Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Plasma renin activity, response to saralasin and exchangeable sodium have been measured in 43 patients with early renal disease. 2. Blood pressure was directly proportional to plasma renin activity. However, mean plasma renin activity was lower in patients with renal disease than in normal controls. 3. Blood pressure fell in response to saralasin infusion in proportion to the pre-infusion plasma renin activity. 4. Exchangeable sodium in hypertensive patients with renal disease did not exceed that in normotensive patients in contrast to earlier reports. Discrepancies may arise from the difficulty in interpreting measured exchangeable sodium in relation to body build.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Sodium and renin in the hypertension of early renal disease. 28 72

1. Direct intra-arterial blood pressure (radial artery) has been compared with indirect blood pressures using a regular sized adult cuff and a thigh cuff, with a mercury sphygmomanometer, in 24 hypertensive patients aged 62--84 years, and in 16 hypertensive patients aged 29--59 years. 2. The patients were studied because they were suspected of having a false elevation of their indirect blood pressure, since they had diastolic pressures over 100 mmHg, without hypertensive retinopathy, cardiac hypertrophy, or nephropathy. 3. Indirect diastolic pressure was falsely elevated by 30 mmHg or more in 12 out of 24 of the subjects over age 60, and in four of the 16 of those under age 60. Pseudohypertension (indirect diastolic greater than 100 mmHg, direct diastolic greater than 90 mmHg) was present in 12 subjects over age 60 and 5 under age 60. 4. Errors in indirect measurement of blood pressure are a serious problem, particularly in the elderly. Direct intra-arterial measurement may be useful in the management of hypertension.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Pseudohypertension in the elderly. 28 97

1. Patients with end-stage renal disease and anephric patients underwent expansion and depletion of body fluids with salt and water. This resulted in four different sequential haemodynamic patterns: (i) no significant increase in blood pressure; (ii) increase in blood pressure associated with a rise in cardiac output and no effect on total peripheral resistance; (iii) increase in cardiac output followed by a rise in blood pressure and total peripheral resistance; (iv) increase in total peripheral resistance and blood pressure without significant changes in cardiac output. 2. It is concluded that an initial rise in cardiac output is not necessary to increase-blood pressure in either anephric man or patients with end-stage renaldisease.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The haemodynamic response to salt and water loading in patients with end-stage renal disease and anephric man. 107 13

1. The National Blood Pressure Study (NBPS) is a single blind trial designed to test the efficacy of active drug treatment in reducing complications from mild hypertension (mean diastolic pressure = 95-109 mmHg). 2. Between 1973 and 1975, four centres screened about 104 000 subjects aged 30-69 years, yielding an estimated prevalence of hypertension (greater than or equal to 95 mmHg diastolic) of 16% and of moderate-to-severe hypertension (greater than of equal to 110 mmHg diastolic) of 1-3%. 3. Some 4000 subjects selected for untreated uncomplicated mild hypertension were randomized to either active treatment (cholorothiazide +alpha-methyldopa and/or a beta-adrenoreceptor antagonist as required) or to matching placebos. 4. At 1 year mean pressures had fallen significantly below entry pressures in both groups but in the active group the fall was greater by a margin of 14-4+/-1-3 (SEM) mmHg systolic and 7-1+/-0-7 mmHg diastolic. At 1 year 5% of subjects in the placebo group had been placed on active treatment on the ethical grounds that pressure had exceeded the mild hypertension limit. 5. Trial end-points (death, morbidity from stroke, hypertensive heart and renal disease, and ischaemic heart disease) number 106 (nine deaths) thus far, of which ischaemic heart disease accounts for 71% and stroke 19%. 6. The duration of trial may need to be extended beyond the original estimate of 5 years.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Report on progress in the Australian National Blood Pressure Study (NBPS). 107 98

1. Healthy subjects, given a long-acting preparation of vasopressin intramuscularly, excreted a significantly less concentrated urine than when subjected to fluid deprivation for 28 h. 2. When fludrocortisone, a potent mineralocorticoid, was given in addition to vasopressin the urine was not significantly less concentrated than after fluid deprivation. 3. Oral urea-loading also enhanced the urine-concentrating power of vasopressin but its effect was less marked than that of fludrocortisone. Oral urea did not increase further the urine concentration achieved by combined fludrocortisone and vasopressin. 4. Renal concentrating power was assessed in fourteen patients with renal disease and impaired concentrating ability. Fludrocortisone significantly enhanced the urine concentration achieved by vasopressin alone and the resultant urine was not significantly less concentrated than that achieved by fluid deprivation. 5. The action of fludrocortisone in enhancing the urine-concentrating effect of vasopressin is similar to that of aldosterone and is probably due to the increased sequestration of solute in the renal medulla, caused by increased reabsorption of sodium chloride in the ascending limb of the loop of Henle. 6. In the clinical assessment of renal concentrating power, the combined use of fludrocortisone and vasopressin has potential advantages over established methods.
Clin Sci Mol Med 1975 Apr
PMID:Assessment of urine-concentrating ability in man: effect of fludrocortisone and urea in enhancing response to vasopressin. 112 20

