuria.

The acute effect of smoking upon arterial blood pressure, urinary albumin excretion rate, glomerular filtration rate and transcapillary escape rate of albumin were investigated in nine normotensive insulin-dependent diabetic patients with microalbuminuria, who had been smoking for 19 (range 4-30) years. In a prospective, open randomized cross-over design, patients were investigated with and without smoking three cigarettes per hour during a 5.5-h period. A rise in systolic blood pressure and heart rate (Takeda TM2420, median (range)) was observed during the smoking day (10(-11 to 14) mmHg and 8 (-1 to 19) beats min-1), compared to the non-smoking day (1 mmHg (-7 to 13) (p = 0.05) and 0 beats min-1 (-2 to 4) (p < 0.01)). Urinary albumin excretion rate (ELISA), glomerular filtration rate (plasma clearance of 51Cr-EDTA) and transcapillary escape rate of albumin (125I-albumin) remained the same with or without smoking. Our study suggests that heavy smoking induces an abrupt rise in systolic blood pressure and heart rate, while vascular leakage of albumin and glomerular filtration rate remain unaltered in normotensive insulin-dependent diabetic patients with microalbuminuria who had been smoking for several years.

Adult↗
PubMed1996

Angiotensin-II type 1 receptor gene polymorphism and diabetic microangiopathy.

BACKGROUND: Genotypic abnormalities of the renin-angiotensin system have been suggested as risk factors for the development of hypertension, diabetic nephropathy and proliferative retinopathy. Most of the known actions of angiotensin-II are exerted through the angiotensin-II type 1 receptor, which is present particularly in vascular smooth muscle cells, myocardium and the kidney. A transversion of adenine to cytosine at nucleotide position 1166 in the gene coding for the angiotensin-II type 1 receptor has been associated with hypertension in the non-diabetic population. METHODS: We studied the relationship between the A1166-->C polymorphism in the angiotensin-II type 1 receptor gene in patients with insulin dependent diabetes mellitus (IDDM) and diabetic nephropathy (121 men, 77 women, age 41 +/- 10 years, diabetes duration 27 +/- 8 years) and in IDDM patients with normoalbuminuria (116 men, 74 women, age 43 +/- 10 years, diabetes duration 27 +/- 8 years). 156 patients (40%) had proliferative retinopathy, 67 patients (17%) had no diabetic retinopathy. RESULTS: There was no difference in genotype distribution between IDDM patients with diabetic nephropathy and normoalbuminuria 103 (52%) / 81 (41%) / 14 (7%) vs. 97 (51%) / 80 (42%) / 13 (7%) had AA/AC/CC genotypes, respectively. The allele frequencies (A/C) in patients with nephropathy (0.73/0.27) and patients with normoalbuminuria (0.72/0.28) were also similar. No difference in genotype distribution between IDDM patients with proliferative retinopathy and without diabetic retinopathy was found either: 77 (50%) / 66 (42%) / 13 (8%) vs. 42 (63%) / 22 (33%) / 3 (4%) had AA/AC/CC genotypes, respectively. CONCLUSIONS: The A1166-->C polymorphism in the angiotensin-II type 1 receptor gene does not contribute to the genetic susceptibility to diabetic nephropathy or proliferative retinopathy in caucasian IDDM patients.

Adult↗
PubMed1995

Long-term comparison of human insulin analogue B10Asp and soluble human insulin in IDDM patients on a basal/bolus insulin regimen.

Recombinant DNA technology allows the production of insulin analogues with faster absorption rates from subcutaneous tissue as compared to soluble human insulin. The human insulin analogue B10Asp (mono/dimeric) is absorbed twice as fast as soluble human insulin (hexameric). A double blind, randomised crossover study with a 1-month run-in period and two 2-month treatment periods was performed in 21 male insulin-dependent diabetic (IDDM) patients aged 18-40 years in order to compare the metabolic control obtained with equimolar doses of the analogue B10Asp vs soluble human insulin (Actrapid) given as mealtime insulin and intermediate acting isophane insulin (Protaphane) at bedtime. At the end of each 2-month study period, the patients were admitted to the metabolic ward. We found significantly higher plasma insulin/analogue levels after breakfast, lunch and dinner with B10Asp as compared to Actrapid (p < 0.05). The plasma insulin/analogue levels were significantly lower before lunch and dinner with B10Asp as compared to Actrapid (p < 0.05). Also, the plasma insulin/analogue level tended to be lower at bedtime when comparing B10Asp to Actrapid. The 24-h blood glucose profiles showed identical fasting blood glucose, significantly lower blood glucose after breakfast with the analogue (p < 0.05), no differences in blood glucose after lunch and dinner but a significantly higher blood glucose at midnight using the analogue (p < 0.05). The overall 24-h mean blood glucose concentrations, the daily insulin dose, HbA1c, diet, home blood glucose monitoring and frequency of hypoglycaemia were almost identical in the two treatment periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Acquired oligonephropathy and diabetic nephropathy.

