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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal histamine concentration, total histamine and protein contents were measured in rats made diabetic via iv streptozotocin injection and held for 13 weeks following diagnosis of diabetes. Insulin (7 U/day) or alpha-hydrazinohistidine (alpha-HH, 25 mg/kg/day) or both drugs were administered to diabetic subgroups the last 2 weeks of the holding period. Untreated diabetics developed significant increases of renal histamine concentration and total histamine content, up 45 and 46%, respectively. Drug interventions reduced the diabetic increases of histamine concentration and content (in order) as follows: diabetic-insulin, down 7 and 8%; diabetic-alpha-HH down 25 and 26%; diabetic-insulin + alpha-HH, down 35 and 36%. Renal tissue protein content was unchanged and qualitative proteinuria was present in all diabetic subgroups. The data indicate that in experimental diabetes there is an increase of the renal inducible histamine pool which is partially reduced by insulin and/or alpha-HH treatments. In view of the long-recognized actions of histamine upon microvascular permeability, elevated renal histamine may be one pathophysiological mediator of the diabetic functional renal microangiopathy manifest as proteinuria.
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PMID:Renal histamine increases in the streptozotocin-diabetic rat. 351 88

The decreasing relative mortality among type I (insulin-dependent) diabetic patients during the last 50 years might be related to the incidence of clinical diabetic nephropathy. We therefore followed 2890 type I diabetic patients (1607 males and 1283 females) diagnosed between 1933 and 1972 and before the age of 31, from admission to death, emigration, or January 1, 1984. All patients had been admitted to the Steno Memorial Hospital. Information on development of proteinuria was obtained in 2658 patients (92%). Five hundred twenty-five patients developed proteinuria due to diabetes and 49 developed nondiabetic proteinuria. When comparing patients diagnosed between 1933 and 1942 with those diagnosed between 1953 and 1962, the incidence of proteinuria decreased by 30% (P less than .03). This might explain the decrease of relative mortality in type I diabetic patients. The incidence decreased with increasing age at onset but was always highest in males. Insulin dose (U/kg) and diabetes duration at admission did not influence the incidence of proteinuria. The incidence peaked after 15-17 yr of diabetes duration independent of sex, age at diagnosis, or calendar year of diagnosis. However, the majority of patients did not develop proteinuria during 40 yr of diabetes. This suggests individual renal susceptibility to the deleterious effect of hyperglycemia.
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PMID:Declining incidence of persistent proteinuria in type I (insulin-dependent) diabetic patients in Denmark. 380 32

To clarify the epidemiological and clinical features of blindness due to diabetic retinopathy, 21 patients were studied. Blind diabetics seen at our clinic numbered 2, 3, 4 and 12 in 1965-1969, 1970-1974, 1975-1979 and 1980-1981 respectively. The ratio of males to females was about 4:3. Patients whose onset was in the 10-19, 20-29, 30-39, 40-49 and 50-59 year age group numbered 4, 5, 6, 3 and 3 respectively. No difference was seen in the duration of the disease between patients whose onset was below and patients whose onset was above 40 years of age. Most of the blind diabetics (81.8%) were treated with insulin and hypoglycemic symptoms had occurred on several occasions in 14 cases. Hypertension was a complication in 10 (45%) and orthostatic hypotension in 7 cases (31.8%). Patellar tendon reflex disappeared in 15 cases (68.2%). Proteinuria was strongly positive in 11 cases (52.4%). It was therefore concluded that the number of blind diabetics has been increasing in our clinic since 1975. Insulin therapy and the association of hypoglycemia were thought to be important precipitating factors of blindness in diabetics. The levels of plasma fibrinogen and soluble fibrin monomer complexes in blind diabetics were higher than those in diabetics without retinopathy.
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PMID:Epidemiological and clinical studies on blindness due to diabetic retinopathy. 668 May 12

We assayed plasma activities of beta-galactosidase, beta-hexosaminidase, alpha-fucosidase and alpha-galactosidase involved in degradation of the glycoprotein molecule in 110 insulin-dependent diabetics aged 3-1/2 to 19 years and compared them to a group of normal youngsters. We correlated the plasma enzyme activities with the duration, control and sequelae of insulin-dependent diabetes. Insulin-dependent diabetics had a significantly higher plasma activity of beta-hexosaminidase and alpha-mannosidase (p less than 0.01) and a significantly lower plasma activity of alpha-fucosidase and alpha-galactosidase (p less than 0.01). Of the 5 enzymes studied, only plasma beta-hexosaminidase correlated with fasting and postprandial blood sugar (p less than 0.01), cholesterol and triglycerides (p less than 0.05). Additionally, poor control of diabetes was also associated with a significantly higher plasma beta-hexosaminidase activity (p less than 0.01). Proteinuria or an abnormal Addis count suggestive of renal involvement was associated with various changes in plasma acidic hydrolases. These changes may be related to insulin deficiency rather than hyperglycemia and may be genetically determined.
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PMID:Plasma acidic glycohydrolases in insulin-dependent diabetes mellitus. 730 74

