Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety-five patients (63 male, 32 female), age 45 +/- 2 years (mean +/- SEM) with chronic renal failure of varied aetiology were randomized to receive either a conventional low protein diet (0.6 g/kg/day protein, 800 mg phosphate; n = 33), a low phosphate diet (providing approximately 1000 mg phosphate plus an orally administered phosphate binder, minimum protein intake 0.8 g/kg/day; n = 30) or to control (minimum protein intake 0.8 g/kg/day, no phosphate restriction; n = 32). Patients were reviewed for a minimum of 6 months before randomization and were withdrawn from the study if plasma creatinine exceeded 900 mumol/l, plasma phosphate was greater than 2.0 mmol/l or at the onset of uraemic symptoms. Following randomization patients were studied for an average of 19 +/- 3 months. Mean plasma creatinine rose from 398 +/- 33 to 600 +/- 50 mumol/l. Dietary protein intake was estimated at 0.69 +/- 0.02 g/kg/day in the low protein group, 1.02 +/- 0.05 in the low phosphate and 1.14 +/- 0.05 in the controls, phosphate intake was 815 +/- 43, 1000 +/- 47, and 1315 +/- 57 mg/day, respectively. Urinary urea excretion and protein catabolic rates were significantly reduced (p less than 0.01) only in those on protein restriction, at 213 +/- 9 mmol/24 hours and 0.71 g/kg/day, respectively. Phosphate excretion was significantly lower (p less than 0.05) in both the low protein group (17.9 +/- 0.8 mmol/24 hours) and the low phosphate group (18.6 +/- 1.0 mmol/24 hours) compared to controls. Changes in body weight, muscle mass and serum transferrin, albumin and immunoglobulins were comparable between the groups. Mean blood pressure following randomization was 150/89 +/- 3/1 (low protein), 148/87 +/- 3/1 (low phosphate) and 146/87 +/- 3/1 (controls). Progression of renal failure was analysed by rate of all of creatinine clearance (ml/min/1.73 m2/month), by rate of deterioration derived from reciprocal plasma creatinine against time plots (1/mmol/year) and to assess individual patient's response to treatment by two phase linear regression ('breakpoint') analysis of reciprocal plasma creatinine/time plots. Progression was analysed only in patients seen for at least 3 months following randomization. The rate of fall of creatinine clearance was not significantly different between the groups (ANOVA): 0.56 +/- 0.08 ml/min/1.73 m2/month (low protein, n = 28), 0.44 +/- 0.07 (low phosphate, n = 23) and 0.69 +/- 0.11 (control, n = 27).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Failure of dietary protein and phosphate restriction to retard the rate of progression of chronic renal failure: a prospective, randomized, controlled trial. 180 Oct 57

In an epidemiological study carried out in Reunion Island, 1,686 randomized school children aged from 11 to 15 years were examined for goitre by cervical palpation. A detailed questionnaire was fully completed by each child and his parents. The iodine level was measured in 168 urinary samples and in the salt and water consumed in the various places investigated. The overall incidence of goitre was 8.2 percent, rising up to 19.7 percent in the mountainous part of the island. The mean urinary iodine level was 40.2 +/- 2.7 micrograms I/g creatinine (m +/- SEM) and fell to 20.0 +/- 3.7 in the highlands. Water and salt contained little iodine. A significant relationship was noted between the presence of goitre on the one hand and sex, familial incidence of goitre, cassava consumption and distance from the coast on the other hand. This study demonstrates that endemic goitre and iodine deficiency are present in a limited area of Reunion Island.
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PMID:[Incidence of endemic goiter on Reunion Island. A search for etiological factors]. 183 62

Plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP) were measured with a specific radioimmunoassay in 19 undialysed patients with chronic renal failure. At the beginning, an extremely high level of plasma hANP (50 fmol/ml) seen in a patient was rejected with Smirnov's test and was excluded from further statistics. The plasma IR-ANP levels in these patients were significantly higher than those of 19 normal subjects matched with age and sex (10.9 +/- 1.6 vs 5.3 +/- 0.6 fmol/ml, mean +/- SEM, p less than 0.01), and positively correlated with mean blood pressure (r = 0.44, p less than 0.05) and the cardiothoracic ratio (r = 0.65, p less than 0.01), but did not correlate with creatinine clearance (r = -0.38, n.s.). Further, a significant correlation was observed between plasma IR-ANP and urinary protein output (r = 0.47, p less than 0.05). On the other hand, urinary protein output did not correlate significantly with variables such as mean blood pressure, the cardiothoracic ratio or creatinine clearance. Since it has been suggested that ANP enhances glomerular capillary permeability, increased ANP responding to volume overload in those patients may play an important role in increasing urinary protein excretion.
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PMID:A possible contribution of endogenous atrial natriuretic peptide to proteinuria in patients with chronic renal failure. 184 Apr 20

Recombinant human insulin-like growth factor I (rhIGF-I) was administered subcutaneously to 6 normal subjects and 2 patients with GH deficiency at a dose of 0.1 mg/kg for 7 consecutive days after breakfast. In normal subjects, plasma IGF-I levels increased from 217 +/- 22 ng/ml (Mean +/- SEM) to maximal levels of 581 +/- 6 ng/ml 4 h after the first administration of IGF-I. The blood glucose levels were statistically depressed 4 h after injection at 69 +/- 2 mg/dl. Similar plasma IGF-I and blood glucose profiles were observed after the seventh administration of IGF-I. The free form of IGF-I in plasma was 2.3 +/- 0.3 ng/ml in normal subjects and increased to maximal levels of 43.5 +/- 5.1 ng/ml 2 h after the first IGF-I administration. A similar pattern for the free form of IGF-I was observed after the seventh administration; however, the values obtained at 0, 1 and 2 h were greater after the seventh administration. In patients with G-deficiency, the plasma IGF-I and blood glucose profiles were similar to those observed in normal subjects, although the total IGF-I levels were low in these patients at all sampling points during the study. Slight decreases in serum insulin, uric acid, and creatinine were observed after the seventh administration of IGF-I. There were no changes in the excretion of urea nitrogen, creatine, creatinine, sodium, potassium, chlorine, calcium or C-peptide in the urine during the 7 days of IGF-I administration.
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PMID:Repeated sc administration of recombinant human insulin-like growth factor I (IGF-I) to human subjects for 7 days. 184 57

1. The aim of the present study was to evaluate the systemic synthesis of cysteinyl leukotrienes in patients with multiple trauma. In order to do this, the urinary excretion of leukotriene E4 was assessed in the first 10 days after trauma. 2. Leukotriene E4 was unequivocally identified by g.c.-m.s. in the urine of healthy subjects and patients with multiple trauma after its conversion to 5-hydroxyeicosanoic acid. Leukotriene E4 was routinely isolated from 24 h urine samples by solid-phase extraction followed by reverse-phase h.p.l.c. and was subsequently quantified by r.i.a. 3. Healthy subjects excreted daily 10 +/- 3 nmol of leukotriene E4/mol of creatinine (mean +/- SEM, n = 16) into urine. 4. Patients with multiple trauma who did not develop adult respiratory distress syndrome (n = 7) excreted 76.8 +/- 6.7 nmol of leukotriene E4/mol of creatinine (mean +/- SEM) daily during the first 10 days after trauma, which was significantly (P less than 0.01) more than did healthy subjects. 5. Excretion of leukotriene E4 was even more enhanced in three patients with multiple trauma who developed adult respiratory distress syndrome. Maximal amounts of 593 +/- 185 nmol of leukotriene E4/mol of creatinine (mean +/- SEM) were excreted on day 9 after trauma by these three patients, which corresponds to a 7.7- and a 59-fold increase in excretion of leukotriene E4 compared with patients with multiple trauma who did not develop adult respiratory distress syndrome and healthy subjects, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced urinary excretion of leukotriene E4 by patients with multiple trauma with or without adult respiratory distress syndrome. 185 91

