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Biomedical subjects

Marcin Adamczak

Publications and source records attributed to Marcin Adamczak.

12 recordsLinked to original sources
PubMed2004

Beneficial Effects of Estrogens on Indices of Renal Damage in Uninephrectomized SHRsp Rats.

Renal diseases tend to be less severe among premenopausal female patients, compared with male patients. Experimental data on the effects of estrogens on renal damage are controversial, and potential underlying mechanisms have not been fully clarified. Three-month-old, female, uninephrectomized (UNX), sham-operated or ovariectomized (OVX) SHRsp rats were left untreated or received either 17beta-estradiol 3-benzoate (25 micro g/d) or estriol (0.02 mg/d) daily. After 3 mo, indices of renal damage (glomerulosclerosis index and tubulointerstitial damage index) and glomerular geometric parameters were investigated. The expression of desmin, TGF-beta, endothelin-1, collagen IV, endothelial nitric oxide synthase, and estrogen receptors alpha and beta in the glomeruli and tubulointerstitium was immunohistochemically evaluated. Estradiol and estriol did not significantly affect kidney weights or BP. Estradiol and estriol caused significant reductions in albuminuria (vehicle-treated UNX/OVX animals, 25.4 +/- 8.52 mg/24 h; estradiol-treated UNX/OVX animals, 15.37 +/- 6.12 mg/24 h; estriol-treated UNX/OVX animals, 6.54 +/- 2.24 mg/24 h). The glomerulosclerosis index was significantly lower in estriol- and estradiol-treated animals (estradiol-treated UNX/OVX animals, 0.69 +/- 0.16; estriol-treated UNX/OVX animals, 0.21 +/- 0.12; P < 0.05), compared with vehicle-treated animals (1.46 +/- 0.09); the tubulointerstitial damage index exhibited a similar pattern. The mean glomerular volume was significantly less in estrogen-treated animals. UNX/OVX animals demonstrated significantly greater expression of TGF-beta and endothelin-1 in immunohistochemical, in situ hybridization, and reverse transcription-PCR assays. This increase was abrogated by estriol but not estradiol. Similarly, significantly higher glomerular and tubulointerstitial expression of proliferating cell nuclear antigen and collagen IV was observed in UNX/OVX animals, and expression was decreased by estriol but not estradiol. It was concluded that, in the UNX model of spontaneous renal damage, glomerular lesions and glomerular hypertrophy were reduced by estriol but less consistently by estradiol. In parallel, loss of podocytes, evidence of podocyte injury (i.e., desmin expression), and expression of mediator systems of glomerular damage were decreased, pointing to a major renoprotective action of estriol.

Animals↗
PubMed2003

Kidney and hypertension-causes. Update 2003.

Renal disease is closely associated with hypertension. On the one hand, kidney disease provokes hypertension. On the other hand, hypertension aggravates the progression of renal dysfunction. The pathomechanisms through which the kidney raises blood pressure have been considerably clarified in recent years. In experimental and clinical studies, it could be shown that "hypertension goes with the kidney". This suggests that some renal anomalies predispose to hypertension. Recently, it could be shown that the kidneys of individuals with so-called essential hypertension have less glomeruli than the kidneys of control individuals. In renal patients the kidney raises blood pressure through several mechanisms. First, the pressure-natriuresis relationship is shifted to the right, i. e., sodium excretion requires higher renal perfusion pressures. Second, there is inappropriate activation of the renin-angiotensin system. Third, as only recently documented in detail, renal injury raises the sympathetic tone, even when whole kidney glomerular filtration rate (GFR) is unchanged. This results from stimulating afferent signals emanating from the kidney. Fourth, there is evidence of impaired endothelial cell dependent vasodilatation even in very early stages of renal dysfunction. Fifth, the pulse pressure profile is altered as a consequence of premature and accelerated aging causing stiffening of the aorta. Knowledge of these pathomechanisms is important for selection of appropriate antihypertensive treatment.

Endothelium, Vascular↗
PubMed2003

Decreased plasma adiponectin concentration in patients with essential hypertension.

