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1. |
Hypokalemia, High Erythrocyte Na+and Low Erythrocyte Na,K-ATPase in Relatives of Patients Dying from Sudden Unexplained Death Syndrome in North-East Thailand and in Survivors from Near-Fatal Attacks |
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American Journal of Nephrology,
Volume 16,
Issue 5,
1996,
Page 369-374
Piyaratana Tosukhowong,
Chulalag Chotigasatit,
Kriang Tungsanga,
Pote Sriboonlue,
Pongsak Pansin,
Visith Sitprija,
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摘要:
The sudden unexplained death syndrome (SUDS) is a sudden death of unknown cause in healthy South-East Asians. In Thailand, it is common in the North-East region. We previously reported high incidences of low erythrocyte sodium and potassium-activated adenosine triphosphatase (NaK-ATPase) activity and of high erythrocyte sodium in North-East Thais and speculated that this metabolic defect might be associated with the high incidence of SUDS in that region. In this communication, we studied plasma sodium and potassium, erythrocyte sodium and potassium, activities of erythrocyte NaK-ATPase, ouabain-insensitive ATPase and total ATPase in healthy Thai blood donors from Central Thailand (group 1), healthy North-East city dwellers (group 2), relatives of SUDS victims (group 3) and survivors from SUDS-like attacks (group 4). Compared with groups 1 and 2, group 3 and 4 subjects had significantly lower plasma potassium (p < 0.0001), higher erythrocyte sodium (p < 0.0001), lower activities of erythrocyte NaK-ATPase (p < 0.0001) and of erythrocyte total ATPase (p < 0.0001). In addition, group 4 subjects had lower plasma potassium, higher erythrocyte sodium and lower activity of total ATPase than those of group 3. The findings suggest that the pathogenesis of SUDS could be related to hypokalemia and a membrane sodium/potassium pump defect.
ISSN:0250-8095
DOI:10.1159/000169027
出版商:S. Karger AG
年代:1996
数据来源: Karger
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2. |
Seasonal Variation in the Incidence of End-Stage Renal Disease |
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American Journal of Nephrology,
Volume 16,
Issue 5,
1996,
Page 375-381
Kunitoshi Iseki,
Osamu Morita,
Koshiro Fukiyama,
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摘要:
The effect of ambient temperature (AMT) on the incidence of end-stage renal disease (ESRD) was examined in Okinawa, Japan, where there is a distinct seasonal variation in monthly AMT but constant intradiurnal temperature change throughout a year. Arbitral continuous and cyclic functions were examined using Fourier analysis and calculation of the cross-correlation coefficient. The calendar month of the start of chronic dialysis was regarded as the time of onset of ESRD. A total of 1,982 patients, 824 females and 1,158 males, was registered with ESRD between 1971 and 1990. The normalized monthly number of new ESRD patients, divided by days of each month, was smallest in August, n = 4.06, and largest in January, n = 6.45, and this pattern was well reproduced by the Fourier synthesized value. The cross-correlation coefficient showed that monthly mean AMT and the normalized number of ESRD patients correlated best with 6 months lag time. Taken together, our results showed that there was strong correlation between the normalized number of ESRD patients and AMT. Uremic symptoms leading to initiate dialysis, such as congestive heart failure, may be aggravated in lower AMT. We speculated a role of an inverse relation between AMT and the sympathetic nerve function. The public health implications of these findings warrant their further investigation.