In order to assess the potential role of the plasma membrane sodium-proton (Na+/H+) exchanger in the pathogenesis of diabetic nephropathy, we investigated 32 insulin dependent (type 1) diabetic patients and 21 control subjects. We tested the Na+/H+ exchange as the rate of amiloride sensitive and sodium dependent volume gain of platelets suspended in sodium propionate. Patients with diabetic nephropathy had significantly increased rates of Na+/H+ exchange (0.31 +/- 0.06 s-1 x 10(-2)) when compared to those without nephropathy (0.24 +/- 0.07, p less than 0.05) or to a control group (0.23 +/- 05, p less than 0.05). Nine patients who were classified as hypertensive had a highly significant increase in the Na+/H+ exchange rates when compared to 23 non-hypertensive diabetic patients: 0.33 +/- 0.04 versus 0.24 +/- 0.06 (p less than 0.001). There was no significant correlation between the Na+/H+ exchange rates and age, diabetes duration, glycated hemoglobin or fructosamine levels on the day of the test. In summary, the data presented here demonstrate an increase in the Na+/H+ exchange rate in insulin-dependent diabetic patients with nephropathy and hypertension.
Mol Cell Biochem 1992 Feb 12
PMID:Increased platelet sodium-proton exchange rates in insulin-dependent (type 1) diabetic patients with nephropathy and hypertension. 132 Jul 32

The Denys-Drash syndrome is characterised by a typical nephropathy, genital abnormalities and also predisposes to the development of Wilms' tumor. These patients eventually go into end stage renal failure. A candidate Wilms' tumor gene, WT1, from the 11p13 chromosome region has recently been cloned. We have analysed the DNA sequence in constitutional cells from eight patients and have shown heterozygous mutations in six of them. Four of the mutations were in exon 9, all resulting in missense mutations. Three were at nucleotide position 1180 resulting in an arg > trp amino acid change. The other was at position 1186 converting an asp > asn in the predicted resultant protein. One patient had a missense mutation in exon 8, converting an arg > his. A single base pair insertion at nucleotide position 821 in exon 6 resulted in the generation of a premature stop codon in the last patient. We were unable to find a mutation in one patient despite complete sequencing of the genomic sequence of the gene. The last patient carried a constitutional deletion of the 11p13 region and no additional mutation was found. There was no obvious correlation between the type of mutation and phenotypic expression. These results further demonstrate that the WT1 gene is important in both the development of the kidney and the genito-urinary system.
Hum Mol Genet 1992 Aug
PMID:Constitutional mutations in the WT1 gene in patients with Denys-Drash syndrome. 133 6

It is now well documented that some enteric bacteria which cause diarrhoeal and/or dysenteric disease produce, at high levels, one or more of a family of protein toxins referred to as Shiga toxin and Shiga-like toxins (SLTs; alternatively called verocytotoxins or VTs). Within the past few years, there have been considerable advancements made in our understanding of the biochemistry and molecular biology of Shiga toxin and SLTs. However, the precise role of the toxins in mediating colonic disease, as well as their contribution to the development of extra-intestinal sequelae (e.g. the haemolytic uraemic syndrome and neurological disorders), remain less clear. In this MicroReview, we will briefly summarize recent progress in Shiga toxin- and SLT-related research and present evidence supporting the concept that these toxins contribute to pathogenesis by directly damaging vascular endothelial cells, thereby disrupting the homeostatic properties of these cells. We will also discuss data which suggest that toxin-mediated damage in the kidney may not be limited to glomerular endothelial cells but may include tubular epithelial cells. Thus, the role of the toxins in renal disease may not be limited to the glomeruli, as was initially hypothesized when the association of infection with toxin-producing strains and the development of acute renal failure was established.
Mol Microbiol 1991 Aug
PMID:The pathogenic mechanisms of Shiga toxin and the Shiga-like toxins. 176 67

Although chronic progressive nephropathy and proteinuria are well-known to affect old laboratory rats, the occurrence of tubular metaplasia of Bowman's capsule (TM) in aging rats has received little attention. We report here that old (24-26 months) male, but not female Sprague-Dawley rats show a high incidence of TM which is significantly (P less than 0.01) correlated with the levels of glomerular sclerosis and intracellular deposits of iron in the tubular epithelium. The incidence of these changes was not correlated with serum testosterone levels, which showed a significant age-related reduction in males. The reported findings suggest that the aging male Sprague-Dawley rat is a useful animal model to investigate the pathogenesis of TM and related morphologic changes in hematuric humans.
Virchows Arch B Cell Pathol Incl Mol Pathol 1990
PMID:Sex-related incidence of tubular metaplasia in Bowman's capsule of aging rats. 197 35

Twenty-three nonobese KK mice with abnormal tolerance to glucose, hyperinsulinemia with insulin resistance and human diabetic-like nephropathy were treated with either saline (12 mice) or glipizide, an oral hypoglycemic compound, 1 mg/kg, (11 mice) from 120 to 360 days of age. These mice develop significant increases in mesangial volume and matrix by 40 days of age. Oral glucose tolerance (OGTT), glucosyltransferase and N-acetyl-beta-glucosaminidase (enzymes involved in synthesis and degradation of kidney glycoproteins, respectively) in the kidney and serum, 24-hr proteinuria, and light microscopy studies of the kidney were performed. Glipizide-treated mice improved their OGTT. There was no difference in body weight; however, a 16% decrease (P less than 0.05) in kidney weight was observed in glipizide-treated mice. Both enzymes were significantly increased in the kidneys of mice treated with glipizide. No difference in serum enzymes was found between the two groups of mice. About 58% of the saline-treated mice had moderate glomerulosclerosis. By contrast, only 27% of glipizide-treated mice had moderate glomerulosclerosis. Also, a significant decrease in proteinuria was found in glipizide-treated mice. These data suggest that glipizide improves glucose metabolism, decreases kidney size, prevents kidney glycoprotein and mesangial matrix accumulation, and reduces proteinuria in type II diabetic KK mice. This indicates that good glycemic control prevents further progression of established diabetic nephropathy in animals.
Exp Mol Pathol 1990 Oct
PMID:Diabetic microangiopathy in KK mice. VI. Effect of glycemic control on renal glycoprotein metabolism and established glomerulosclerosis. 214 55


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