Adipocytes secrete several biologically active substances that are presumed to be involved in obesity-related hypertension. There are no reports that deal with the relationship between plasma adiponectin concentration and blood pressure (BP). To evaluate the role of adiponectin in essential hypertension 33 patients with essential hypertensive (EHP) (12 women, 21 men) and 33 body mass index-matched normotensive healthy subjects (NHS) (13 women, 20 men) were studied. In EHP plasma adiponectin concentration was significantly lower than in NHS (9.1 +/- 4.5 v 13.7 +/- 5.2 microg/mL, respectively). In all subjects a significant negative correlation was found between plasma adiponectin concentration and mean, systolic, and diastolic BP, suggesting that adiponectin contributes to the clinical course of essential hypertension.

Adiponectin↗
PubMed2003

Why is coronary heart disease of uraemic patients so frequent and so devastating?

On September 6, 2001, Professor Fernando Valderrabano (Hospital Gregorio Marañon, Madrid) died at the age of 59 years. He was a leading figure in Spanish nephrology, a full professor of Medicine/Nephrology at the University Complutense of Madrid, and an outstanding scientist who published more than 300 articles in medical journals. He was a very intelligent and cultured person, and a man of great style who enjoyed a wide range of hobbies and interests in addition to his medical work. All his colleagues and friends mourn his passing.

Comorbidity↗
PubMed2003

Reversal of glomerulosclerosis after high-dose enalapril treatment in subtotally nephrectomized rats.

Interventions to block the renin-angiotensin system (RAS) halt the progression of renal lesions in renal damage models. It has recently also been reported that established glomerulosclerosis can be reversed by pharmacologic blockade of the RAS. It was the aim of this study to confirm that high doses of angiotensin-converting enzyme (ACE) inhibitors reverse established glomerulosclerosis and to extend the findings by providing quantitative information on glomerular geometry, podocytes and other glomerular cells, renal vessels and tubulointerstitial tissue. Male Sprague Dawley rats were subjected to subtotal surgical renal ablation (SNX) (n = 27) or sham operation (n = 31) and fed using a pair-feeding protocol. Eight weeks after surgery, rats were either sacrificed or allocated to two arms: enalapril treatment (48 mg/kg body wt per day administered in the drinking fluid for 4 wk) or no treatment. Renal morphology was evaluated after 8 or 12 wk, respectively, by stereology in tissue fixed by pressure-controlled perfusion. Both systolic BP and albumin excretion rate were significantly higher in SNX compared with sham-operated controls. They were significantly reduced in SNX after delayed enalapril treatment. The glomerulosclerosis (GSI), tubulointerstitial (TII), and vascular (VI) damage indices were significantly higher in all SNX groups than in sham-operated controls. At the end of the experiment (12 wk after SNX) GSI, TII, and VI were significantly lower in SNX with delayed enalapril treatment (0.77 +/- 0.18, 0.63 +/- 0.19 and 0.43 +/- 0.16, respectively) compared with untreated SNX (1.64 +/- 0.14, 1.16 +/- 0.34 and 0.67 +/- 0.29, respectively). GSI, TII, and VI were also significantly lower in SNX with delayed enalapril treatment compared with SNX sacrificed without treatment 8 wk after SNX. The same was true for glomerular volume. The number of podocytes was not affected by SNX, but podocyte volume was increased. Both indices remained unaffected by treatment. The numbers of cells within the mesangium and endothelial cells per glomerulus were significantly lower in SNX after delayed enalapril treatment compared with untreated SNX. These results strongly suggest regression of preexisting lesions, i.e., glomerular, tubular, and vascular remodeling as well as reversal of glomerular hypertrophy by ACE inhibitor treatment. The study confirms that high-dose ACE inhibitor treatment causes partial reversal of glomerular as well as interstitial lesions in subtotally nephrectomized rats.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

Does plasma leptin concentration predict the nutritional status of hemodialyzed patients with chronic renal failure?

