Analytical estimation of non-local deformation-mediated magneto-electric coupling in soft composites.

For a long time, the search for magneto-electric materials concentrated on multi-ferroics and hard-matter composites. By contrast, rather recently the exploitation of strain-mediated magneto-electric (ME) coupling in soft composites was proposed. The basic idea behind this approach is to combine the magneto- and electro-mechanical responses of composites consisting of a soft matrix carrying magnetic inclusions. Despite that such composites are straightforward to manufacture and have cheap constituents, they did not gain much attention up to now. In this contribution, we demonstrate that ME coupling induced by finite deformations could be of significant magnitude. Our approach relies on shape effects as a special non-local phenomenon in magneto- and electro-elasticity. Based on that we characterize an up to now overlooked ME coupling mechanism which purely relies on these shape effects in soft-matter-based magnetic and electric media. While soft magnetic media are commonly realized as composites, the coupling effect to be highlighted exists independently of the origin of a body's magnetic and electric properties. We show that the magnitude of the effect is indeed significant and, among ellipsoidal bodies, most pronounced for those of spherical to moderately prolate shape. Finite-element simulations are performed to assess the quality of the analytical predictions.

Smoking as a risk factor for end-stage renal failure in men with primary renal disease.

BACKGROUND: It is not known whether smoking increases the risk of end-stage renal failure (ESRF) in patients with primary renal disease. METHODS: We performed a retrospective multicenter case-control study including 582 patients from nine centers in Germany, Italy and Austria. The diseases investigated were IgA glomerulonephritis (IgA-GN) as a model of inflammatory renal disease and autosomal dominant polycystic kidney disease (ADPKD) as a model of non-inflammatory renal disease. Cases were patients who had progressed to ESRF and controls were patients who were not in ESRF, that is, whose serum-creatinine failed to progress to >3 mg/dl during the observation period and who did not require renal replacement therapy. Matching for renal disease (IgA-GN, ADPKD), gender, age at renal death and region of residence resulted in 102 individually matched pairs (IgA-GN N = 54, ADPKD N = 48). Multiple conditional logistic regression was used to estimate adjusted odds ratios for independent tobacco effects. RESULTS: In men (matched pairs: IgA-GN N = 44, ADPKD N = 28), a significant dose-dependent increase of the risk to progress to ESRF was found (non-adjusted). The baseline risk was defined as <5 pack-years (PY): (i) 5 to 15 PY, odds ratio 3.5 (95% CI 1.3 to 9.6), P = 0.017; (ii) >15 PY = 5.8 (2.0 to 17), P = 0.001. Systolic blood pressure, ACE inhibitor treatment and age at diagnosis emerged as potential confounders. After adjustment, the risk for ESRF in men with >5 PY was highly increased for patients without ACE inhibitor treatment [10.1 (2.3 to 45), P = 0.002] but not with ACE inhibitor treatment [1.4 (0.3 to 7.1), P = 0.65]. CONCLUSION: Smoking increases the risk of ESRF in men with inflammatory and non-inflammatory renal disease.

Concentration of dimethyl-L-arginine in the plasma of patients with end-stage renal failure.

Abstract. NGNG dimethyl-L-arginine (asymmetric dimethyl-L-arginine; ADMA) and NGNG dimethyl-L-arginine (symmetric dimethyl-L-arginine; SDMA) are naturally occurring analogues of L-arginine, the substrate for nitric oxide (NO) synthesis. ADMA is a potent inhibitor of NO synthesis, and accumulates in the plasma of patients with renal failure. However the precise concentration of ADMA and SDMA in renal patients is still controversial. This study was performed to measure plasma ADMA and SDMA concentrations by two different HPLC techniques in nine healthy controls and 10 uraemic subjects, and to investigate the effects of haemodialysis. In controls, the mean (+/-SEM) plasma concentrations of ADMA and SDMA were 0.36 +/- 0.09 and 0.39 +/- 0.05 mumol/l respectively, yielding an ADMA/SDMA ratio of 1.2 +/- 0.17. In uraemic patients, the plasma concentrations of ADMA and SDMA were 0.9 +/- 0.08 mumol/l (P < 0.001 compared to controls) and 3.4 +/- 0.3 mumol/l (P < 0.001 compared to controls) with an ADMA/SDMA ratio of 0.27 +/- 0.015 (P < 0.001). In the course of one 4 h haemodialysis session, ADMA concentrations decreased from 0.99 +/- 0.13 to 0.77 +/- 0.3 mumol/l and SDMA concentrations from 3.38 +/- 0.44 to 2.27 +/- 0.21 mumol/l. The plasma ADMA/creatinine ratio tended to increase from 1.26 +/- 0.20 x 10(-3) to 2.01 +/- 0.41 x 10(-3). It is concluded that there is a modest (3-fold) but definite increase in plasma ADMA concentration in uraemic patients compared to controls. SDMA accumulates to a greater degree (8-fold increase) and more closely parallels creatinine concentration than ADMA. The change in the ADMA/SDMA ratio is not accounted for by greater renal or dialysis clearance of ADMA, and, even though alternative explanations are not excluded, greater metabolism of ADMA than SDMA is the most likely explanation. Although small in magnitude, the increase in ADMA concentration might by biologically significant.