Twelve-h overnight urine and serum samples obtained simultaneously at 20-min intervals were assayed for growth hormone (GH). Ninety-one children, 5 to 16 y (Tanner stage 1 to 3) participated; group 1 were healthy children, group 2 were children with organic GH deficiency, and group 3 had idiopathic growth failure and normal GH stimulation tests. Serum pool GH concentrations in group 1 were similar to those in group 3 (3.3 +/- 0.3 versus 3.4 +/- 0.2 micrograms/L); group 2 had significantly lower GH concentrations (1.6 +/- 0.2 micrograms/L). Plasma IGF-I levels were significantly greater in groups 1 (14.2 +/- 2.6 nmol/L, p less than 0.001) than in groups 2 and 3 (2.6 +/- 0.5 and 5.5 +/- 0.7 nmol/L, respectively). Urinary GH (mean +/- SEM) standardized for body weight (micrograms/kg) in group 1 (0.31 +/- 0.02) was significantly greater than in group 2 (0.14 +/- 0.01) and group 3 (0.20 +/- 0.01). However, when expressed as microgram/mol creatinine, the output of GH was similar in group 1 (4.0 +/- 0.3) and group 3 (3.4 +/- 0.3); both groups had significantly greater output compared to group 2 (1.3 +/- 0.2). Urinary IGF-I (nmol/kg) in group 1 (0.22 +/- 0.02) was significantly greater than in group 2 (0.12 +/- 0.01) or group 3 (0.07 +/- 0.01). Urinary GH correlated with serum pool GH concentration (r = 0.64, p less than 0.001). Although urinary GH output reflects endogenous GH secretion, the overlap between groups 1 and 3 precludes using urinary GH measurements as a diagnostic test for GH deficiency in children with idiopathic growth failure.
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PMID:Diagnostic significance of urinary growth hormone measurements in children with growth failure: correlation between serum and urine growth hormone. 186 20

The success of anti-rejection therapy was evaluated in 65 cadaveric renal allografts immunosuppressed with cyclosporin. All first rejection episodes were treated with 0.5 g methylprednisolone given daily for 3 days. Second rejection episodes were treated with either a further identical 3-day course of methylprednisolone or a 10-14-day course of the monoclonal antibody OKT3. The peak creatinine during second rejection episodes was higher in patients treated with OKT3 (481 +/- 54 mumol/l; mean +/-SEM) than in those treated with methylprednisolone (320 +/- 59 mumol/l) (P = 0.036), suggesting more severe rejection in the OKT3 group. Despite this the rejection reversal rate was higher in the OKT3-treated group (100%) when compared to the high-dose methylprednisolone group (64%) (P less than 0.05) and the creatinine at 6 months was less in the OKT3 group (162 +/- 17 mumol/l) than in the methylprednisolone group (230 +/- 22 mumol/l). These data suggest that OKT3 is a very effective treatment for second rejection episodes following renal transplantation and yields improved renal functions in comparison with high-dose steroids.
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PMID:Anti-rejection therapy in renal transplantation: Use of the monoclonal antibody OKT3. 188 82

Serum creatinine, blood urea nitrogen and creatine phosphokinase were measured in 32 women during the last 3 weeks of pregnancy and, in a further 39 women, during and after labor. The serum creatinine increased from 61.9 +/- 0.9 to 69.8 +/- 1.8 mumol/l (mean +/- SEM) (P less than 0.05) in the third stage of labor and returned to normal by 72 h after delivery. The muscle creatine phosphokinase increased from 54 +/- 7 to 77 +/- 9.9 units (P less than 0.05) during the third stage and remained high (87 +/- 13.3 units) 72 h later. We conclude that these changes are due to muscle contraction and injury during delivery.
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PMID:The rise of serum creatinine levels during labor. 189 22

