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  1. 4 Folia Histochemica et Cytobiologica

  2. 3 Archivum Immunologiae et Therapiae Experimentalis

  3. 3 Polish Journal of Environmental Studies

  4. 2 Acta Biochimica Polonica

  5. 2 Journal of Physiology and Pharmacology. Supplement

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  1. 2 Danilewicz M.

  2. 2 Skrzypczak W.

  3. 2 Wagrowska-Danilewicz M.

  4. 1 Adaszek L.

  5. 1 Aleksandrowicz E.

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  1. 1 2021

  2. 2 2020

  3. 1 2019

  4. 1 2018

  5. 1 2012

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1

Proteinuria and the intensity of gymnast training load

100%
Potylicki K., Szot Z.
Polish Journal of Environmental Studies
|
1999
|
tom 08
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nr 5
2

Microalbuminuria in weight lifters - the adaptive response induced by training

88%
Suchanowski A.
Polish Journal of Environmental Studies
|
1999
|
tom 08
|
nr 5
3

Expression of angiogenic factor with G patch and FHA domains 1 (AGGF1) in placenta from patients with preeclampsia

75%
An L.-F., Chi S. Q., Zhang J., Wang H.-B., Ouyang W.-X.
Folia Histochemica et Cytobiologica
|
2020
|
tom 58
|
nr 2
4
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Content available

Proteinuria - selected issues

75%
Skrzypczak W.
Acta Scientiarum Polonorum. Zootechnica
|
2021
|
tom 20
|
nr 3
5

Canine renal amyloidosis: a case report

75%
Szczepankiewicz B., Paslawska U., Grzegory M., Jonkisz P., Borecka P., Marzec M., Brzozowska M., Nowak M.
Medycyna Weterynaryjna
|
2018
|
tom 74
|
nr 05
Amyloidosis is a disease caused by the deposition of amorphous extracellular protein, leading to impaired kidney function. Canine and feline amyloidosis is associated with the deposition of AA protein. The disease is hereditary and is related to breed but not sex. Predisposed breeds include the Shar Pei dog and Abyssinian cat. Proteinuria resulting in hypoalbuminemia due to changes in renal glomeruli is the first clinical sign. In addition, a decreased appetite, anorexia, vomiting, lethargy, polyuria and polydipsia may be observed. In order to diagnose the disease, serum amyloid A levels may be measured. However, a definitive diagnosis is made on the basis of an intravital renal biopsy and the presence of amyloid in the histopathological examination. The main goal of treatment is to reduce inflammation and proteinuria. If nephrotic syndrome occurs, the prognosis is guarded to poor, and the majority of patients do not survive one year. The definitive diagnosis is based on the post-mortem examination, in which the presence of amyloid deposits is confirmed in the kidney tissue. We present the case of a 7-year-old female Shar Pei diagnosed with kidney amyloidosis, on the basis of which we have developed a prevention scheme for clinical practice.
6

Effect of pentoxifylline on proteinuria, markers of tubular injury and oxidative stress in non-diabetic patients with chronic kidney disease - placebo controlled, randomized, cross-over study

75%
Renke M., Tylicki L., Rutkowski P., Knap N., Zietkiewicz M., Neuwelt A., Aleksandrowicz E., Lysiak-Szydlowska W., Wozniak M., Rutkowski B.
Acta Biochimica Polonica
|
2010
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tom 57
|
nr 1
119-123
 Background: Inhibition of the renin-angiotensin-aldosterone system (RAAS) with angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) is a common strategy used in the management of patients with chronic kidney disease (CKD). However, there is no universal therapy that can stop progression of CKD. Pentoxifylline (PTE) is a non-specific phosphodiesterase inhibitor with anti-inflammatory properties. It has been reported to have promising effects in CKD treatment. Methods: In a placebo-controlled, randomized, cross-over study we evaluated the influence of PTE (1200 mg/day) added to RAAS blockade on proteinuria, surrogate markers of tubular injury and oxidative stress-dependent products in 22 non-diabetic patients with proteinuria (0.4-4.3 g per 24 h) with normal or declined kidney function [eGFR 37-178 mL/min]. In an eight-week run-in period, therapy using ACEI and/or ARB was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: PTE/washout/placebo or placebo/washout/PTE. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. Results: The PTE therapy reduced proteinuria (by 26 %) as compared to placebo. There were no differences in α1-microglobulin, urine excretion of N-acetyl-β-d-glucosaminidase (NAG), hsCRP, the urinary excretion of 15-F2t-isoprostane, blood pressure (BP), eGFR and serum creatinine between the PTE and placebo groups. Conclusion: Pentoxifylline may decrease proteinuria in non-diabetic patients with CKD.
7