BACKGROUND: Patients with chronic renal failure are characterized by hyperleptinemia, and leptin is presumed to be an anorectogenic hormone. The aim of this prospective study was to analyze changes in body composition and parameters of nutritional status in relation to changes in plasma leptin concentration in uremic patients during the first year of hemodialysis therapy. MATERIAL/METHODS: 21 patients (10 F, 11 M, mean age 51+/- 3 years, BMI 24.3+/-1.1 kg/m2) were enrolled in this study. Nutritional status was evaluated by anthropometric parameters, estimation of body composition (DEXA method), and biochemical markers (plasma concentrations of albumin, cholesterol, triglycerides, transferrin) and plasma leptin concentration. Tests were performed twice: immediately after initiation of hemodialysis therapy and again 12 months later. RESULTS: After 12 months of hemodialysis therapy, the changes in body mass (-2.6+/-0.8 kg; p=0.23), total fat mass (TFM) (-0.3+/-0.8 kg; p=0.68) and total lean mass (TLM) (+0.5+/-0.8 kg; p=0.26) were insignificant. Plasma leptin concentration and estimated biochemical nutritional parameters did not change markedly. A significant positive correlation was noticed between TFM and plasma leptin concentration (R=0.521; p=0.02) at the beginning of hemodialysis therapy and between changes in TFM and plasma leptin concentration (R=0.466; p=0.04) after one year. CONCLUSIONS: Plasma leptin concentration does not predict forthcoming changes in body composition and changes of nutritional status in uremic patients after the first year of hemodialysis.

Body Composition↗
PubMed2002

Effect of antioxidant therapy with dl-alpha-tocopherol on cardiovascular structure in experimental renal failure.

BACKGROUND: Chronic renal failure is characterized by remodeling of the structure of the heart and the vasculature, for example, left ventricular hypertrophy, myocardial fibrosis, capillary/myocyte mismatch, as well as thickening of intramyocardial arteries and of peripheral arteries and veins. Furthermore, uremia is a state of increased oxygen stress. It was the purpose of this study to examine whether these findings are interrelated. METHODS: To investigate whether antioxidative therapy with dl-alpha-tocopherol (Toco; vitamin E) interferes with the development of abnormal cardiovascular structure in experimental renal failure, 28 male Sprague-Dawley rats were subjected to partial renal ablation (subtotal nephrectomy, SNX) or to sham operation (sham). SNX were either left untreated or received the antioxidant Toco (2 x 1500 IE/kg BW/week in the pellets). Blood pressure was measured using tail plethysmography. The experiment was terminated after 12 weeks. Heart and left ventricular weight were determined and the following parameters were measured using morphometry and stereology: volume densities of cardiomyocytes, capillaries and non-vascular interstitium; length density and total length of cardiac capillaries, wall thickness of intramyocardial arterioles and of the aorta. RESULTS: Systolic blood pressure and body weight were comparable in all groups. Treatment with Toco led to significantly increased plasma concentrations of Toco. Left ventricular weight and wall thickness of intramyocardial arteries were significantly higher in both SNX groups compared to sham controls. Volume density of the cardiac interstitial tissue was significantly higher in untreated SNX than in Toco treated SNX and sham control rats. Length density of capillaries was significantly lower in untreated SNX than in control rats; however, the values were significantly higher, and even higher than in sham controls, when SNX were treated with Toco. CONCLUSIONS: Treatment with the antioxidant dl-alpha-tocopherol prevented cardiomyocyte/capillary mismatch, and to some extent also myocardial fibrosis in rats with renal failure. The results point to a role of oxidative stress in the genesis of myocardial interstitial fibrosis and capillary deficit of the heart.

Animals↗
PubMed2002

Kidney and hypertension.

