Biomedical subjects

Barbara Rantner

Publications and source records attributed to Barbara Rantner.

5 recordsLinked to original sources

PubMed2006

Association of ankle-brachial index and plaques in the carotid and femoral arteries with cardiovascular events and total mortality in a population-based study with 13 years of follow-up.

AIMS: Peripheral arterial occlusive disease is associated with a high risk of cardiovascular morbidity and mortality. We prospectively examined the association of the ankle-brachial index (ABI) and arterial plaques in carotid and femoral arteries with incident myocardial infarctions (MIs) and cardiovascular and total mortality in 1325 participants of the population-based MONICA Augsburg Survey 1989/90. METHODS AND RESULTS: At baseline, 6.1% of men and 2.6% of women had an ABI < or =0.9. At least one plaque in the carotid or femoral arteries was identified in 51.8% of men and 36.3% of women. During a 13-year follow-up, 58 persons (4.4%) suffered a MI before age 75 and 189 persons (14.3%) died, 86 (6.5%) of them from cardiovascular causes. Kaplan-Meier curves confirmed both measurements as strong predictors for all three endpoints (P<0.0001). Cox regression analysis revealed an increase of the risk for MI and cardiovascular and total mortality of 22 (P=0.012), 35, and 32% (P<0.00001), respectively, per 0.1 unit decrease in ABI. Correction for measurement error in ABI increased these estimates. The increase in risk for MI and cardiovascular and total mortality was 52, 70, and 45%, respectively, for each increase in the number of plaque-affected arteries (P<0.0001). CONCLUSION: Both ABI and number of plaque-affected arteries are strong predictors for incident MI and cardiovascular and total mortality.

Adult↗

PubMed2006

Atherosclerosis as a risk factor for benign prostatic hyperplasia.

OBJECTIVES: To evaluate the relationship between clinical benign prostatic hyperplasia (BPH) and atherosclerosis, using colour Doppler ultrasonography (CDUS) and symptom scores. PATIENTS, SUBJECTS AND METHODS: CDUS was used to evaluate prostatic vascularity in four groups of men, comprising young healthy subjects, patients presenting with coronary artery disease (CAD), diabetes mellitus, or peripheral arterial occlusive disease (PAOD). Resistive index (RI) measurements and computer-assisted quantification of colour pixel density (CPD) were used to objectively evaluate perfusion. The International Prostate Symptom Score (IPSS) and the International Index of Erectile Function were used to quantify symptoms. RESULTS: In diabetic patients and men with PAOD, perfusion of the transition zone (TZ) of the prostate was significantly lower (P < 0.001) and the RI of the TZ was significantly higher (P < 0.001) than in healthy controls and men with CAD. In diabetics and men with PAOD, the mean prostate volume was greater than in healthy controls and men with CAD. The IPSS in patients with vascular damage (diabetes, PAOD) was significantly worse than in the control group. CONCLUSIONS: The significantly lower CPD and higher RI values of the TZ in patients with vascular disease than in healthy subjects support the hypothesis that an age-related impairment of blood supply to the prostate has a key role in the development of BPH.

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PubMed2006

Role of the kidney in the metabolism of apolipoprotein A-IV: influence of the type of proteinuria.

Increased plasma concentrations of apolipoprotein A-IV (apoA-IV) in chronic renal disease suggest a metabolic role of the kidney for this antiatherogenic protein. Therefore, we investigated patients with various forms of proteinuria and found increased serum concentrations of apoA-IV in 124 nephrotic patients compared with 274 controls (mean 21.9 +/- 9.6 vs. 14.4 +/- 4.0 mg/dl; P < 0.001). Decreasing creatinine clearance showed a strong association with increasing apoA-IV levels. However, serum albumin levels significantly modulated apoA-IV levels in patients with low creatinine clearance, resulting in lower levels of apoA-IV in patients with low compared with high albumin levels (21.4 +/- 8.6 vs. 29.2 +/- 8.4 mg/dl; P = 0.0007). Furthermore, we investigated urinary apoA-IV levels in an additional 66 patients with a wide variety of proteinuria and 30 controls. Especially patients with a tubular type of proteinuria had significantly higher amounts of apoA-IV in urine than those with a pure glomerular type of proteinuria and controls (median 45, 14, and 0.6 ng/mg creatinine, respectively). We confirmed these results in affected members of a family with Dent's disease, who are characterized by an inherited protein reabsorption defect of the proximal tubular system. In summary, our data demonstrate that the increase of apoA-IV caused by renal impairment is significantly modulated by low levels of serum albumin as a measure for the severity of the nephrotic syndrome. From this investigation of apoA-IV in urine as well as earlier immunohistochemical studies, we conclude that apoA-IV is filtered through the normal glomerulus and is subsequently reabsorbed mainly by proximal tubular cells.

