Experimental nephrology最新文献_第3页

Reduction in mean glomerular pore size coincides with the development of large shunt pores in patients with diabetic nephropathy. 糖尿病肾病患者肾小球平均孔径的减小与大分流孔的形成一致。

Experimental nephrology Pub Date : 2001-01-01 DOI: 10.1159/000020698

R Oberbauer, V Nenov, C Weidekamm, M Haas, T Szekeres, G Mayer

{"title":"Reduction in mean glomerular pore size coincides with the development of large shunt pores in patients with diabetic nephropathy.","authors":"R Oberbauer, V Nenov, C Weidekamm, M Haas, T Szekeres, G Mayer","doi":"10.1159/000020698","DOIUrl":"https://doi.org/10.1159/000020698","url":null,"abstract":"The glomerular size selectivity was determined by neutral dextran clearance sieving technique and plasma cystatin C levels in two groups of patients with long-standing type I diabetes mellitus and different stages of albuminuria but normal glomerular filtration rate and in a group of healthy controls. The sieving characteristics of the glomerular filter were determined using a mathematical model of log normal pore size distribution. Patients with albuminuria above 200 microg/min exhibited a significant increase of cystatin c plasma concentrations and a significant reduction in mean glomerular filtration slit size. Only these patients exhibited large, unrestrictive pores in the glomerular filter (shunt). The plasma cystatin c levels correlated significantly with 26-angstrom neutral dextran plasma levels in microalbuminuric patients and in patients with albuminuria above 200 microg/min. We conclude that a reduction in average pore size of the glomerular filter does not occur earlier than the development of large shunt pores. The renal clearance of cystatin c in patients with proteinuric diabetic nephropathy but a normal glomerular filtration rate is reduced due to its molecular size.","PeriodicalId":12179,"journal":{"name":"Experimental nephrology","volume":"9 1","pages":"49-53"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000020698","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21882253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 29

Intrarenal renin-angiotensin system contributes to tubular acidification adaptation following uninephrectomy. 肾内肾素-血管紧张素系统有助于肾切除术后肾小管酸化适应。

Experimental nephrology Pub Date : 2001-01-01 DOI: 10.1159/000020700

C Amorena, C Damasco, P Igarreta, M MacLaughlin

{"title":"Intrarenal renin-angiotensin system contributes to tubular acidification adaptation following uninephrectomy.","authors":"C Amorena, C Damasco, P Igarreta, M MacLaughlin","doi":"10.1159/000020700","DOIUrl":"https://doi.org/10.1159/000020700","url":null,"abstract":"Background/aims: Reduction in renal mass by uninephrectomy induces a functional compensation in the remnant kidney. The activity of the angiotensin-converting enzyme (ACE) as well as renin mRNA in the proximal convoluted tubule (PCT) of uninephrectomized (UNx) rats increases. The aim of this work was to determine whether the increased activity of the local renin-angiotensin system (RAS) participates in the adaptation of renal function after uninephrectomy.Method: We utilized normal two-kidney (2K) and 3-week UNx rats to study the activity of the ACE in vesicles obtained from luminal membranes of proximal tubular cells and the acidification kinectics in PCTs using micropuncture techniques.Results: The converting enzyme activity was significantly larger in UNx (5.87+/-0.69 nmol x min(-1) x mg protein(-1)) than in 2K rats (2.43+/-0.13 nmol x min(-1) x mg protein(-1); p<0.05). The acidification rate constant (kappa) in PCT of 2K rats was 0.18+/-0.02 s(-1) and in UNx rats 0.30+/-0.04 s(-1) (p<0.001). In UNx rats, microperfusion with 10(-5) M ramipril or 10(-5) M losartan decreased kappa to 0.19+/-0.02 and 0.18+/-0.02 s(-1), respectively, but had no effect on 2K rats. Luminal steady-state pH (pH(infinity)) was the same in 2K and UNx rats, and was not modified by addition of 10(-5) M ramipril or 10(-5) M losartan in both groups. The proximal H(+) flux (J(H(+))), calculated from pH(infinity) and kappa, was 1.12 nmol x cm(-2) x s(-1) in 2K rats and, 1.77 nmol. cm(-2). s(-1) in UNx rats (p<0.001). In 2K rats, this value was not changed by 10(-5) M ramipril or 10(-5) M losartan, but in UNx rats J(H(+)) decreased 25 and 30% with ramipril or losartan, respectively (p<0.001).Conclusions: These data suggest that the increase in the local RAS activity could be an adaptive change that contributes to maintain the homeostasis of body fluids after uninephrectomy.","PeriodicalId":12179,"journal":{"name":"Experimental nephrology","volume":"9 1","pages":"60-4"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000020700","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21882255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