ISSN:0250-8095
DOI:10.1159/000169028
出版商:S. Karger AG
年代:1996
数据来源: Karger
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3. |
Serum Bicarbonate Is an Independent Determinant of Protein Catabolic Rate in Chronic Hemodialysis |
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American Journal of Nephrology,
Volume 16,
Issue 5,
1996,
Page 382-385
Bahar Bastani,
Mary McNeely,
Paul G. Schmitz,
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摘要:
Serum bicarbonate is an independent determinant of protein catabolic rate in chronic hemodialysis. Recent biochemical studies suggest that metabolic acidosis induces an increase in protein catabolic rate. Therefore, we retrospectively examined the relationship between serum total CO2, normalized protein catabolic rate (NPCR), midweek BUN, KT/V, and serum albumin in 70 chronic hemodialysis patients over a period of 4-6 months (total of 270 determinations). Multiple regression analysis indicated an independent and inverse association of tCO2 with NPCR (p < 0.0001). Subsequent analysis of the data indicated a nonlinear relationship between serum CO2 and NPCR. Indeed, the slope of the regression abruptly increased from -0.015 ± 0.005 to -0.108 ± 0.032 when analyzed for serum CO2 < 15 mEq/1. We conclude that metabolic acidosis may modulate protein kinetics in patients receiving maintenance hemodialysis. Moreover, this relationship appears to be exaggerated at moderate to severe reductions in tCO2. Thus, this analysis suggests that decreases in tCO2 have a detrimental effect on protein catabolism in stable patients maintained on chronic hemodialysi
ISSN:0250-8095
DOI:10.1159/000169029
出版商:S. Karger AG
年代:1996
数据来源: Karger
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4. |
Hypocalcemia, Morbidity, and Mortality in End-Stage Renal Disease |
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American Journal of Nephrology,
Volume 16,
Issue 5,
1996,
Page 386-393
Robert N. Foley,
Patricks S Parfrey,
John D. Harrnett,
Gloria M. Kent,
Lingqun Hu,
Regan O’;Dea,
David C. Murray,
Paul E. Barre,
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摘要:
Background: Hypocalcemia and hyperphosphatemia with secondary hyperparathyroidism are characteristic of end-stage renal disease (ESRD). Although calcium levels critically affect almost all cellular processes, the impact of chronic hypocalcemia and other abnormalities of calcium-phosphate homeostatis on the prognosis of ESRD patients is unknown. Methods: An inception cohort of 433 patients starting ESRD therapy was followed prospectively for an average of 41 months. Serum calcium and other parameters were measured monthly. The mean calcium levels were 9.4 ± 0.7 mg/dl. 23% of the patients had mean calcium levels < 8.8 mg/dl. After adjusting for baseline age, diabetes mellitus, ischemic heart disease, smoking and cholesterol levels, as well as serial albumin, hemoglobin, mean arterial blood pressure, phosphate and alkaline phosphatase levels, chronic hypocalcemia was strongly associated with mortality (RR 2.10, p = 0.006 for a mean calcium level < 8.8 mg/dl). The association with mortality was similar in hemodialysis (RR 2.10, p = 0.006) and peritoneal dialysis patients (2.67, p = 0.034). Using similar covariate adjustment, chronic hypocalcemia was associated with de novo ischemic heart disease (RR 5.23, p < 0.001), recurrent ischemic heart disease (RR 2.46, p = 0.006), de novo cardiac failure (RR 2.64, p < 0.001), and recurrent cardiac failure (RR 3.30, p < 0.001). Hypocalcemia retained its independent impact on morbidity and mortality when analyzed as a time-dependent covariate. Conclusions: Chronic hypocalcemia, a very common, reversible feature of chronic uremia, is independently associated with morbidity and mortality in ESRD patients.
ISSN:0250-8095
DOI:10.1159/000169030
出版商:S. Karger AG
年代:1996
数据来源: Karger
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5. |
Neutral-Lipid Transfers and Cholesteryl Ester Transfer Protein in Hemodialyzed Patients |
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American Journal of Nephrology,
Volume 16,
Issue 5,
1996,
Page 394-401
Véronique Reade,
Hafid Mezdour,
Richard Reade,
Majid Kandoussi,
Michel Dracon,
Jean-Charles Fruchart,
Claude Cachera,
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摘要:
Abnormalities in cholesteryl ester transfers may play a role in the development of atherosclerosis observed in patients with end-stage renal failure treated by chronic hemodialysis. Net neutral-lipid transfers and cholesteryl ester transfer protein activity and mass were investigated in 20 hemodialyzed patients, arbitrarily divided into two groups based on fasting triglyceride levels, and compared to triglyceride-matched control groups. In the hypertriglyceridemic subjects (plasma triglyceride values > 150 mg/dl), high-density lipoprotein cholesterol was decreased, and the net cholesteryl ester transfer rates were significantly higher than the rates in normolipidemic subjects. The comparison of subjects matched for plasma triglyceride and cholesterol levels showed no significant difference in cholesteryl ester or triglyceride transfer rates between patients and controls. Our results suggest that normal or elevated net neutral-lipid transfers are not related to the renal status of the subjects, but rather to their plasma triglyceride levels.