Essential edema-proteinuria-hypertesion [EPH] gestosis and gestosis superimposing pre-existing renal disease: comparison of cellular immunity parameters

75%
Malinowski A., Szpakowski M., Tchorzewski H., Zeman K., Oszukowski P., Podciechowski L.
Archivum Immunologiae et Therapiae Experimentalis
|
1994
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tom 42
|
nr 5-6
8

The role of heparanase in diseases of the glomeruli

63%
Szymczak M., Kuzniar J., Klinger M.
Archivum Immunologiae et Therapiae Experimentalis
|
2010
|
tom 58
|
nr 1
45-56
9
Content available remote

Urinary excretion of low molecular weight proteins in goats during the neonatal period

63%
Ozgo M., Skrzypczak W., Drzezdzon D., Lepczynski A., Dratwa-Chalupnik A., Michalek K., Herosimczyk A.
Journal of Physiology and Pharmacology. Supplement
|
2009
|
tom 60
|
nr 3
119-125
10

Anti-Qa2 animal models for preeclampsia preclinical studies: a pathological elevation of blood pressure and proteinuria

63%
Hikmah E. M., Liben P., Widjiati
Folia Biologica
|
2019
|
tom 67
|
nr 2
11

Utility of urinary markers in the assessment of renal dysfunction in familial glomerulonephritis in Dobermann dogs

63%
Winiarczyk D., Adaszek L., Madany J., Winiarczyk M., Winiarczyk S.
Journal of Veterinary Research
|
2020
|
tom 64
|
nr 1
12

The transcriptional regulation of podocin [NPHS2] by Lmx1b and a promoter single nucleotide polymorphism

63%
Harendza S., Stahl R. A. K., Schneider A.
Cellular and Molecular Biology Letters
|
2009
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tom 14
|
nr 4
679-691
Podocin (NPHS2) is a component of the glomerular slit membrane with major regulatory functions in the renal permeability of proteins. A loss of podocin and a decrease in its resynthesis can influence the outcome of renal diseases with nephrotic syndrome, such as minimal change glomerulonephritis, focal segmental glomerulosclerosis (FSGS) and membranous nephropathy. The transcriptional regulation of podocin may play a major role in these processes. We defined the transcriptional regulation of the human podocin gene and the influence of single nucleotide polymorphisms (SNPs) within its promoter region in the podocytes using reporter gene constructs and gel shift analysis. In addition, we took genomic DNA from healthy Caucasian blood donors and from biopsies of kidneys with defined renal diseases and screened it for podocin promoter SNPs. Our data shows that the transcription of podocin is mainly regulated by the transcription factor Lmx1b, which binds to a FLAT-F element and displays enhancer function. With the SNP variant −116T, there was a significant reduction in luciferase activity, and nuclear protein binding was observed, while the SNP −670C/T did not display functionality. The allelic distribution of −116C/T in patients with kidney diseases leading to nephrotic syndrome was not significantly different from that in the control group. Our data indicates that among other factors, podocin is specifically regulated by the transcription factor Lmx1b and by the functional polymorphism -116C/T. However, there is no association between −116C/T and susceptibility to minimal change glomerulonephritis, focal segmental glomerulosclerosis or membranous nephropathy.
13

The effect of pre-eclamptic umbilical cord serum on fibroblast division in culture

63%
Pawlicka E., Romanowicz L., Bankowski E., Chyczewski L., Jaworski S.
Folia Histochemica et Cytobiologica
|
2002
|
tom 40
|
nr 4
14