ACE inhibition preserves heparan sulfate proteoglycans in the glomerular basement membrane of rats with established adriamycin nephropathy. ACE抑制可保留阿霉素肾病大鼠肾小球基底膜中的硫酸肝素蛋白多糖。

Experimental nephrology Pub Date : 2001-01-01 DOI: 10.1159/000020704

F H Wapstra, G J Navis, H van Goor, J van den Born, J H Berden, P E de Jong, D de Zeeuw

{"title":"ACE inhibition preserves heparan sulfate proteoglycans in the glomerular basement membrane of rats with established adriamycin nephropathy.","authors":"F H Wapstra, G J Navis, H van Goor, J van den Born, J H Berden, P E de Jong, D de Zeeuw","doi":"10.1159/000020704","DOIUrl":"https://doi.org/10.1159/000020704","url":null,"abstract":"The gradual onset of the antiproteinuric effects of ACE inhibition suggests that structural effects on the glomerular basement membrane (GBM) may be involved in their renoprotective action. To test this hypothesis, we studied the effects of lisinopril (5 mg/kg/24 h) on proteinuria, focal glomerulosclerosis (FGS) and glomerular heparan sulfate (HS) proteoglycan (HSPG) GBM staining in rats with established Adriamycin nephrosis. Treatment was started 6 weeks after disease induction. As expected, lisinopril reduced blood pressure, proteinuria and the FGS score. In control rats, Adriamycin nephrosis was associated with significantly impaired GBM staining for both HSPG core protein (assessed from BL-31 staining) and HS staining (assessed from JM-403 staining) 12 weeks after disease induction. In rats treated with lisinopril (5 mg/kg/24 h) GBM staining was significantly better preserved for HS as well as for HSPG core protein. These data suggest that structural effects on the GBM, improving glomerular permselectivity, may be involved in the renoprotective effects of ACE inhibition in proteinuria-induced renal damage.","PeriodicalId":12179,"journal":{"name":"Experimental nephrology","volume":"9 1","pages":"21-7"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000020704","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21881150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 34

Low leptin mRNA level in adipose tissue and normoleptinemia in experimental chronic renal failure. 实验性慢性肾功能衰竭脂肪组织瘦素mRNA水平低与正常瘦素血症的关系。

Experimental nephrology Pub Date : 2001-01-01 DOI: 10.1159/000020699

J Swierczynski, J Korczynska, M Szolkiewicz, J Karbowska, Z Kochan, T Nieweglowski, E Kusiak, B Rutkowski

{"title":"Low leptin mRNA level in adipose tissue and normoleptinemia in experimental chronic renal failure.","authors":"J Swierczynski, J Korczynska, M Szolkiewicz, J Karbowska, Z Kochan, T Nieweglowski, E Kusiak, B Rutkowski","doi":"10.1159/000020699","DOIUrl":"https://doi.org/10.1159/000020699","url":null,"abstract":"Background: Anorexia and weight loss frequently accompany chronic renal failure (CRF). Although multiple metabolic changes occur during CRF, a bulk of evidence indicates that the decrease in caloric intake plays a major role in CRF-induced weight loss. Recently, it has been suggested that elevated plasma leptin concentrations could contribute to anorexia and to downregulation of leptin gene expression in CRF patients. However, in some CRF patients, plasma leptin concentrations have been found to be lower than one could expect. Thus we assumed that inhibition of leptin synthesis plays an important role in the regulation of plasma leptin concentrations in CRF patients.Methods: To test this assumption, the leptin mRNA level in rat white adipose tissue from ad-libitum-fed control (sham operated), pair-fed control (sham operated) and rats with experimentally induced CRF has been measured by Northern blotting analysis. In addition, serum leptin concentration (by radioimmunoassay) was determined in all three groups of animals.Results: The results of the present study indicate that in experimental CRF the leptin mRNA level is decreased by about 50% as compared to the sham-operated animals (ad-libitum-fed and pair-fed controls). The mean serum leptin concentration in CRF rats was essentially similar to the leptin concentration in sham-operated ones.Conclusion: The data obtained suggest that in CRF animals the serum leptin concentration might be affected not only by the decrease in leptin removal in the kidney, but also by the decrease in leptin secretion from adipose tissue. Furthermore, the results of the study suggest that leptin may be only one of many factors involved in the pathogenesis of malnutrition associated with CRF.","PeriodicalId":12179,"journal":{"name":"Experimental nephrology","volume":"9 1","pages":"54-9"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000020699","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21882254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 26