There is a unique relationship between the kidney and blood pressure (BP): on the one hand, renal dysfunction and particularly renal disease cause an increase in BP, while on the other hand, high BP accelerates loss of function of the diseased kidney. Transplantation studies, both in experimental animals and humans, documented that "blood pressure goes with the kidney," a normotensive recipient of a kidney genetically programmed for hypertension (HT) will develop HT, while conversely hypertensive patients with renal failure receiving the kidney of a normotensive donor may develop normotension. Family studies showed higher BP values and more frequent HT in first degree relatives of patients with primary glomerulonephritis or diabetic nephropathy, both type 1 and type 2. The notion that HT accelerates the loss of renal function has been proposed at the turn of the century, but definite evidence by observational and interventional studies has only been provided in the last two decades. The issue has been much confounded by the mistaken believe that damaged kidneys require higher BP values in order to function properly. The mechanisms of BP increase in renal disease comprise: salt retention, inappropriate activity of the renin-angiotensin system (RAS) and of the sympathetic nerve system as well as impaired endothelial cell-mediated vasodilatation. There is ample evidence both in primary renal disease (AIPRI and REIN trials) and in nephropathy of type 1 and type 2 diabetes (IDNT, RENAAL) that pharmacological blockade of the RAS by angiotensin-converting enzyme inhibitors or angiotensin II type 1 receptor blockers has BP-independent renoprotective effects. More recently, it has also been shown that blockade of the sympathetic nerve system has BP-independent effects on albuminuria and on glomerulosclerosis.

Humans↗
PubMed2002

[Influence of aging on plasma leptin concentration].

Aging is associated both with clinically important hormonal changes and with a decrease of energy expenditure. Leptin is a protein hormone, predominantly produced by adipocytes, which is presumed to be involved in the regulation of appetite and energy expenditure. The present study aimed to assess the relationship between leptinaemia and age. 144 healthy subjects (72 females and 72 males) age from 20 to 93 years were enrolled in this study. All studied subjects were divided according to the age into five groups (group A comprised subjects aged 20 to 40 years, group B--from 41 to 60 years, group C--from 61 to 70 years, group D--from 71 to 80 years and group E--aged over 81 years). In all examined subjects plasma leptin, insulin and glucose concentrations were estimated at 8 a.m., 4 p.m. and 12 p.m. respectively. Body mass index (BMI) was also calculated in all studied subjects. Basal (8 a.m.) plasma leptin concentration did not differ significantly in all age groups: A = 10.4 +/- 1.33; B = 12.5 +/- 2.18; C = 9.8 +/- 1.48; D = 14.4 +/- 3.12; E--10.5 +/- 1.99 ng/ml). In all examined groups plasma leptin concentrations were significantly higher at 12 p.m. than at 8 a.m. and 4 p.m. respectively. Females were characterized by significantly higher plasma leptin concentration in all age groups. A significant positive correlation was found between plasma leptin concentration and BMI in all age groups (except group A). No relationship between age and plasma leptin concentration were found, as analyzed both by correlation and multivariate regression analysis, respectively. From results obtained in this study we may conclude that age does not influence significantly leptinaemia.

Adult↗
PubMed2002

Effect of renin-angiotensin system activation by dietary sodium restriction and upright position on plasma leptin concentration in patients with essential hypertension.

BACKGROUND: Both leptin and the renin-angiotensin system (RAS) are involved in the regulation of arterial blood pressure. This study was undertaken to assess the relationship between RAS and plasma leptin concentration in hypertensive patients under conditions of normal and restricted sodium supply and upright position. MATERIAL/METHODS: In 31 patients with essential hypertension (EHP - 14 F, 17 M, age 44I14 years, BMI 29.3I6.4 kg/m2) and 8 healthy subjects (NHS - 4 F, 4 M, age 37(17 years, BMI 25.3I6.6 kg/m2) plasma leptin concentration, plasma renin activity (PRA), and 24-hour urinary sodium excretion (UNa) were evaluated twice: first on a diet containing 100-120 mmol sodium per day and after 8 hours overnight bed rest, and a second time after 3 days of dietary sodium restriction (10-20 mmol daily) and 3 hours in upright position. RESULTS: Dietary sodium restriction and upright position was followed by a significant increase in PRA and decrease of UNa. By contrast, plasma leptin concentration showed a moderate decrease both in EHP and NHS. No significant correlation was found between PRA and plasma leptin concentrations in either of the groups examined. CONCLUSIONS: From the results obtained in this study we may conclude that dietary sodium restriction and upright position exerts only a moderate effect on plasma leptin concentration, in contrast to PRA, in both hypertensive and normotensive subjects.

Adult↗