Congenital or acquired nephron number reduction and diabetes mellitus both induce hyperfiltration and intrarenal hypertension. These hemodynamic factors have been suggested to play an important role in the initiation and progression of diabetic and nondiabetic glomerulopathies. In a prevalence cohort of all 50 albuminuric (> or = 300 mg/24 hr), non-insulin-dependent diabetic mellitus (NIDDM) patients (aged < 66 years) attending a diabetic clinic during 1987, we identified four patients with acquired oligonephropathy who had developed diabetic nephropathy. Three patients only had a single functioning kidney (nephrectomy in two cases), and the remaining patient had unilateral severely reduced kidney function and elevated plasma renin concentration. These patients represent 8% of our NIDDM population with albuminuria, and are the only patients in our NIDDM population younger than 66 years (n = 363) known to have single kidneys. However, systematic renography screening was not performed. During the observation period, which ranged from 16 to 100 months, albuminuria increased from 2.3 g/24 hr (range, 1.2 to 3.4 g/24 hr) to 3.2 g/24 hr (range, 0.7 to 9.4 g/24 hr), glomerular filtration rate decreased to 6 mL/min/yr (range, 4 to 12 mL/min/yr), and blood pressure remained stable at 142/92 mm Hg. Three patients received antihypertensive medication. Two of the patients died after 16 and 26 months of observation, respectively, due to acute myocardial infarction and stroke. The results of our study of NIDDM patients support the concept that reduced nephron number predispose patients to the development of diabetic nephropathy.

Adult↗
PubMed1995

Angiotensin-converting enzyme inhibition in diabetic nephropathy: ten years' experience.

The aim of our prospective study was to evaluate putative progression promoters, kidney function, and prognosis during long-term treatment with angiotensin-converting enzyme inhibition in insulin-dependent diabetes mellitus patients suffering from diabetic nephropathy. Eighteen consecutive hypertensive insulin-dependent diabetes patients with nephropathy (mean age, 33 years) who had not been treated previously were all treated with captopril in combination with frusemide or bendrofluazide. The four patients who were refractory to this regimen also received nifedipine. Treatment was continued for a median of 8.9 years (range, 6.3 to 9.8, years). Renal function was assessed every 6 months by measurement of glomerular filtration rate (GFR) (single-bolus 51Cr-EDTA technique) and albuminuria by radioimmunoassay. Baseline values (+/- SE) were mean arterial blood pressure 146/93 +/- 3/1 mm Hg, albuminuria (geometric mean +/- antilog SE) 982 +/- 1.2 micrograms/min, and GFR 98 +/- 5 mL/min/1.73 m2. Angiotensin-converting enzyme inhibition induced a significant reduction during the whole treatment period of blood pressure (137/85 +/- 3/1 mm Hg; P < 0.01) and albuminuria (392 +/- 1.4 microns/min; P < 0.01), and the rate of decline in GFR was 4.4 +/- 0.7 mL/min/yr, in contrast to previous reports of 10 to 14 mL/min/yr (natural history). Univariate analysis revealed a significant correlation between the rate of decline in GFR and mean arterial blood pressure (r = 0.58, P = 0.01), albuminuria (r = 0.67, P < 0.01), hemoglobin A1c (r = 0.69, P < 0.01), and serum total cholesterol concentration (r = 0.51, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Screening and management of microalbuminuria in patients with diabetes mellitus: recommendations to the Scientific Advisory Board of the National Kidney Foundation from an ad hoc committee of the Council on Diabetes Mellitus of the National Kidney Foundation.

All individuals with diabetes mellitus should be screened yearly with a spot urine albumin:creatinine ratio to identify those who are at increased risk for the development of complications of diabetes mellitus, including nephropathy, retinopathy, and cardiovascular disease. Once these high-risk individuals are appropriately identified, it is recommended that therapy with an angiotensin-converting enzyme (ACE) inhibitor be initiated. In addition, cardiovascular risk factors should be investigated, and when appropriate, therapeutic interventions should be initiated according to existing recommendations.

