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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 361 records · Page 20Linked to original sources
PubMed1995

The effect of dietary salt on insulin sensitivity.

Acute reduction of salt intake causes an increase in serum lipid and insulin levels in healthy volunteers and patients with essential hypertension, suggesting induction of insulin resistance by salt restriction. Direct measurements of insulin sensitivity using the euglycaemic clamp showed no significant change after 7 days of salt restriction. Our previous study showed a time dependent course of dyslipidaemia after institution of a low salt diet. We therefore assessed insulin sensitivity (M-value) under euglycaemic conditions (clamp technique) at discrete time points using a parallel group design. Two groups of healthy males were examined on high (200 mmol d-1) and low (20 mmol d-1) salt intake. One group (n = 7, 25 +/- 3 years, BMI 22.4 +/- 2.1 kg m-2) received high and low salt diet in random order each for 7 days. The other group (n = 7, 26 +/- 3 years, 22.1 +/- 1.9 kg m-2) received the respective diet in random order for 3 days. A significantly (P < 0.01) different mean M-value was noted in the group receiving the diets for 3 days, i.e. after low salt intake it was 7.4 +/- 1.2 mg kg-1 min-1 and after high salt intake 8.6 +/- 1.1 mg kg-1 min-1. In contrast, the mean M-value was similar after low and high salt periods in the group of individuals who had been studied after 7 days on either salt take (7.8 +/- 1.8 on low salt vs. 7.6 +/- 1.3 mg kg-1 min-1 on high salt).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Quantification of urinary insulin-like growth factors (IGFs) and IGF binding protein 3 in healthy volunteers before and after stimulation with recombinant human growth hormone.

We examined excretion of urinary insulin-like growth factors I and II (IGF-I and IGF-II) and their major binding protein IGFBP-3 in comparison to their respective serum concentration in nine healthy female volunteers (median age 25 years, range 22-27) under baseline conditions and after stimulation with recombinant human growth hormone (rhGH), 4.5 IU twice daily subcutaneously for a period of 3 days. The IGFs were measured in unconcentrated urine by use of recently developed, highly sensitive radioimmunoassays. The IGFBP-3 was measured by a specific radioimmunoassay. The mean (+/- SD) urinary concentrations of IGF-I (0.08 +/- 0.07 micrograms/l), IGF-II (1.02 +/- 0.47 micrograms/l) and IGFBP-3 (19.1 +/- 6.9 micrograms/l) were two to three orders of magnitude lower than in serum. The ratio of IGF-II over IGF-I concentration in urine (13:1) was five times higher than in serum (2.5:1), and the ratio of IGFBP-3 over the sum of IGF-I and IGF-II in urine (17:1) was four times higher than in serum (4:1). Urinary excretion was 63.3 +/- 46.6 ng.m-2.24h-1 for IGF-I, 1002 +/- 598 ng.m-2.24h-1 for IGF-II and 18039 +/- 4983 ng.m-2.24h-1 for IGFBP-3. Using fast protein liquid exclusion chromatography, only immunoreactive IGFBP-3 components of less than 60 kD were detected in urine, with a major peak at 20 kD. Urinary IGFBP-3 excretion correlated with serum IGFBP-3 (r = 0.61, p < 0.01) and the glomerular filtration rate (r = 0.56, p < 0.05) measured by steady-state inulin infusion clearances.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Renin gene expression in human kidney biopsies from patients with glomerulonephritis or graft rejection.

The expression of renin mRNA was determined by a quantitative polymerase chain reaction assay in 27 human kidney samples: (1) 15 biopsies of patients with glomerulonephritis with or without angiotensin-converting enzyme inhibitor (ACEI) treatment; (2) biopsies of six renal allografts with graft rejection; and (3) six biopsy samples from unaffected parts of tumor nephrectomy specimens as controls. After isolation of RNA, 0.5 to 1 microgram of total RNA was used for reverse transcription to generate cDNA. The human renin gene was subsequently amplified by the use of two primers spanning the second and third exons. Renin expression was quantified with a renin cDNA mutant as the internal standard. It exhibited the same primer binding sites as the endogenous gene but carried a 155-basepair deletion, thus yielding a shorter amplification product. The number of glomeruli was counted by microscopic transillumination immediately after biopsy (median, 9 per biopsy; range, 2 to 23). Renin mRNA was expressed as femtograms of renin mRNA per glomerulus. Renin gene expression was lower in glomerulonephritic patients without ACEI treatment compared with that in control tumor nephrectomy samples, i.e., 63 +/- 20 (N = 7) versus 250 +/- 50 fg (N = 6) of renin mRNA/glomerulus, (P < 0.02), although plasma renin concentration in the glomerulonephritic patients was in the normal range. Significantly higher renin mRNA expression was found in glomerulonephritic patients treated with ACEI, i.e., 210 +/- 50 (N = 8) compared with 63 +/- 20 (N = 7) fg of renin mRNA/glomerulus in patient not treated with ACEI (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

More adverse renal prognosis of autosomal dominant polycystic kidney disease in families with primary hypertension.

Marked variability of age at renal death is noted in autosomal dominant polycystic kidney disease (ADPKD). The hypothesis that the coexistence of primary hypertension and ADPKD within families is associated with earlier renal death was tested. Of a total of 162 ADPKD patients treated in one Austrian and three German centers, 57 propositi were identified whose families provided (1) information concerning blood pressure; (2) documented presence of ADPKD (by sonography or autopsy) in one parent; and (3) age at renal death in the propositus. Hypertension of the unaffected parent was defined as blood pressure above 140/90 mm Hg or antihypertensive treatment before age 60 yr. Age at renal death in the propositus was defined as the start of renal replacement therapy. Median age at renal death of 23 offspring (11 male, 12 female) from families with a history of primary hypertension of the nonaffected parent was lower than that of 34 offspring (16 male, 18 female) from families without a known history of primary hypertension of the nonaffected parent, i.e., 49 yr (26 to 64) versus 54 yr (28 to 82) (P < 0.03). The data are consistent with the notion that genetic predisposition to primary hypertension is associated with an earlier onset of terminal renal failure in families with ADPKD.

