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At least 145 records · Page 8Linked to original sources
PubMed2003

Renal allograft loss as the result of polyomavirus interstitial nephritis after simultaneous kidney-pancreas transplantation: results with kidney retransplantation.

BACKGROUND: Polyomavirus (PV) infection in kidney transplant patients has been reported to cause interstitial nephritis and subsequent graft loss. The cornerstone of current therapy is a reduction in immunosuppression, which can subsequently lead to kidney allograft rejection. This dilemma becomes even more challenging in the setting of simultaneous kidney-pancreas transplantation, because a reduction in immunosuppression may result in rejection of the pancreas allograft. Antiviral therapy has not been shown to be clinically successful in decreasing the risk of graft loss secondary to PV infection. Furthermore, because of limited experience, the decision to perform retransplantation in patients who lost their primary kidney grafts to PV interstitial nephritis becomes a difficult one. METHODS: Retrospective review and case studies. RESULTS: We report two successful living donor kidney retransplants in simultaneous kidney-pancreas transplant patients who lost their first kidney grafts to PV infection. Both patients are receiving rimantadine therapy and performing well, with functioning kidney and pancreas grafts and no evidence of recurrent PV interstitial nephritis 22 and 37 months after retransplantation. CONCLUSIONS: Although follow-up is limited, our initial experience would indicate that graft loss secondary to PV interstitial nephritis is not an absolute contraindication for kidney retransplantation.

Adult↗
PubMed1983

"Structural autoregulation" of blood flow and GFR in the two renal vascular beds from two-kidney, one-clip renal hypertensive rats, as compared with kidneys from uni-nephrectomized and intact normotensive rats.

Both kidneys from two-kidney, one-clip renal hypertensive rats (RHR) and the hypertrophied kidney of uni-nephrectomized rats (UNR) were investigated during artificial perfusion with 2% Dextran solution and kerosene at maximal vasodilatation, and studied with respect to organ weight, vascular resistance, preglomerular/postglomerular resistance ratio and glomerular filtration capacity. Paired perfusions were throughout used, isolated kidneys from age-matched normotensive rats serving as controls. The untouched, "high-pressure" RHR kidney had increased 40% in weight/100 g b.w. while its vascular resistance at maximal dilatation had increased almost 60%/g organ weight. Glomerular filtration capacity and preglomerular/postglomerular resistance ratio remained, however, largely unchanged. The clipped "low-pressure", RHR kidney was reduced 40% in weight and 45% in renal vascular resistance/g organ weight. It also showed a reduced pre/postglomerular resistance ratio and some reduction of filtration capacity. The remaining hypertrophied kidney in UNR had increased 40% in weight, while its vascular resistance and filtration capacity/g organ weight, as well as its pre/postglomerular resistance ratio were unchanged. It is concluded that the kidney in renovascular hypertension rapidly adapts structurally not only in tissue mass, but also concerning total vascular resistance and pre/postglomerular resistance ratio, so as to chronically "autoregulate" GFR to match the altered pressure situation. Likewise, after unilateral nephrectomy the remaining, normotensive kidney increases in mass, with matched increases in blood flow and glomerular filtration capacity, while total resistance/g organ weight and the pre/postglomerular resistance ratio remain at normotensive levels.

Adaptation, Physiological↗
PubMed2005

Identification of differentially expressed genes between fetal and adult mouse kidney: candidate gene in kidney development.

BACKGROUND: The kidney development involves a wide variety of developmental processes requiring a lot of genes expressed in a sequential manner. The aim of the present study is to identify new genes involved in these processes. METHODS: To obtain a view of the mouse embryonic kidney transcriptome we used the SADE method, which allows large-scale quantitative gene expression measurements. RESULTS: 7,689 tags were sequenced from our library. Among the 4,507 unique transcripts yielded, 64% correspond to known genes, 22% ESTs, 12% unidentified genes. 472 genes were differentially expressed as compared to published adult kidney library. Among these, we identified several candidate genes and focused on a particular one: thymosin beta4 (Tbeta4), an actin-sequestering protein more highly expressed in fetal kidney. First we studied the in vivo expression patterns of Tbeta4 transcript during kidney development. Tbeta4 increases throughout the kidney development and remains high during active nephrogenesis. Moreover, the spatial distribution of Tbeta4 mRNA was analysed and reveals that during active nephrogenesis (i.e., 18 dpc) Tbeta4 is localised in differentiating glomeruli. In adult kidney, Tbeta4 remains expressed in podocytes and collecting ducts. CONCLUSION: Our results provide the first demonstration of Tbeta4 production in vivo by embryonic kidney and further show that Tbeta4 is implicated in kidney organogenesis.