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.

The role of the parathyroid glands in the uremic syndrome.

The genesis of hyperparathyroidism in uremia has turned out to be quite complex, involving low calcitriol, low ionized calcium, and possibly direct effects of high phosphate as well as the action of local factors and modifier genes determining the hyperplastic response of the gland. Growth is initially polyclonal and later monoclonal. In addition, the response of target tissues to parathyroid hormone (PTH) is attenuated ("PTH resistance"), and this may be due, at least in part, to diminished phenotypic expression of PTH receptors. In a series of elegant studies, it has been shown that PTH acts not only on the classical target organs of calcium homeostasis (ie, bone and kidney), but also on nonclassical. The role of PTH excess in the genesis of several features of the uremic syndrome, for example muscle dysfunction, cardiomyopathy, leukocyte and T-cell dysfunction or insulin secretion by pancreatic islet cells, has been established. These studies have borne out the prediction that PTH is a "uremic toxin."

[Nonocclusive intestinal ischemia as a complication of hemodialysis treatment]. / Nicht-okklusive Darmischämie als Komplikation der Hämodialysebehandlung.

A 52-year-old man on haemodialysis treatment for chronic glomerulonephritis also had a nephrotic syndrome, hypercholesterolaemia, severe arterial hypertension and peripheral vascular disease in stage IIb. He also was a heavy smoker. Following a nonspecific diarrhoeal illness, which caused haemoconcentration, he developed abdominal pain and fever. WBC count (29,000/microliter) and serum lactate level (18.2 mmol/l) were elevated, and there were clinical signs of lower abdominal peritonitis. Laparotomy revealed multiple ischaemic segments. The arteries were not thrombosed but had severe atheromatous changes. There is an increasing incidence of such nonocclusive intestinal ischaemia because there are more elderly people and more patients with high-risk factors among those requiring dialysis.

Immunogenetic findings in glomerulonephritis.

In the 19th century, several authors recognized that some renal diseases tend to run in families. Alport pointed to the constellation of nephritic urinary sediment, hearing loss and progression into renal failure. Today this is recognized to result from abnormal basement membrane (BM) collagen synthesis. Recently it has been recognized, however, that other forms of glomerulonephritis may also run in families. In about 10% of patients with glomerulonephritis one or more sibling also suffers from glomerulonephritis. Genetically determined derangements of immune regulation may play a role in the genesis of primary chronic glomerulonephritis. Potentially associated immunogenetic abnormalities include inherited defects of the complement system, increased prevalence of certain HLA-types, altered frequencies of polymorphisms in immunoglobulins and TCR genes and others. This overview summarizes immunogenetic studies performed in patients with glomerulonephritis with special emphasis on patients with mesangial IgA GN.

Structural causes of cardiac dysfunction in uremia.

While coronary heart disease is undoubtedly a major cause of cardiac morbidity and mortality in uremia, important noncoronary problems contribute to the common presence of cardiac problems. Based on clinical and experimental studies, we could show: (i) Left ventricular hypertrophy (LVH) can be dissociated, at least in part, from elevation of blood pressure. (ii) In uremia, PTH-dependent intermyocardiocytic fibrosis occurs; it may account, at least in part, for disturbed LV compliance and contribute to the arrhythmogenic potential. (iii) Blood pressure-independent abnormalities of intracardiac arterioles and reduced myocardial capillary supply are observed.

Albuminuria of hypertensive patients.

Renal dysfunction as a consequence of malignant hypertension has been recognized for decades in patients with essential hypertension. It has been shown only recently, however, that albuminuria (including underlying albuminuria not detectable by conventional tests, i.e. microalbuminuria) has emerged as a frequent sequela of essential hypertension. Furthermore, renal dysfunction of the elderly as a result of ischemic nephropathy, in the absence of malignant hypertension, has turned out to be an important long-term outcome in the patient with essential hypertension. The presence of albuminuria is a strong predictor of cardiovascular events. Albuminuria is associated with more severe hypertension and with evidence of more advanced target organ damage (e.g. LVH). It is more prevalent in the elderly. It is unknown whether the predictive value of albuminuria reflects its association with more severe hypertension and end-organ damage, or whether albuminuria serves as an indicator of capillary leakiness which causes detectable abnormalities in the renal microcirculation but reflects more generalized endothelial barrier dysfunction predisposing to accelerated atherogenesis.