Previous studies have indicated that cephaloridine nephrotoxicity was reduced in diabetic rats. This study determined whether the reduction in toxicity was due to streptozotocin or the diabetic state. Male Fischer-344 rats were injected intraperitoneally with 35 mg/kg streptozotocin to induce diabetes. Insulin (5 U/day, subcutaneously) was begun within 72 h and continued for 10 days. Toxicity was quantitated 48 h after injection of cephaloridine (1500 mg/kg, i.p.) in normoglycemic (NC), diabetic (DC) and diabetic animals treated with insulin (DIC). Cephaloridine produced diuresis, glucosuria, proteinuria, elevated kidney weight and decreased renal cortical slice accumulation of organic ions in the NC group. Cephaloridine toxicity was reduced in the DC group since kidney weight, BUN level and renal cortical slice accumulation of organic anions were similar between treated and control animals. Cephaloridine treatment of the DIC group was associated with increased BUN levels, proteinuria and diminished renal cortical slice accumulation of organic cations. These results indicated that the diabetic state, and not streptozotocin, reduced cephaloridine nephrotoxicity.
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PMID:Cephaloridine nephrotoxicity in diabetic rats: modulation by insulin treatment. 762 67

We assessed the clinical characteristics of newly-diagnosed diabetic patients presenting to the Mulago Hospital Diabetic Clinic for the first time between 1 January 1993 and 10 August 1994. There were 252 patients: 117 men and 135 women. Mean age at onset of diabetes was 45 years (range 2-87 years) and peak incidence was at 40-49 years. Body mass index (BMI) was available in only 71 patients, of whom 53.5% (33.8% female, 19.7% male) were overweight (BMI > 25 in women, in > 27 men) and 11.3% (8.5% men, 2.8% women) were underweight (BMI < 20). Obesity was more marked in young women. Almost all patients presented with the classical symptoms of diabetes, and the majority were severely hyperglycaemic. A family history of diabetes was identified in 16%. Concurrent illnesses at diagnosis of diabetes were unusual. Sepsis was commonest (11.9%), followed by malaria (7.8%), tuberculosis (1.2%), AIDS (1.2%) and pancreatitis (0.8%). Peripheral neuropathy was present in 46.4% of patients, hypertension (BP > 150/100) in 27.3%, impotence in 22.2% of the men, proteinuria in 17.1%, ischaemic heart disease in 4.8%, foot ulcers in 4.0% and cataracts in 3.2%. Insulin was the most commonly prescribed treatment (52.8%); 31% of patients received oral hypoglycaemic agents, only 15.1% were managed on diet only, and 1.2% opted for herbal medicine.
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PMID:The presentation of newly-diagnosed diabetic patients in Uganda. 891 47

Although insulin resistance has been involved in the pathogenesis of essential hypertension in non-diabetic patients, few studies were performed regarding to the association between insulin resistance, hypertension and nephropathy in diabetes mellitus. We observed the changes of blood pressure and proteinuria for 7 years in normotensive 28 patients with non-insulin-dependent diabetes mellitus (NIDDM), following measurement of insulin sensitivity. Patients were over 40 years old and not obese, and fasting plasma glucose levels were less than 140 mg/dl. Insulin sensitivity was determined using glucose-clamp method or glucose, insulin, and somatostatin infusion method. In 28 subjects, 12 subjects developed hypertension and 16 subjects were remained normotensive. Insulin induced glucose clearance was significantly decreased in subjects developed hypertension (30 +/- 12 ml/kg/10 min) than in subjects remained normotensive (50 +/- 19 ml/kg/10 min). Furthermore, we found significantly higher incidence of proteinuria in patients developed hypertensive (7 out of 12 patient) than in patients remained normotensive (one out of 16 patients; p < 0.05). These results suggest that insulin resistance is involved in the etiology of hypertension in NIDDM patients, and that this derangement has an important role for the progression of diabetic nephropathy.
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PMID:Insulin resistance, hypertension and nephropathy. 924 Jul 60