Aging↗
PubMed1996

Vascular and cardiac overexpression of endothelin-1 gene in one-kidney, one clip Goldblatt hypertensive rats but only in the late phase of two-kidney one clip Goldblatt hypertension.

OBJECTIVE: To investigate a model of experimental hypertension that exhibits severe hypertrophy of small blood vessels but in which deoxycorticosterone acetate (DOCA) and salt are absent: the one-kidney, one clip model of Goldblatt renovascular hypertension, which is non-renin-dependent, and compare it with the renin-dependent two-kidney, one clip Goldblatt hypertensive rat, in which additionally vascular hypertrophy is less severe. METHODS: Endothelin-1 gene expression in blood vessels and in the heart was examined by Northern blot analysis. RESULTS: After 2 or 4 weeks of application of the silver clip to unilaterally nephrectomized rats, the aorta and mesenteric arteries exhibited a significant increase in the intensity of the 2.3 kb band corresponding to hybridization with endothelin-1 messenger RNA (mRNA) in comparison with results obtained in control unilaterally nephrectomized rats. No increase was noted in the blood vessels of the two-kidney, one clip hypertensive rat at 2 or 4 weeks, but significant increases were found at 8 weeks in aorta, but not in mesenteric arteries. Cardiac abundance of endothelin-1 mRNA was also increased in ventricles and in the left atria of one-kidney, one clip hypertensive rats, but only in the late phase (at 8 weeks) in two-kidney, one clip hypertensive rats. CONCLUSION: Because one-kidney, one clip hypertensive rats presented severe vascular hypertrophy whereas two-kidney, one clip hypertensive rats only did so in the late phase of hypertension, these results lend further support to there being a relationship between vascular hypertrophy and endothelin-1 vascular overexpression in experimental models of hypertension. They also demonstrate that enhancement of the expression of endothelin-1 gene in blood vessels and in the heart of hypertensive rats may occur in the absence of exposure to DOCA and salt, and that endothelin-1 gene overexpression in experimental hypertension occurs early in non-renin-dependent, volume-expanded models such as the one-kidney, one clip or the DOCA-salt hypertensive rat, but only in the progressively non-renin-dependent late phase of the initially renin-dependent volume-contracted two-kidney, one clip hypertensive rat.

Animals↗
PubMed2005

[Establishment of rat model of transplantation of kidney containing adrenal implants and its protective effects on the transplanted kidney].

OBJECTIVE: To establish a rat model of transplantation of kidney containing adrenal implants and to explore the protective effects of the adrenal implants on the transplanted kidney. METHODS: Fragments of adrenal cortex of the left adrenal gland were obtained and implanted into the left kidneys of the same would-be donor rats. Twenty-four Lewis rats were transplanted with the left kidneys containing adrenal gland implants of SD rats (Group I), and another Lewis rats were transplanted with the unprepared left kidneys of 24 SD rats (Group II). Seven days after the implantation the right kidneys of the recipient rats were resected. No immunosuppressant was used. The survival time was observed. Blood samples were collected at different time points to examine the serum corticosterone, creatinine, and urea nitrogen. Light microscopy was used to observe the morphology of the implanted kidneys and the adrenal implants. RESULTS: Histological examination showed that the adrenal gland implants survived well with good blood supply. Seven days after the resection of the right kidneys microscopy showed atrophy of the adrenal implants. There were no significant differences in serum corticosterone, creatinine, and urea nitrogen between the levels before and 7 days after transplantation and between the 2 groups. The survival time of Group I was 10.2 d +/- 2.2 d, significantly longer than that of Group II (7 d +/- 2 d, P < 0.05). CONCLUSION: Adrenal implants that survive and recover their endocrinal function have protective effect on the transplanted kidney in early period.