Adult↗
PubMed1995

Association of M235T variant of the angiotensinogen gene with familial hypertension of early onset.

A higher frequency of a variant of the angiotensinogen gene characterized by a transition in exon 2 causing a replacement of methionine by threonine (M235T) has recently been found in hypertensive individuals, but not all authors were able to confirm this observation. We examined (i) 219 patients with primary hypertension, (ii) 92 normotensive controls (spouses), and (iii) a sample of the general population (blood donors, n = 139). Analysis of genomic DNA was performed by PCR amplification and alleles were separated on agarose gels. In the general population and in normotensive spouses the respective frequencies of the T and M alleles were: general population: M = 0.6, T = 0.4; normotensive spouses: M = 0.59, T = 0.41. A significantly higher frequency of the 235T allele was found in hypertensive individuals with a family history of hypertension and an onset of hypertension before 50 years of age (spouses: 0.41 versus HT with age of onset < or = 50 years and family history of HT: 0.56; P = 0.01 by chi 2). In conclusion, the present study confirms the observation of a higher frequency of the 235T allele of the angiotensinogen gene in hypertension and identifies individuals with family history and early onset of hypertension as individuals at risk.

Adolescent↗
PubMed1995

Influence of ACE inhibition on glucose tolerance in patients with stable chronic renal failure.

ACE inhibitors improve glucose tolerance and insulin sensitivity in hypertensive patients with normal renal function. Hypertensive patients with renal failure are a high-risk group who are particularly glucose intolerant and insulin resistant. We have therefore studied whether ACE inhibition improve glucose tolerance in this group as well. In a double-blind placebo-controlled crossover study 10 patients with stable moderate chronic renal failure (mean endogenous creatinine clearance 40 +/- 16 ml/min/1.73 m2) were examined. Patients were randomly allocated to receive either placebo or the ACE inhibitor perindopril (2 mg/day per os) for 14 days. After 7 days of wash-out they received the alternative medications in random order for another 14 days. Before and after each of the two treatment periods (day 1 and day 15) an intravenous glucose tolerance test (i.v. GTT) with concomitant determination of insulin levels was performed. The glucose disappearance rate (K value) was calculated to express changes in glucose tolerance. An i.v. GTT was also performed in a group of healthy volunteers. The mean K value was significantly (P < 0.05) lower, i.e. glucose tolerance was impaired, in patients compared with healthy controls. In addition, baseline and peak insulin levels after the i.v. GTT were significantly higher (P < 0.05) in patients than in healthy subjects. The K values in patients before and after placebo treatment (1.33 +/- 0.31 and 1.41 +/- 0.45 respectively) were not significantly different from the values with perindopril treatment (1.35 +/- 0.37 and 1.41 +/- 0.48 respectively). Furthermore, no significant differences between placebo and perindopril treatment were found with respect to the insulin response to the glucose load. The peak (5 min) insulin concentrations after the i.v. glucose load were 49.0 +/- 19.2 microU/ml (day 1) and 50.0 +/- 24.9 (day 15) with placebo and 49.2 +/- 19.3 (day 1) and 46.8 +/- 17.9 (day 15) with perindopril.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Immunological determination of advanced glycosylation end-products in human blood and urine.

Advanced glycosylation end-products (AGE) in human blood and urine were investigated with the aid of an AGE-specific enzyme-linked immunosorbent assay. Evidence is presented that AGE are natural constituents of human serum and urine. In diabetics with normal renal function only a small increase in serum AGE levels was found as compared to normal controls, while no difference in urinary excretion rate was discernible. Urinary excretion rate of AGE from diabetic and non-diabetic patients with end-stage renal disease was reduced, while high serum AGE levels were observed. AGE in serum occur in a low-molecular-weight fraction and in a possibly protein-bound high-molecular-weight fraction. In urine from normal controls three immunologically reactive fractions were detected whose apparent molecular mass ranged from 100 to 1000 Daltons, while in urine from patients with end-stage renal failure additional high-molecular-weight fractions appeared.

Adolescent↗
PubMed1995

Renal reserve in the elderly.

The increase in glomerular filtration rate after an amino acid load, the so-called renal reserve, was found to be impaired in the aged rat. Renal diseases progress more rapidly in the elderly. Whether the renal reserve predicts progression of renal disease is controversial, however, and generally little information on renal reserve in elderly subjects is available. We examined renal hemodynamics before and after an amino acid infusion in 15 healthy normotensive subjects of young age (median age, 26 years [23 to 32]) and in 10 of old age (70 years [61 to 82]). Median basal inulin (Cin) and paraaminohippurate (Cpah) steady-state clearances were significantly lower in the elderly (102 and 339 mL/min/1.73 m2) than in the young subjects (122 and 647 mL/min/1.73 m2), but virtually all GFR values of the elderly were still within the normal range. The median percent rise of Cin was +16% in young and +17% elderly subjects (independent of gender). A well-preserved renal reserve was also confirmed by two other studies; one in chronically ill elderly patients treated for various nonnephrological diseases using an amino acid load and the other in healthy elderly volunteers in which renal reserve was tested with a protein (meat) meal. The mean absolute renal reserve in the three cohorts studied was between 16 and 26 mL/min/1.73 m2, the oldest patient studied was 89 years. The results of these studies document that in humans renal functional reserve is preserved at least until age 90 years in women and men.

Adult↗