ISSN:0250-8095
DOI:10.1159/000169031
出版商:S. Karger AG
年代:1996
数据来源: Karger
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6. |
Alpha-V/Beta-3 and Alpha-V/Beta-5 Integrin Distribution in Neoplastic Kidney |
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American Journal of Nephrology,
Volume 16,
Issue 5,
1996,
Page 402-408
Hamid Rabb,
Elvira Barroso-Vicens,
Richard Adams,
Julio Pow-Sang,
German Ramirez,
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摘要:
Integrins are transmembrane glycoproteins that mediate cell-cell and cell-matrix interactions. Altered integrin expression may contribute to tumor progression, invasiveness and metastases. The alpha-V/beta-3 (αvβ3; osteopontin/ vitronectin receptor) has recently been implicated in neovascularization and tumor-induced angiogenesis. αv-Subunit also associates with β5 to form an αvβ5-complex, another vitronectin receptor. We studied tissue distribution of αv β3 and αv β5-integrins, as well as α1- and β1-subunits in nephrectomy samples from 7 subjects with localized renal cell carcinoma. Grossly and histologically uninvolved regions (‘normal’) from the same nephrectomy specimens were used for comparison. Integrin expression was studied with specific monoclonal antibodies and the immunoperoxidase technique. αvβ3 was expressed in the glomerular epithelial cells, Bowman’s capsule, vascular endothelium, and weakly in tubular epithelial cells. αvβ5 had a similar distribution except for minimal expression on vascular endothelium. α1-Expression was observed in mesangium and but weakly in Bowman’s capsule. β1-Expression was seen in glomerular epithelial cells, Bowman’s capsule, vascular epithelium and tubular epithelial cells. Unlike in ‘normals’, neoplastic expression was more heterogeneous. αvβ3 was expressed in tumor cells in 4/7 cases, vascular endothelium in 6/6, and in stroma in 4/7. αvβ5 was weakly expressed in tumor cells in 4/5, vascular endothelium in 5/5, and stroma in 4/5 cases. α1-Expression was seen in tumor cells in 3/7, vascular endothelium in 4/7 and in stroma in 7/7 cases. β1-Expression was seen in tumor cells in 7/7 cases, vascular endothelium in 7/7, and in stroma in 4/7 cases. This study delineates the pattern of expression of the αvβ3- and αvβ5-integrins in ‘normal’ and neoplastic human kidney. Variations in αvβ3- and αvβ5-integrin expression may play a role
ISSN:0250-8095
DOI:10.1159/000169032
出版商:S. Karger AG
年代:1996
数据来源: Karger
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7. |
Plasma Phospholipids and Platelet Function in Uremic Patients |
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American Journal of Nephrology,
Volume 16,
Issue 5,
1996,
Page 409-411
Ana Vecino,
José L. Teruel,
José L. Navarro,
Jesús M. Cesar,
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摘要:
An increased activity of phospholipase A2 has been observed in the plasma of patients with uremia. This enzyme converts phosphatidylcholine to lysophosphatidylcholine (LPC), an inhibitor of platelet aggregation. We measured the levels of plasma phospholipids including LPC, and platelet aggregation in 7 patients with uremia. Platelet response to agonists was defective, mainly with collagen (p < 0.001). The patients’ levels of LPC in plasma were similar to those of controls (109.7 ± 41.6 vs. 80.4 ± 16.8 nmol/ml) and did not correlate with the platelet response to adenosine diphosphate (r = -0.51). The amount of phosphatidylcholine was increased with respect to normal plasma (1,041.0 ± 201.8 vs. 760.8 ± 142.7 nmol/ml, p < 0.01), while the levels of other phospholipids were normal. These results do not suggest a participation of plasma LPC in the genesis of the platelet defect observed in patients with u