Adrenal Glands↗
PubMed1984

Study of renovascular hypertension in rats: I. The role of the contralateral, non-clipped kidney in two-kidney, one-clip hypertension in rats.

We attempted to produce two-kidney one-clip renovascular hypertension in SD rats, using hemoclips 0.2mm in diameter. After 12 weeks, 10 of the 16 rats were hypertensive. At this point, one-kidney, one-clip models were prepared by contralateral nephrectomy in five of the 10 hypertensive rats and in all six normotensive rats. Postoperatively, these 11 rats developed hypertension. Four to 6 weeks later, the clip was removed from the renal artery in five two-kidney and 11 one-kidney hypertensive rats. After unclipping, all the rats became normotensive although the extent of the fall in blood pressure in the one-kidney model was significantly greater than in the two-kidney model. The roles of the contralateral non-clipped kidney in the evolution of two-kidney, one-clip Goldblatt hypertension appear to be dual; sometimes depressing elevated blood pressure and sometimes maintaining it. Thus, it is postulated that in the six initially normotensive rats, its action was predominantly antihypertensive, while in the other 10 hypertensive rats, the presence of a contralateral non-clipped kidney served to develop and maintain hypertension even after unclipping.

Angiotensin II↗
PubMed1997

Pancreas and kidney allograft-infiltrating cells in simultaneous pancreas-kidney transplantation.

BACKGROUND: Rejection after pancreas-kidney transplantation may occur isolated or concurrently in both grafts. To get more insight into the cellular mechanisms underlying these rejection episodes, we compared the functional characteristics of pancreas and kidney graft-infiltrating T cells. METHODS: Graft-infiltrating T cell (GIC) lines were cultured from simultaneously taken pancreas and kidney biopsies from eight patients. CD4 to CD8 ratios were determined by fluorescence-activated cell sorter and cytotoxicity toward donor proximal tubular epithelial cells (PTEC) and donor spleen cells (DSC) using a standard cytotoxicity assay. Cytokine production was determined by enzyme-linked immunosorbent assay. RESULTS: CD4 to CD8 ratios were comparable between the pancreas and kidney lines for each patient, but differences were observed in cytotoxicity toward PTEC and DSC. For four of eight patients, the lysis of PTEC by pancreas GIC was less than the lysis induced by kidney GIC. This was also seen in three of five patients for lysis of DSC. The specificity of GIC lines toward mismatched donor antigens was studied for two patients and appeared to be comparable for pancreas and kidney. Most GIC lines produced interferon (IFN)-gamma (75.5+/-22.7 pg/ml), but no IL-10, indicating that the cell lines consisted primarily of Th1 and type 1 CD8+ cells. Mean production of IL-6 was 465.6+/-193.6 pg/ml. No major differences were observed between kidney and pancreas GIC for either cytokine. CONCLUSIONS: We conclude that pancreas and kidney GIC lines have the same phenotype, cytokine production, and allospecificity. Differences were, however, seen for lysis of PTEC and DSC, suggesting that tissue-specific antigens might play a role.

Biopsy↗
PubMed1983

Urinary excretion of thermostable kidney antigen (BE antigen) in patients with various renal diseases. A case of membranous nephropathy with kidney BE antigen in the urine.

Urine samples of 17 patients with nephropathy were tested with precipitating anti-thermostable-kidney antigen sera (anti-kidney BE antigen), which had been made kidney specific by absorption with diverse tissues. Kidney BE antigen was demonstrated in the concentrated urine of a patient (case I.T.) with membranous nephropathy, in whom membranous nephropathy appeared to be associated with exposure to chromium. Kidney BE antigen was, however, not demonstrated in the concentrated urine from the other 16 patients with nephropathy (chronic glomerulonephritis, 7; acute glomerulonephritis, 3; lupus nephritis, 3; membranous nephropathy, 2; diabetic nephropathy, 1). Kidney BE antigen was localized in the tubular cells but not in the glomeruli, by indirect immunofluorescent staining. Kidney BE antigen was not demonstrated in the glomeruli in case I.T., even after acid elution of the sections. The possible role of kidney BE antigen in the pathogenesis of membranous nephropathy is discussed.

Adult↗