Insulin resistance (IR) and secondary hyperinsulinaemia are major risk factors of atherosclerosis and probably also of related glomerulosclerosis. Angiotensin converting enzyme inhibitors (ACEI), while improving IR in essential hypertension, do not improve it in patients with chronic renal disease. Thus, the combination of ACEI and low protein diet was evaluated. Thirty-eight patients with various kidney diseases and mild to moderate impairment of kidney function were included in the study. Thirteen of them suffered from IR. Their dietary protein intake was decreased from > or = 1.0 g/kg/d to 0.6-0.7 g/kg/d. Moreover, they were treated by ACEI enalapril at dosages of 2-10 mg/d depending on the absence/presence and severity of hypertension. The patients were followed for 8 months. No clinically relevant kidney disease progression (KDP) was found. IR patients improved remarkably. IR was examined by the oral glucose tolerance test and glucose, insulin and C-peptide determinations. Their increased plasma triglyceride, VLDL concentrations and proteinuria decreased, HDL concentration increased. Acid-base balance and anaemia did not change. It is concluded that protein restriction in combination with ACEI treatment improve IR and the associated dyslipoproteinaemia and proteinuria.
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PMID:Dietary protein restriction in combination with angiotensin converting enzyme inhibitor improves insulin resistance in patients with chronic renal disease. 940 10

Insulin resistance and hyperinsulinemia are associated with essential hypertension. There is also evidence of hyperinsulinemia in women who developed hypertension in pregnancy (P). The present study examines whether chronic hyperinsulinemia in pregnant rats plays a role in the development of hypertension in pregnancy. A sustained-release insulin pellet was implanted subcutaneously in 15 Wistar rats (P-INS) 1 wk before and on day 7 of pregnancy; 14 control rats were sham-implanted (P-SHAM). Tail-cuff systolic BP (SBP), serum triglycerides, glucose, insulin, renal function, and urinary excretion of Na+ and of metabolites of nitric oxide were determined throughout pregnancy. Data were analyzed by ANOVA with basal body weight as covariate analysis of covariance. Results are expressed as the mean +/- SD. Body weight; water and food intake; urine volume; creatinine clearance; and level of proteinuria at the end of pregnancy were similar in both groups. The number of fetuses was 9 +/- 2.3 in P-INS versus 11 +/- 2.4 in pregnant control rats (P < 0.05). Before mating, SBP was similar, but at the end of pregnancy SBP was 110 +/- 18 mmHg in P-INS versus 85 +/- 12 mmHg in pregnant rats (P < 0.05). Serum triglycerides and Na+ were also higher in P-INS rats. The fractional excretion of Na+ was 3.1 +/- 1.0 versus 4.4 +/- 1.5, respectively (P < 0.01). The percent increase in nitric oxide metabolite excretion was 233 +/- 14 versus 370 +/- 17%, respectively (P < 0.01). Chronic hyperinsulinemia, without sugar supplementation, and hypertriglyceridemia may cause a decrease in the synthesis of nitric oxide in P-INS rats. The development of hypertension in these rats may be associated with an impaired vasodilatation, together with an increased renal sodium reabsorption.
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PMID:Chronic exogenous hyperinsulinemia in pregnancy: a rat model of pregnancy-induced hypertension. 944 81

The SHROB rat is a unique strain with genetic obesity, hypertriglyceridemia, hyperinsulinemia, renal disease with proteinuria, and genetically determined hypertension, characteristics paralleling human Syndrome X. The obese phenotype results from a single homozygous recessive trait, designated faK, and is allelic with the Zucker fatty trait (fa), but of distinct origin. The faK mutation is a premature stop codon in the extracellular domain of the leptin receptor, resulting in a natural receptor knockout. The SHROB are glucose intolerant compared to heterozygous or wild-type SHR, but retain fasting euglycemia even on a high sucrose diet, suggesting that diabetes requires polygenic interaction with additional modifier genes. Insulin-stimulated phosphorylation of tyrosine residues on the insulin receptor and on the associated docking protein IRS-1 are reduced in skeletal muscle and liver compared to SHR, due mainly to diminished expression of insulin receptor and IRS-1 proteins. Despite multiple metabolic derangements and severe insulin resistance, hypertension is not exacerbated in SHROB compared to SHR. Thus, insulin resistance and hypertension are independent in this model. Increased activity of the sympathetic nervous system may be a common factor leading by separate pathways to hypertension and to insulin resistance. We studied the chronic effects of sympathetic inhibition with moxonidine on glucose metabolism in SHROB. Moxonidine (8 mg/kg/day), a selective I1-imidazoline receptor agonist, not only reduced blood pressure but also ameliorated glucose intolerance. Moxonidine reduced fasting insulin by 47% and plasma free fatty acids by 30%. Moxonidine enhanced expression and insulin-stimulated phosphorylation of IRS-1 in skeletal muscle by 74 and 27%, respectively. Thus, central sympatholytic therapy not only counters hypertension but also insulin resistance, glucose tolerance, and hyperlipidemia in the SHROB model of Syndrome X.
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PMID:Molecular pathology in the obese spontaneous hypertensive Koletsky rat: a model of syndrome X. 1084 68


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