We have utilized specific, irreversible inhibitors of cysteine proteinases to examine the role of renal cathepsin B and cathepsin L in the proteinuria which occurs in an experimental model of human glomerular disease. Administration of trans-epoxysuccinyl-L-leucylamido-(3-methyl)butane (Ep475) a specific, irreversible inhibitor of cysteine proteinases, including cathepsins B and L, significantly reduced proteinuria in rats with experimentally induced, neutrophil-independent, anti-GBM antibody disease (controls: 10 +/- 1 mg/24 h, N = 8; anti-GBM antibody disease: 203 +/- 30 mg/24 h, N = 8; anti-GBM antibody disease + Ep475: 112 +/- 13 mg/24 h, mean +/- SEM, N = 6, P less than 0.05). There was a marked reduction in the activity of both cathepsin B and cathepsin L in renal cortices obtained from Ep475-treated rats compared to either saline-treated controls or rats treated with anti-GBM IgG only. Administration of Z-Phe-Tyr(O-t-butyl)CHN2, a specific, irreversible cysteine proteinase inhibitor with a high degree of selectivity toward cathepsin L, also caused a reduction in anti-GBM antibody-induced proteinuria (90 +/- 18 mg/24 h, N = 6, P less than 0.05). This reduction in proteinuria was accompanied by a marked decrease (-84%) in the specific activity of renal cortical cathepsin L in Z-Phe-Tyr(O-t-butyl)CHN2-treated rats. However, cathepsin B activity was unchanged. There was no significant change in the renal anti-GBM antibody uptake, plasma urea nitrogen, or plasma creatinine values in the Z-Phe-Tyr(O-t-butyl)CHN2-treated rats compared to rats treated with anti-GBM IgG only or saline-treated controls. These data document the ability of cysteine proteinase inhibitors to decrease the proteinuria which occurs in a neutrophil-independent model of human anti-GBM antibody disease and suggest an important role for cathepsin L in the pathophysiology of the proteinuria which occurs in this model.
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PMID:Evidence suggesting a role for cathepsin L in an experimental model of glomerulonephritis. 189 42

We have previously reported that during 2 months of strenuous exercise, untrained young women with documented ovulatory menstrual cycles developed secondary oligoamenorrhea and luteal phase defects. In this study we tested the hypothesis that such abnormalities arise by altered neuroendocrine regulation of menstrual hormone secretion and that weight loss potentiates such effects. We supply a detailed analysis of the 20 cycles, of the total of 53, in which luteal phase abnormalities occurred. During the control month and 2 exercise months, all subjects collected daily overnight urine samples for the determination of LH, FSH, estriol (E3), and free progesterone (P) excretion by RIAs and creatinine by chemical assay. The characteristics of the abnormal luteal phase cycles were determined by comparing the excreted hormone levels and patterns during the control cycles with those of exercise cycles. The area under the curve (AUC) for each hormone was calculated for the follicular and luteal phases of each cycle. Six of the exercise cycles exhibited an inadequate luteal phase. This was characterized by a mean integrated P area of 202.4 (SEM, -61.8) nmol/day.nmol creatinine, compared with 331.7 (SEM, 64.7) during the corresponding control cycles, over a period of 9 or more days after the urinary LH peak to the onset of menses. Fourteen of the exercise cycles exhibited a short luteal phase. This was characterized by a mean integrated P area of 75.9 (30.9) nmol/day.nmol creatinine, compared to 267 (61.7) during the corresponding control cycles, over a span of 8 days or less from the urinary LH peak to the onset of menses. Additional abnormalities occurred only in the short luteal phase cycles. These included an increase in the length and AUC for E3 of the follicular phase and a decrease in the AUC of LH during the luteal phase. We conclude that the initiation of strenuous endurance training in previously ovulating untrained women frequently leads to corpus luteum dysfunction associated with insufficient P secretion and, in the case of short luteal phase cycles, decreased luteal phase length. That exercise may alter the neuroendocrine system is suggested by a delay in the ovulatory LH peak in spite of increased E3 excretion; moreover, less LH is excreted during the luteal phase. The lack of positive feedback to estrogens and decreased LH secretion during the luteal phase could compromise corpus luteum function. In contrast, decreased free P excretion was the sole abnormality noted in menstrual cycles with an inadequate luteal phase.
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PMID:Exercise induces two types of human luteal dysfunction: confirmation by urinary free progesterone. 190 47


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