Nephrotoxic effects of environmental and occupational exposure to mercury compounds: a review and our study

63%
Rutowski J., Moszczynski P.
Polish Journal of Environmental Studies
|
1998
|
tom 07
|
nr 2
Mercury is present in nature as metallic mercury, inorganic and organic compounds. Mercury levels constantly increase in the human natural environment. A similar rise of mercury content has been observed in human tissues. Kidney disease arising from exposure to heavy metals, mainly during occupational exposure to mercury, may play a special role in nephrology. Long-term exposure to mercury may cause progressive degenerative changes in the kidneys, possibly leading to renal insufficiency. The main renal changes caused by mercury are indicated by the both glomerular and tubular disfunction. Early renal damage may usually be monitored by measurements in urine excretion of very sensitive small proteins and of some enzymes. This article reviews data concerning the nephrotoxic effects of mercury compounds in animals and humans induced by exposure to mercury compounds with the results of our study in changes of proteins in urine excretion in groups of workers occupationally exposed to mercury vapours, (depending on degree and duration of exposure).
15

Tubular NF-kappaB is overexpressed in proteinuric patients with IgA nephropathy

51%
Danilewicz M., Wagrowska-Danilewicz M.
Folia Histochemica et Cytobiologica
|
2012
|
tom 50
|
nr 1
16

SOCS3 and SOCS5 mRNA expressions may predict initial steroid response in nephrotic syndrome children

51%
Ostalska-Nowicka D., Smiech M., Jaroniec M., Zaorska K., Zawierucha P., Szaflarski W., Malinska A., Nowicki M.
Folia Histochemica et Cytobiologica
|
2011
|
tom 49
|
nr 4
17

Selective cobalamin malabsorption and the cobalamin-intrinsic factor receptor

51%
Grasbeck R.
Acta Biochimica Polonica
|
1997
|
tom 44
|
nr 4
The disease is characterised by cobalamin (Cbl) deficiency in children 0-5 years old, causing failure to thrive, infections, megaloblastic anaemia, neuropathy, and mild general malabsorption; slight proteinuria is common. Cbl injections produce remission, but Cbl malabsorption and proteinuria persist. About 250 cases have been reported. Dogs also have it. The heredity is autosomal and recessive. The physiological and pathological absorption mechanisms are described: Cbl liberated from food by digestion is first bound to haptocorrin, but in the intestine it is transferred to intrinsic factor. In the ileum the complex attaches to a receptor on the enterocytes; this requires neutral pH and Ca2+. The receptor is a membrane-bound glycoprotein consisting of multiple subunits. The receptor-ligand complex is endocytosed and degraded in lysosomes, and the vitamin is transferred to transcobalamin which carries it to tissues. The same receptor is strongly expressed in the kidneys, but urine also contains its activity which can be assayed for diagnosis. The basic lesion is an error in the ileal receptor. In the affected dogs the synthesised receptor is retained intracellularly. Urine and ileal biopsies from human cases contained little receptor but it had conserved affinity for the ligand. Recently examined Arab patients did not excrete reduced amounts of the receptor. Apparently, the disease has subsets, such as different structural errors in the receptor and possibly faulty transport inside the enterocyte. The cause of the proteinuria is unknown but kidney damage due to severe Cbl deficiency and an error in a multiligand renal receptor are among the possibilities.
18

Monoclonal antibody analysis of glomerular and renal interstitial immune cells in steroid-resistant and steroid-responsive minimal change disease in children

51%
Wagrowska-Danilewicz M., Danilewicz M.
Archivum Immunologiae et Therapiae Experimentalis
|
1996
|
tom 44
|
nr 2-3
19
Content available remote

Decorin deficiency in diabetic mice: Aggravation of nephropathy due to overexpression of profibrotic factors, enhanced apoptosis and mononuclear cell infiltration

45%
Merline R., Lazaroski S., Babelova A., Tsalastra-Greul W., Pfeilschifter J., Schluter K. D., Gunther A., Iozzo R. V., Schaefer R. M., Schaefer L.
Journal of Physiology and Pharmacology. Supplement
|
2009
|
tom 60
|
nr 4
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