Mechanisms of renal calcium transport. 肾钙转运机制。

Experimental nephrology Pub Date : 2000-11-01 DOI: 10.1159/000020688

P A Friedman

{"title":"Mechanisms of renal calcium transport.","authors":"P A Friedman","doi":"10.1159/000020688","DOIUrl":"https://doi.org/10.1159/000020688","url":null,"abstract":"The kidneys play a key role in the integrated regulation of calcium homeostasis. Calcium absorption takes place throughout the nephron. Proximal tubules, thick ascending limbs of Henle's loop, and distal tubules are the major sites of calcium absorption. The mechanisms of absorption vary significantly from one segment to another, as does the extent of hormonal regulation. At one extreme is the considerable reabsorption by proximal tubules that proceeds primarily, if not entirely, by a paracellular pathway that is not regulated by hormones or drugs. In thick ascending limbs, calcium absorption occurs through a combination of transcellular and paracellular routes. The active, transcellular component is regulated by parathyroid hormone (PTH) and calcitonin, whereas the passive, paracellular route is governed by the extent of concomitant sodium absorption. At the other extreme is the distal tubule, where calcium absorption is entirely transcellular and is regulated by PTH,1,25[OH(2)] vitamin D(3), calcitonin, and by calcium-sparing drugs such as thiazide-type diuretics. The present review focuses on recent insights into the mechanisms of transcellular calcium movement and highlights the discovery of an epithelial calcium channel, ECaC, that may mediate calcium entry in distal tubules.","PeriodicalId":12179,"journal":{"name":"Experimental nephrology","volume":"8 6","pages":"343-50"},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000020688","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21846546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 71

Defects in processing and trafficking of cystic fibrosis transmembrane conductance regulator. 囊性纤维化跨膜传导调节剂的加工和转运缺陷。

Experimental nephrology Pub Date : 2000-11-01 DOI: 10.1159/000020687

K Kunzelmann, R Nitschke

引用次数: 10

Disorders of the epithelial Na(+) channel in Liddle's syndrome and autosomal recessive pseudohypoaldosteronism type 1. Liddle综合征和常染色体隐性假醛固酮增多症1型中上皮Na(+)通道的紊乱

Experimental nephrology Pub Date : 2000-11-01 DOI: 10.1159/000020685

Y S Oh, D G Warnock

{"title":"Disorders of the epithelial Na(+) channel in Liddle's syndrome and autosomal recessive pseudohypoaldosteronism type 1.","authors":"Y S Oh, D G Warnock","doi":"10.1159/000020685","DOIUrl":"https://doi.org/10.1159/000020685","url":null,"abstract":"The epithelial Na(+) channel (ENaC) is the key step in many Na(+)-absorptive epithelia, such as kidney and distal colon, that controls the overall rate of transepithelial Na(+) transport. ENaC is composed of three homologous subunits, alpha, beta, and gamma. The alpha subunit is the key subunit for the formation of a functional ion channel, while the beta and gamma subunits can greatly potentiate the level of expressed Na(+) currents. ENaCs belong to the recently identified DEG/ENaC supergene family, sharing the same basic structure with cytoplasmic amino and carboxy termini, two transmembrane regions, and a large extracellular loop. The human ENaC genes have been cloned, and using genetic linkage analysis the involvement of ENaC gene mutations in two distinct human diseases, Liddle's syndrome and autosomal recessive pseudohypoaldosteronism type 1 (PHA-1), has been demonstrated. In Liddle's syndrome, gain-of-function mutations in the beta or gamma ENaC subunits have been found; all identified mutations so far reside in the carboxy terminus of the protein, either deleting or modifying the functionally important PY motif. In PHA-1, loss-of-function mutations in the alpha, beta, or gamma subunits have been found; these mutations either truncate a significant portion of the structure or modify an amino acid that plays an important role in channel function. In this review, our current understanding about ENaC and the pathophysiology of Liddle's syndrome and PHA-1 caused by ENaC mutations will be discussed.","PeriodicalId":12179,"journal":{"name":"Experimental nephrology","volume":"8 6","pages":"320-5"},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000020685","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21847364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 30

Defective processing and trafficking of water channels in nephrogenic diabetes insipidus. 肾源性尿崩症的水渠加工和运输缺陷。

Experimental nephrology Pub Date : 2000-11-01 DOI: 10.1159/000020686

E J Kamsteeg, P M Deen, C H van Os

引用次数: 22

Severely impaired urine-concentrating ability in mice lacking the CLC-K1 chloride channel. 缺乏CLC-K1氯离子通道的小鼠尿浓缩能力严重受损。

Experimental nephrology Pub Date : 2000-11-01 DOI: 10.1159/000020690

S Uchida, F Marumo

引用次数: 8

Molecular pathology of renal chloride channels in Dent's disease and Bartter's syndrome. 登特病和巴特综合征肾氯离子通道的分子病理学研究。

Experimental nephrology Pub Date : 2000-11-01 DOI: 10.1159/000020689

R V Thakker

引用次数: 31