摘要:

The thyroid function was evaluated before and after 6 months of recombinant human erythropoietin (rhEPO) treatment (1,500-9,000 U/week) in 22 hemodialysis patients with hematocrit levels 5% (group I) and 11 patients with an increase < 5% (group II). Before rhEPO administration, the levels of thyroid hormones, especially free thyroxine (T4) and free triiodothyronine (T3), were below the normal range despite normal thyrotropin values in most of the patients (low T4:7 cases in group I and 9 in group II; low T3:10 cases in group I and 10 in group II). RhEPO treatment significantly increased both total amount and free fractions of thyroid hormones in group I, whereas it did not affect these values in group II. Consequently, the pretreatment low T4 or low T3 status was resolved in a substantial number of the patients in group I (low T4:5 cases, low T3:4 cases). In addition, there was a significant correlation between the increases in hematocrit and free T3 in all studied subjects (r = 0.603; p < 0.05). These results suggest that anemia may participate to some extent in the pathogenesis of thyroid dysfunction in hemodialysis patients with renal anemia.

ISSN:1660-8151    

DOI:10.1159/000187828

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

According to the urea kinetic model it is considered that the urea distribution volume (V) is that of body water, and that it is distributed in only one compartment. Since the V value is difficult to measure, it is normal to use 58% of body weight, in spite of the fact that it may range from 35 to 75%. In this study, we have calculated the value of V by using an accurate method based on the total elimination of urea from the dialysate. We have studied the V, and also whether the different dialysis characteristics modify it. Thirty-five patients were included in this study, 19 men and 16 women, under a chronic hemodialysis programme. The dialysate was collected in a graduated tank, and the concentration of urea in plasma and in dialysate were determined every hour. Every patient received six dialysis sessions, changing the blood flow (250 or 350 ml/min), the ultrafiltration (0.5 or 1.51/h), membrane (cuprophane or polyacrylonitrile) and/or buffer (bicarbonate or acetate). At the end of the hemodialysis session, the V value ranged from 43 to 72% of body weight; nevertheless, this value was practically constant in every patient. The V value gradually increased throughout the dialysis session, 42.1 ± 6.9% of body weight in the first hour, 50.7 ± 7.5% in the second hour and 55.7 ± 7.9% at the end of the dialysis session. The change of blood flow, ultrafiltration, membrane or buffer did not alter the results. The V value was significantly higher in men in comparison with women, 60.0 ± 6.6% vs. 50.5 ± 5.9% of body weight (p < 0.

ISSN:1660-8151    

DOI:10.1159/000187829

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

The strain of FGS/Nga mouse is reported to develop proteinuria and progressive glomerulosclerosis. We studied the renal pathology of that strain periodically for 1 year. Focal and segmental glomerulosclerosis was observed 3 months after birth and the lesion progressed to the glomerular obsolescence in a year. Electron microscopic study revealed electron dense deposits (DD) in the mesangium and the splitting of glomerular basement membrane. Studies using immunofluorescence and immunoelectron microscopy revealed that these DD were contained IgA, IgM, C3 and the retroviral envelope antigen (gp70). Clinically, proteinuria began at the age of 3 months and the renal function was decreased on time course. No other organs were involved. We studied the renal lesions of FGS mice by the histological and immunohistochemical methods and concluded that this mouse strain provides the tool for studying the mechanisms of the progression of glomerulosclerosis.

ISSN:1660-8151    

DOI:10.1159/000187830

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

To understand the role of thymus-derived T cells in the development of IgA nephropathy (IgAN), we performed neonatal thymectomies on ddY mice, in which this disease occurs spontaneously. Although these thymectomized mice developed a renal lesion closely resembling that typical of IgAN, the extent of their mesangial IgA deposition was significantly milder than in control sham-operated mice. The immunological mechanisms responsible for curbing this mesangial deposition of IgA were then analyzed. The percentage of splenic T cells and the magnitude of mitogenic responses both decreased markedly in thymectomized compared with control mice. These results suggested the hypofunction of thymus-derived T cells. However, serum IgA levels were almost identical in both groups. Furthermore, sera from both groups contained similar amounts of macromolecular IgA, of the type formerly eluted from the affected glomeruli of patients with IgAN. These results strongly indicate that thymus-derived T cells or their products determine the amount of IgA deposited in the kidneys of ddY mice.