Adult↗

PubMed2004

The apolipoprotein(a) size polymorphism is associated with nephrotic syndrome.

BACKGROUND: The atherogenic serum lipoprotein(a) [Lp(a)] is significantly elevated in patients with nephrotic syndrome. The underlying mechanism for this elevation is poorly understood. METHODS: We investigated in 207 patients with nondiabetic nephrotic syndrome and 274 controls whether the apolipoprotein(a) [apo(a)] kringle-IV repeat polymorphism explains the elevated Lp(a) levels in these patients. RESULTS: Patients showed a tremendous elevation of Lp(a) concentrations when compared to controls (mean 60.4 vs. 20.0 mg/dL and median 29.8 vs. 6.4 mg/dL, P < 0.0001). Primary and secondary causes contributed to this elevation. The primary causes became apparent by a markedly elevated number of low-molecular-weight apo(a) phenotypes which are usually associated with high Lp(a) levels. This frequency was 35.7% in patients compared to only 24.8% in controls (P= 0.009). In addition, secondary causes by the pathogenetic mechanisms of the nephrotic syndrome itself resulted in a different increase of Lp(a) in the various apo(a) isoform groups. Based on the measured Lp(a) concentrations in each subject, we calculated separately the Lp(a) concentrations arising from the two expressed isoforms by estimating the relative proportion of the two serum isoforms in the sodium dodecyl sulfate (SDS) agarose gel electrophoresis. Low-molecular-weight isoforms were associated with 40% to 75% elevated Lp(a) concentrations when compared to matched isoforms from controls. High-molecular-weight apo(a) isoforms showed 100% to 500% elevated Lp(a) levels compared to matched isoforms from controls. The severity of the nephrotic syndrome as well as the degree of renal impairment did not influence the Lp(a) concentrations. CONCLUSION: The tremendously increased Lp(a) levels in nephrotic syndrome ar caused by primary genetic as well as disease-related mechanisms.

Adult↗

PubMed2004

Lipoprotein(a)- and low-density lipoprotein-derived cholesterol in nephrotic syndrome: Impact on lipid-lowering therapy?

BACKGROUND: Patients with nephrotic syndrome have the highest lipoprotein(a) [Lp(a)] concentrations known. Lp(a) is an low-density lipoprotein (LDL)-like particle consisting of 45% cholesterol. The usual methods to determine LDL cholesterol do not distinguish between cholesterol derived from LDL and Lp(a) and are thus the net result of cholesterol levels from both lipoproteins. High Lp(a) concentrations therefore significantly contribute to the measured or calculated LDL cholesterol levels. Since statins have no influence on Lp(a) levels, it can be expected that the LDL cholesterol-lowering effect of statins may be diminished in patients who have a pronounced elevation of Lp(a) levels accompanied by only moderate elevations of LDL cholesterol. METHODS: We investigated 207 patients with nondiabetic nephrotic syndrome in whom Lp(a) concentrations were strikingly elevated when compared to 274 controls (60.4 +/- 85.4 mg/dL vs. 20.0 +/- 32.8 mg/dL, P < 0.0001). RESULTS: According to National Kidney Foundation Dialysis Outcomes Quality Initiative (K/DOQI) Clinical Practice Guidelines for Managing Dyslipidemias, almost 95% of these patients are candidates for a therapeutic intervention to lower LDL cholesterol. LDL cholesterol levels corrected for Lp(a)-derived cholesterol, however, were 27 mg/dL lower than uncorrected concentrations (compared to only 9 mg/dL in controls). If Lp(a)-corrected levels instead of total LDL cholesterol levels were used, 25.7% of patients with low-molecular-weight (LMW) apolipoprotein(a) [apo(a)] isoforms were classified no longer to be in need of LDL cholesterol-lowering therapeutic intervention compared to only 2.3% of patients with high-molecular-weight (HMW) apo(a) phenotypes (P < 0.00001). This ("pseudo") pharmacogenetic effect results in incorrect determination of LDL cholesterol. CONCLUSION: Our observation has an impact on the indication for, and assessment of efficacy of intervention. This potential artifact should be investigated in ongoing large trials in renal patients as well as in nonrenal African American subjects who have on average markedly higher Lp(a) levels. In nonrenal Caucasian subjects with much lower Lp(a) concentrations, this issue will be less relevant.

Adult↗