Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growing male rats were fed dietary Pirimiphos-methyl at 0, 500, 1000 and 1500 ppm for 28 days and selected blood and urine constituents were measured at weekly intervals. Dietary intake of Pirimiphos-methyl induced an initial, transient hypoglycemia and a marked elevation in blood urea at all dosages. Though it did not produce any significant change in the urine output initially, marked oliguria was observed after 12 days of feeding. The alterations observed in urine constituents were: increased urea, proteinuria, transient increase in creatinine and significant increase in the excretion of glucuronic acid and ethereal sulfate at all intervals. However, since no pathological alterations were evident in the kidney, the anomalous urinary excretion of various body constituents might be due to the anticholinesterase action of the insecticide at the central nervous system.
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PMID:Toxicity of pirimiphos-methyl: II. Effect of dietary feeding on blood and urine constituents in albino rats. 338 34

Although kidney enlargement occurs in Type I glycogen storage disease, renal disease has not been considered a major problem. Death from renal failure in three patients known to us prompted a study of renal function in this disorder. Of the 38 patients with Type I glycogen storage disease under our care, the 18 children under 10 years old had normal renal function. Fourteen of the 20 older patients (13 to 47 years) had disturbed renal function, manifested by persistent proteinuria; many also had hypertension, hematuria, or altered creatinine clearance. Progressive renal insufficiency developed in 6 of these 14 patients, leading to three deaths from renal failure. At the onset of proteinuria, creatinine clearance was increased in seven patients (3.05 +/- 0.68 ml per second per 1.73 m2 of body-surface area; range, 2.47 to 4.13 [normal range, 1.33 to 2.33 ml per second per 1.73 m2]). Renal biopsies were performed in three patients after an average of 10 years of proteinuria. All three biopsies demonstrated focal segmental glomerulosclerosis in various stages of progression. Our data suggest that chronic renal disease is a frequent and potentially serious complication of Type I glycogen storage disease. In addition to treating hypoglycemia vigorously, physicians should monitor renal function carefully in patients with this disorder.
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PMID:Renal disease in type I glycogen storage disease. 342 4

Atenolol was compared with placebo in a randomised and double-blind prospective study of 120 women with mild to moderate pregnancy-associated hypertension who were also initially managed conventionally by bed rest. Atenolol given once daily significantly reduced blood-pressure, prevented proteinuria, and reduced the number of hospital admissions. Loss of blood-pressure control leading to withdrawal from the study was commoner among the placebo group, whose babies had a high morbidity. Respiratory distress syndrome occurred only in the placebo group. Intrauterine growth retardation, neonatal hypoglycaemia, and hyperbilirubinaemia occurred with the same frequency in the two groups. Neonatal bradycardia was more common after atenolol but the systolic blood-pressure of the babies was the same in both groups. There was no difference between the groups in maternal symptoms which could have been attributed to beta-blocker therapy. Thus atenolol is more effective than conventional obstetric management in this form of hypertension and does not adversely affect mother or baby.
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PMID:Placebo-controlled trial of atenolol in treatment of pregnancy-associated hypertension. 613 Nov 64

Hypertension in pregnancy has implications for both maternal and fetal welfare. Extrapolation from concepts of mechanisms operating in hypertension in general to pregnancy-related hypertension is not justified. In the latter, the major features are a hyper-adrenergic state, plasma volume reduction and an increased systemic resistance. A reduction in uteroplacental perfusion may result from or may activate the mechanisms that elevate blood pressure. Humoral factors (e.g. hormonal attenuation of vascular reactivity) and prostacyclin deficiency may be central to the disordered physiology. Treatment of hypertension in pregnancy should aim at avoiding the vascular damage due to blood pressure elevation but not cause a reduction in uteroplacental perfusion. Unlike earlier antihypertensive regimens using centrally acting sympatholytics, adrenergic neuron blockers or diuretics, regimens using beta-blockers or combinations of beta-blockers with alpha-blockers or vasodilating agents such as hydralazine permit effective blood pressure control, even in severe hypertension, and pregnancy can often proceed until term or until fetal maturity is secured. Adverse effects on the fetus (growth retardation, cardiorespiratory depression, hypoglycaemia, hyperbilirubinaemia) formerly attributed to beta-blockers are more likely related to poorly controlled hypertension. Specific benefits of maternal beta-adrenoceptor blockade are suggested by evidence for prevention of proteinuric deterioration and a decrease in the incidence and severity of respiratory distress in premature infants. Hypertension in pregnancy still presents a formidable therapeutic challenge and requires comprehensive management with close monitoring of fetal welfare. The presence or development of proteinuria in a hypertensive pregnant woman implies a major increase in risk to the fetus and warrants immediate admission to hospital for specialist management.
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PMID:Hypertension in pregnancy. Pathophysiology and management. 614 40