Albuminuria↗
PubMed1995

Increased glomerular filtration rate after withdrawal of long-term antihypertensive treatment in diabetic nephropathy.

Initiation of antihypertensive treatment (AHT) in hypertensive insulin-dependent diabetic (IDDM) patients with diabetic nephropathy (DN) induces a faster initial (0 to 6 months) and a slower subsequent (6 months to end of observation) decline in GFR [delta GFR (ml/min/month) approximately 1.5 vs. 0.35]. Whether this initial phenomenon is reversible (hemodynamic) or irreversible (structural damage) after prolonged AHT is not known. To elucidate these mechanisms we investigated 42 hypertensive IDDM patients (16F/26M, age 40 +/- 7 years, mean +/- SD) with DN receiving AHT (angiotensin converting enzyme inhibition, N = 30) for 6 (2 to 15) years [median (range)]. GFR (ml/min/1.73 m2), arterial blood pressure (BP, mm Hg) and albuminuria (mg/24 hr) were measured the last day on AHT and one month after withdrawal of AHT. The measured variables were all significantly elevated after withdrawal of AHT: GFR [mean(SEM)] from 76(4) to 81(4) (P < 0.0001), BP [mean(SEM)] from 140/82 (2/1) to 151/89 (2/1) (P < 0.0005) and albuminuria [geometric mean (antilog SEM)] from 704 (1.2) to 1122 (1.2) (P < 0.0001). A correlation between relative rise in systolic blood pressure (delta Sys%) and relative change in GFR (delta GFR%) was found (r = 0.44, P < 0.005). Our results render some support of the hypothesis that the faster initial decline in GFR is due to a functional (hemodynamic) effect of AHT, which does not attenuate over time, while the subsequent slower decline reflects the beneficial effect on progression of diabetic nephropathy.

Adult↗
PubMed1995

Whole-body glucose metabolism in obese patients with type 2 diabetes mellitus: the impact of hypertension and strict blood glucose control.

We have examined the impact of hypertension and blood glucose control on insulin sensitivity in obese Type 2 (non-insulin-dependent) diabetic patients. Glucose metabolism in the basal state and in response to insulin was examined using the euglycaemic, hyperinsulinaemic (2 mU kg-1 min-1) clamp technique in combination with 3-[3H]-glucose infusion and indirect calorimetry in 60 obese Type 2 diabetic patients (30 normotensive patients and 30 hypertensive patients on antihypertensive treatment) and 10 obese normotensive control subjects. In the basal state and during hyperinsulinaemia, glucose disposal rates (total, oxidative, and nonoxidative) were similar in Type 2 diabetic patients with or without hypertension (230 +/- 83 vs 270 +/- 114 mg m-2 min-1 (NS), 83 +/- 28 vs 95 +/- 7 mg m-2 min-1 (NS), 148 +/- 70 vs 180 +/- 89 mg m-2 min-1 (NS), treated hypertensive vs normotensive subjects, respectively). However, compared to obese control subjects (403 +/- 65 mg m-2 min-1) both groups of diabetic patients had significantly decreased insulin-stimulated glucose disposal rates (p < 0.005). Even in a subset of Type 2 diabetic patients with long-term (> 6 months) near normal blood glucose control (HbA1c < 6.1%) significant defects were detectable in whole-body glucose and lipid metabolism when compared to control subjects. These results indicate that treated hypertension does not significantly aggravate the insulin insensitivity that is already present in Type 2 diabetes mellitus. Furthermore, Type 2 diabetic patients with long-term good metabolic control continue to demonstrate insulin insensitivity in peripheral tissues.

Adult↗
PubMed1995

Albuminuria and poor glycemic control predict mortality in NIDDM.

