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At least 37 records · Page 2Linked to original sources
PubMed1981

Immune response in experimentally induced uremia. II. Suppression of PHA response in uremia is mediated by an adherent, Ia-negative and indomethacin-insensitive suppressor cell.

The characteristics of the adherent suppressor cell in uremic rats were examined. We found that: 1) adherent spleen cells from uremic rats display a more potent suppressor activity than do control adherent cells; 2) the suppression that is mediated by uremic adherent spleen cells cannot be eliminated by pretreatment with indomethacin, whereas the suppression that is mediated by naturally present adherent cells in the control rat is reversed by pretreatment with indomethacin; 3) the uremic adherent suppressor cell does not have Ia antigens that can be detected by the monoclonal antibodies OXL, whereas control adherent cells have Ia antigens on their surface; 4) both the control and uremic adherent suppressor cells are insensitive to mitomycin C and do not have any detectable levels of Thy 1 antigens on their surface. It appears that immune suppression in uremic rats is mediated by an adherent cell that differs from adherent cells present in control animals. The suppression in uremic rats is either not mediated by prostaglandins or may be mediated by preformed prostaglandin synthetase products.

Animals↗
PubMed1981

Sexual dysfunction in the male patient with uremia: a reappraisal.

Partial or complete impotence is common in uremia. It is not clear whether the impotence is organic or psychogenic in nature and whether uremia itself or the state of chronic illness is responsible for it. We examined these questions, by psychiatric interviews and nocturnal penile tumescence (NPT), in 50 normal subjects, 48 patients with chronic uremia, including 23 patients treated with maintenance dialysis, and 22 patients with chronic illness and normal renal function. About 40 to 50% of patients with uremia, but not those with chronic illness and normal renal function, complained of erectile dysfunction and reported a significant decrease in frequency of intercourse. There were no significant differences between patients with uremia prior to initiation of therapy and those treated with maintenance hemodialysis. NPT declines after 40 years of age. In all age groups, NPT was significantly (P less than 0.01) lower in uremics than in normals or those with chronic illness. There was no correlation between erectile complaints, frequency of intercourse or NPT, and the presence or absence of depression. The frequency of intercourse correlated significantly (r = 0.68, P less than 0.01) with NPT in patients with uremia. Data indicate that 50% of male patients with uremia have partial or complete impotence, which is most probably organic in nature and is related to uremia or its metabolic or hormonal consequences rather than to the state of chronic illness.

Adolescent↗
PubMed1996

Phosphorus intake regulates intestinal function and polyamine metabolism in uremia.

This study found that 5/6-nephrectomized uremic rats showed secondary hyperparathyroidism as reflected by an increase in their serum parathyroid hormone (PTH) level in association with a decrease in serum 1,25-dihydroxyvitamin D [1,25-(OH)2D]. These changes recovered partially upon phosphorus restriction. Calcium absorption and gene expression of calbindin-D9k were decreased in uremia and were also improved by phosphorus restriction. In uremia, intestinal spermidine/spermine N1-acetyltransferase activity was decreased, while ornithine decarboxylase (ODC) activity and its gene expression were potentiated. Enhancement of c-fos and c-jun gene expressions was also observed in uremia. These phenomena suggest that the intestinal villus may proliferate in uremia. Phosphorus restriction prevented increases in the expression of ODC, c-fos and c-jun observed in uremia. Since phosphorus restriction caused a rise in the serum 1,25-(OH)2D level, the role of 1,25-(OH)2D in uremia-induced intestinal dysfunction was examined. A single injection of 1,25-(OH)2D3 to uremic rats caused an increase in the steady-state calbindin-D9k mRNA level, and decreases in steady state c-fos and ODC mRNA levels, suggesting that the deficiency of 1,25-(OH)2D3 is responsible for intestinal dysfunction in uremia. In conclusion, altered polyamine metabolism caused by 1,25-(OH)2D deficiency is intimately involved in intestinal dysfunction and the development of the proliferative state of the intestinal villus in uremia.

Absorption↗
PubMed1997

Decreased hepatic insulin-like growth factor (IGF)-I and increased IGF binding protein-1 and -2 gene expression in experimental uremia.