ISSN:0250-8095
DOI:10.1159/000169033
出版商:S. Karger AG
年代:1996
数据来源: Karger
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8. |
Isolated Hematuria in Adults: IgA Nephropathy Is a Predominant Cause of Hematuria Compared with Thin Glomerular Basement Membrane Nephropathy |
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American Journal of Nephrology,
Volume 16,
Issue 5,
1996,
Page 412-416
Hiroshi Tanaka,
Sung-Teh Kim,
Masayuki Takasugi,
Akio Kuroiwa,
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摘要:
We examined kidney biopsy specimens obtained from 40 adult patients with isolated hematuria to determine the renal pathology and the incidence of thin glomerular basement membrane nephropathy (TGBMN). Light microscopy showed minor glomerular abnormalities in 26 patients (65%), focal and segmental lesions in 3 patients (8%), and mild diffuse proliferative glomerulonephritis in 11 patients (28%). Immunofluorescence microscopy showed IgA nephropathy (IgA-N) in 16 patients (40%), in whom no progressive lesions were identified. We measured the glomerular basement membrane (GBM) thickness using electron microscopy, and TGBMN was identified in 4 patients (10%). Our results suggest that IgA is a major pathological finding in adult patients with isolated hematuria. GBM thinning does not appear to be a major cause of glomerular hematuria.
ISSN:0250-8095
DOI:10.1159/000169034
出版商:S. Karger AG
年代:1996
数据来源: Karger
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9. |
A 19-Year-Old Female with Fever, Acroparesthesia, and Progressive Deterioration of Renal Function |
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American Journal of Nephrology,
Volume 16,
Issue 5,
1996,
Page 417-424
Mohamed A. El-Shahawy,
Carlos Mesa,
Michael Koss,
Vito M. Campese,
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ISSN:0250-8095
DOI:10.1159/000169035
出版商:S. Karger AG
年代:1996
数据来源: Karger
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10. |
Interrelationship between Renal Mass and Renotropin Activity in Consecutive Generations of Uninephrectomized Mice |
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American Journal of Nephrology,
Volume 16,
Issue 5,
1996,
Page 425-430
Zhan Averbukh,
Joshua Weissgarten,
Sylvia Berman,
Mirel Cohn,
David Modai,
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摘要:
In offspring of uninephrectomized mouse mothers at ages 3, 5 and 7 weeks (n = 8 in each group) fresh and dry kidney weights, protein content, mean number of glomeruli per microscopic field (GN), mean cumulative fractional glomerular area per microscopic field (GA) and mean number of nuclei per glomerulus (GC) were all significantly increased compared to age-matched control offspring of sham nephrectomized mothers. Sera from mice at ages 3 and 5 weeks, offspring of uninephrectomized mothers, stimulated mesangial cell proliferation in culture. Surprisingly, fresh and dry renal weight, GN, GA and GC were all significantly increased in offspring of sham nephrectomized mothers, daughters of uninephrectomized grandmothers. We speculate that elevated maternal renotropin transferred via the placenta introduces a modification in the embryonal interrelationship between renal mass and endogenous renotropin. This modification results in exaggerated embryonal serum renotropic activity extending to puberty. Whether the humoral agent responsible for enhanced mesangial cell proliferation in vitro is identical to renotropin remains to be elucidated.
ISSN:0250-8095
DOI:10.1159/000169036
出版商:S. Karger AG
年代:1996
数据来源: Karger
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