The impact of microalbuminuria and macroalbuminuria on mortality was evaluated prospectively in 328 Caucasian patients with non-insulin-dependent diabetes mellitus (NIDDM) followed for 5 years. One hundred ninety-one (109 men and 82 women) patients with normoalbuminuria (albumin excretion rate [AER] < 30 mg/24 h), 86 (50 men and 36 women) patients with microalbuminuria (AER 30-299 mg/24 h), and 51 (43 men and 8 women) patients with macroalbuminuria (AER > or = 300 mg/24 h) < 66 years old at entry were followed from 1987 until death or until 1 January 1993. Mean age at entry was 54 (SD 9) years. In January 1993, 8% of patients with normoalbuminuria, 20% of patients with microalbuminuria, and 35% of patients with macroalbuminuria had died (predominantly from cardiovascular disease) (P < 0.01 [normoalbuminuria versus micro- and macroalbuminuria] and P < 0.05 [microalbuminuria versus macroalbuminuria]). Cox multiple regression analysis revealed significant predictors of all-cause mortality to be preexisting coronary heart disease (relative risk [95% confidence interval]), 2.9 (1.6-5.1); log10AER (factor 10), 1.9 (1.4-2.6); HbA1c level (%), 1.2 (1.0-1.4); and age (years), 1.08 (1.03-1.13). Significant predictors of cardiovascular mortality included preexisting coronary heart disease, 6.1 (2.8-13.5); macroalbuminuria, 2.5 (1.1-5.8); HbA1c level (%), 1.3 (1.1-1.6); and systolic blood pressure (10 mmHg), 1.2 (1.0-1.4). Univariate Cox survival analysis in the normoalbuminuric group revealed that AER above the median of 8 mg/24 h was associated with an increased all-cause mortality risk of 2.7 (0.93-7.69) (P = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Low birth weight. A risk factor for development of diabetic nephropathy?

It has been demonstrated that intrauterine growth retardation, defined as birth weight below the 10th percentile, gives rise to a reduction in nephron number. Oligonephropathy has been suggested to increase the risk for systemic and glomerular hypertension in adult life as well as enhance risk for expression of renal disease after exposure to potentially injurious renal stimuli. The aim of this study was to determine if low birth weight is a risk factor for development of diabetic nephropathy. In a case-control study, we investigated 184 (110 men) insulin-dependent diabetes mellitus (IDDM) patients with diabetic nephropathy (persistent albuminuria > 300 mg/24 h) (age [mean +/- SD] 41.0 +/- 9.3 years, duration of diabetes 26.9 +/- 8.2 years) and 182 (111 men) normoalbuminuric (< 30 mg/24 h) IDDM patients (age 42.1 +/- 9.8 years, duration of diabetes 25.8 +/- 8.6 years). Information about weight at birth was obtained from the midwife's original registrations. In women below the 10th percentile in birth weight (< or = 2,700 g, n = 16), 75% had nephropathy compared with only 35% among patients whose birth weights were above the 90th percentile (> or = 4,000 g, n = 17) (P = 0.05). In men below the 10th percentile in birth weight (< or = 2,910 g, n = 22), the prevalence of patients with nephropathy (50%) was similar to the prevalence among patients above the 90th percentile in birth weight (> or = 4,200 g, n = 24) (54%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Lack of relationship between an insertion/deletion polymorphism in the angiotensin I-converting enzyme gene and diabetic nephropathy and proliferative retinopathy in IDDM patients.

Genotypic abnormalities of the renin-angiotensin system have been suggested as a risk factor for the development of diabetic nephropathy and proliferative retinopathy. We studied the relationship between an insertion(I)/deletion (D) polymorphism in the angiotensin-converting enzyme (ACE) gene in insulin-dependent diabetes mellitus (IDDM) patients with diabetic nephropathy (121 men and 77 women, age 40.9 +/- 10 years, diabetes duration 27 +/- 8 years) and in IDDM patients with normoalbuminuria (118 men and 74 women, age 42.7 +/- 10 years, diabetes duration 26 +/- 8 years). A total of 155 patients (40%) had proliferative retinopathy, and 67 patients (17%) had no diabetic retinopathy. There was no difference in genotype distribution between IDDM patients with diabetic nephropathy and those with normalbuminuria: 63 (32%)/95 (48%)/40 (20%) vs. 67 (35%)/77 (41%)/46 (24%) had DD/ID/II genotypes, respectively. Patients with nephropathy had higher plasma ACE levels (609 [151-1,504] micrograms/l) compared with patients with normoalbuminuria (428 [55-1,630] micrograms/l) (P < 0.001). Multiple linear regression analysis revealed that the plasma ACE level in patients with nephropathy is partially determined by ACE/ID polymorphism, mean arterial blood pressure, and glomerular filtration rate (r2 = 0.30, P < 0.001). There was no difference in genotype distribution between IDDM patients with proliferative retinopathy and those without diabetic retinopathy: 52 (34%)/74 (48%)/29 (19%) vs. 26 (39%)/25 (37%)/16 (24%) had DD/ID/II genotypes, respectively. There was also no difference in plasma ACE concentration detected among patients with no, simplex, or proliferative retinopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