ISSN:1660-8151    

DOI:10.1159/000187831

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Glomerular basement membrane thickening and mesangial expansion are the main pathological features in diabetic nephropathy – glomerulosclerosis with the biochemical correlate of increased collagen accumulation. We studied a new principle to reduce collagen accumulation in the glomerulus: thiaproline, known to inhibit protein synthesis by blocking the elongation, led in our studies to a morphological reduction of the glomerular basement membrane thickening and to a decreased collagen content. As the thiaproline analogue is incorporated into collagen, the mechanism of increased degradation of the modified collagen is being discusse

ISSN:1660-8151    

DOI:10.1159/000187832

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

This paper investigates factors involved in mesangial cell (MC) proliferation by focussing on the proliferative effects of phorbol myristate acetate (PMA) on mouse MC in culture in comparison to those of fetal calf serum (FCS). The potential roles of cyclooxygenase and lipoxygenase products of arachidonic acid metabolism and of hydroxyl radicals on their proliferation are addressed. The results indicate: (1) that PMA can induce proliferation of MC; (2) that inhibition of prostaglandin synthesis by indomethacin does not modify PMA-induced proliferation but enhances the proliferative response to FCS, and (3) that stimulation of MC proliferation by PMA or FCS is inhibited by agents interfering with the generation of products of the lipoxygenase pathway and hydroxyl radical scavengers. The role of lipoxygenase products and reactive oxygen species in MC proliferation deserves further investigation.

ISSN:1660-8151    

DOI:10.1159/000187833

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Metabolic acidosis is a well-known mediator of compensatory renal hypertrophy; however, the underlying mechanism is still poorly understood. The aim of the present study was to investigate whether metabolic acidosis can influence the proteolytic activity in the proximal tubule. Metabolic acidosis was induced in rats by 0.28 M NH4C1 which was mixed to drinking water. The development of metabolic acidosis was documented by a significant increase in urinary pH. After 11 days of 0.28 MNH4Cl treatment, the experimental animals developed mild proteinuria (9.52 ± 0.99 versus 17.65 ± 1.63 mg/day). The kidney weigth increased significantly (1,653.56 ± 27.84 versus 1,753.33 ± 56.11 mg) and tubular proteinase activity, measured at pH 5.4, was markedly reduced (60.3 ± 1.2 versus 52.2 ± 2.4 U/mg protein, or 2,105.5 ± 92.0 versus 1,631.0 ± 97.2 mU/μg DNA). In summary, these results suggest that compensatory renal hypertrophy induced by metabolic acidosis might at least partly be due to the suppression of tubular proteinase

ISSN:1660-8151    

DOI:10.1159/000187834

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

We present a 57-year-old man with end-stage renal failure due to chronic glomerulonephritis, who had been on hemodialysis for 13.5 years and had suffered from recurrent painful swelling of the left leg for 4.7 years. A diagnosis of deep venous thrombosis was made by the phlebography. Coagulation studies showed decreased protein C activity despite a normal protein C antigen level. None of his relatives had decreased protein C activity, and the levels of the other coagulation factors synthesized by the liver were all normal. Accordingly, the patient was diagnosed as having acquired type II protein C deficiency.

ISSN:1660-8151    

DOI:10.1159/000187835

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

A case of human T-cell lymphotrophic virus type I (HTLV-I)-associated myelopathy (HAM) occurring in a 62-year-old Japanese male with a history of hemodialysis and repeated blood tranfusions due to chronic renal failure (CRF) is reported. The patient was a lifelong resident of Chiba Prefecture, a nonendemic area for HTLV-I infections. The clinical course was characterized by abrupt onset and rapid progression of neurological signs and symptoms, which appeared to have responded quite well to prednisolone. Although patients with a history of CRF, hemodialysis, and transfusion of blood units which were not screened for anti-HTLV-I antibodies appear to belong to the high risk group for HTLV-I infections and subsequent development of HAM, reports on such cases have been scanty. Only 3 cases have been reported to date. It appears quite possible that many patients with CRF and HAM remain misdiagnosed.

ISSN:1660-8151    

DOI:10.1159/000187836

出版商:S. Karger AG    

年代:1994

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000187837

出版商:S. Karger AG    

年代:1994

数据来源: Karger