The imbalance between normal insulin-like growth factor-I (IGF-I) and markedly increased IGF binding protein (IGFBP) plasma levels plays a pathogenic role for growth retardation and catabolism in children with chronic renal failure. To investigate the mechanism of these alterations, experiments were performed in an experimental model of uremia in rats (5/6 nephrectomy) and in pair-fed and ad libitum-fed sham-operated controls Using a specific solution hybridization/RNase protection assay, we observed a marked reduction of hepatic IGF-I messenger RNA (mRNA) abundance at steady state in uremic animals (37 +/- 5% of control) compared both with pair-fed (65 +/- 10%) and ad libitum-fed controls (100 +/- 11%) (P < 0.001). Reduced IGF-I gene expression was clearly organ-specific; it was most pronounced in liver (significant vs., pair-fed controls) and lung and muscle tissue (significant vs., ad libitum-fed controls); no change was observed in kidney and heart tissue. To determine a potential mechanism of reduced hepatic IGF-I gene expression in uremia, the hepatic GH receptor gene expression in the same experimental animals was analyzed by specific solution hybridization/RNase protection assay. Uremic animals had a 20-30% reduction of hepatic GH receptor mRNA abundance compared with controls. Hepatic GHBP expression in uremia was decreased in parallel. Despite the reduction of hepatic IGF-I mRNA abundance, plasma IGF-I levels in uremia were not different from ad libitum-fed controls. This discrepancy is explained by an increased concentration of IGFBPs in uremic plasma. By RIA, plasma IGFBP-1 levels in uremia were increased 4-fold; by Western immunoblot, plasma IGFBP-2 levels were increased 7-fold and plasma IGFBP-4 levels were increased 2-fold compared with both control groups. Intact IGFBP-3 (M(r), approximately 48 kDa) and low molecular IGFBP-3 fragments were not significantly different among the three groups. By Northern blot analysis, hepatic IGFBP-1 mRNA levels in uremia were 2-fold higher than in controls. IGFBP-2 mRNA abundance in liver tissue was increased 4-fold, whereas in kidney there was a significant reduction of IGFBP-2 mRNA (30% of control). IGFBP-4 mRNA was increased by 50% in kidney but not in liver. Plasma insulin and corticosterone levels were not different among the groups. Our study shows that hepatic IGF-I gene expression was specifically reduced in uremia, partially as the consequence of a reduced hepatic GH receptor gene expression. One of the mechanisms contributing to increased IGFBP levels in uremia is increased hepatic gene expression of IGFBP-1 and IGFBP-2. The imbalance between reduced hepatic IGF-I production and increased hepatic IGFBP-1 and 2 production is likely to play a pathogenic role for catabolism and growth failure in CRF.

Animal Nutritional Physiological Phenomena↗
PubMed2006

Evaluation of cardiac global function using the myocardial performance index by tissue Doppler echocardiography in patients with uremia.

OBJECTIVE: The purpose of this study was to assess global ventricular function in patients with uremia by means of the myocardial performance index (MPI) derived from tissue Doppler echocardiography. METHODS: According to the left ventricular mass index and pericardial effusion, 45 patients with uremia were classified into 2 groups: a uremia group and a uremia with pericardial effusion group. To calculate left ventricular MPI (LVMPI) and right ventricular MPI (RVMPI) by tissue Doppler echocardiography, the isovolumic contraction time (ICT), isovolumic relaxation time (IRT), and ejection time (ET) were measured at different sites in the mitral and tricuspid annuli. RESULTS: The mean ICT and IRT were longer, the ET was shorter, and the LVMPI and RVMPI were higher in the 2 disease groups than in a control group, and the indices were higher in the uremia with pericardial effusion group than in the uremia group. The increase of the LVMPI was more obvious than that of the RVMPI. There was a significant difference in the mean LVMPI and RVMPI among the 3 groups (P<.01). The MPI was positively correlated with the IRT and the sum of the ICT and IRT and negatively correlated with the ET. CONCLUSIONS: Both left and right ventricular systolic and diastolic function are impaired in patients with uremia. The MPI could be measured by tissue Doppler echocardiography, and we suggest that this index provides a novel, noninvasive method for clinical research on global myocardial performance in patients with uremia.

Adult↗
PubMed1998

Cardiovascular response to hemodialysis: the effects of uremia and dialysate buffer.

Cardiovascular instability continues to be one of the primary clinical problems in hemodialysis. Acetate buffer in dialysate is one of the factors that may induce hypotension. Since uremia may have a direct effect on the regulation of the cardiovascular system, the present study was designed to investigate the separate effects of uremia and acetate hemodialysis on blood pressure in anesthesized dogs, as well as the hemodynamic parameters determined by invasive cardiovascular monitoring. Animals were separated into four groups: (1) group I, hemodialysis with acetate in controls; (2) group II, hemodialysis with acetate in uremic dogs; (3) group III, hemodialysis with bicarbonate in controls; and (4) group IV, hemodialysis with bicarbonate in uremic dogs. Acute uremia was induced by bilateral ureteral ligation and a 90-minute hemodialysis (acetate or bicarbonate) procedure was performed 72 hours later. The results obtained in this study show that, compared with dogs with normal renal function, acute uremia resulted in an elevation in mean arterial pressure (MAP; 178 +/- 13 vs. 115 +/- 23 mm Hg, P < 0.01), which was associated with an increase in cardiac index (CI) and left ventricular stroke work index (LVSWI). In these dogs, the pulmonary capillary wedge pressure (PCWP; preload) and the systemic vascular resistance index (SVRI; afterload) were not different than controls. In uremic dogs, hemodialysis with acetate, but not with bicarbonate, decreased the MAP to values similar to controls. The decrease in MAP induced by acetate hemodialysis in uremic dogs was associated with a decrease in SVRI and PCWP. These results suggest that in dogs with acute uremia, acetate hemodialysis (HD) decreases myocardial contractility that was previously increased by a direct effect of uremia. In controls, acetate produced a moderate decrease in MAP that was the result of a mild decrease in CI and SVR. Since PCWP was not significantly decreased after acetate HD, the decrease in CI can be attributed to a mild decrease in myocardial performance. In conclusion, this study in dogs suggests that uremia enhances myocardial contractility directly. Acetate hemodialysis reduces this elevated myocardial contractility to normal values.

Acetates↗