A 59-year-old Japanese farmer with asymptomatic fasting hypoglycemia and with exaggerated hypoglycemic episodes induced by insulin and oral hypoglycemic agent administered for his postprandial hyperglycemia was diagnosed as glycogen storage disease type I. This diagnosis was suggested by unresponsiveness of blood glucose level to glucagon and confirmed by 13% normal level of glucose 6-phosphatase activity in liver biopsy specimen and by the presence of PAS positive amylase digestable glycogen in liver specimen. This case was associated with an incomplete type of Fanconi syndrome characterized by hyperphosphaturic hypophosphatemia, partial aminoaciduria, mild proteinuria and hyperuricosuric normouricemia in spite of the lactic acidemia due to glycogen storage disease type I. The etiology for the absence of hypoglycemia and other typical manifestations of glycogen storage disease type I was studied. The glucose production from glycogen by lysosomal alpha 1,4-glucosidase especially at prolonged fasting and the presence of postprandial hyperglycemia by insulin deficiency are regarded as responsible for keeping this patient free from typical manifestations of glycogen storage disease type I.
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PMID:A case of glycogen storage disease type I associated with an incomplete type of Fanconi syndrome; the protective role of lysosomal alpha 1,4-glucosidase and insulin deficiency against hypoglycemia. 639 62

To investigate the quality of glycaemic control that is achievable in diabetic patients with persistent proteinuria and asymptomatic but declining renal function three matched groups of patients were studied. The first comprised diabetics with proteinuria receiving continuous subcutaneous insulin infusion; the second, diabetics without proteinuria receiving continuous subcutaneous insulin infusion; and the third, diabetics with proteinuria receiving conventional insulin treatment. Glycaemic control in patients receiving continuous subcutaneous insulin infusion was shown to be appreciably worse during the daytime in diabetics with proteinuria than in diabetics without proteinuria, although greatly superior to that in diabetics with proteinuria receiving conventional insulin treatment. The loss of glycaemic control in patients with proteinuria receiving continuous subcutaneous insulin infusion probably occurred as a response to daytime hypoglycaemia and a consequent reduction in the proportion of the total insulin dose given prandially. Difficulty in controlling blood glucose concentrations may be a factor in the failure of intensified insulin regimens to influence the progression of diabetic renal disease.
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PMID:Glycaemic control in diabetic nephropathy. 642 82

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

A portable pump, programmed to administer intermittent pulses of insulin subcutaneously, supplemented by premeal boluses, was used by 8 patients for periods up to 12 months. Two boys, 11 and 16 years of age, sought improved growth; four young adults age 19 to 26 years desired normalization of metabolism to forestall microvascular complications already manifest; a 14-year-old girl had been incapacitated by unstable diabetes and a 26-year-old woman had been unable to attain sufficient control to gain weight without developing hypoglycemia. Maximal possible control with conventional insulin administration was attempted prior to pump use and such control was measured by glycohemoglobin (HgbA1) percentage and urine and blood sugar levels during a 24-hour period and compared with control with pump use. All initially had marked reduction in 24-hour urine volume (mean 3.3 L +/- .4 SEM to 1.4 +/- 0.2), urine glucose (mean 198 g +/- 81 to 14 +/- 4) and glycemia (mean 258 mg/dl +/- 29 to 133 +/- 12). HgbA1% declined markedly in all but the 14-year-old girl over the first weeks and reached normal or near normal levels in three patients. Four patients continued to use the pump after 3.5 to 12 months because of improved sense of well being, weight control, and in one, marked reduction in proteinuria. Both boys had a doubling of growth pace. Four patients are no longer using the pump after 3 to 8 months because of inconvenience, manipulation with intermittent usage, intolerance of normoglycemia, or overzealous control attempts with dangerous hypoglycemia. Pump use may permit the attainment of levels of control previously not possible, but is extremely demanding for patients and health personnel and must remain an experimental method in carefully selected and monitored patients.
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PMID:Ambulatory diabetes management with pulsed subcutaneous insulin using a portable pump. 699 94

Optimal control of diabetes should achieve not only euglycemia and normal levels of glycosylated hemoglobin but also absence of the reversible concomitants of diabetes such as red cell rigidity, hyperlipidemia, increased capillary permeability, enlargement of the kidneys, proteinuria, etc. Unfortunately, in most patients consistent euglycemia cannot be assured even with two daily injections of insulin. However, self-measurement of blood glucose as a guide to insulin taken before each meal and at bedtime can, in selected patients, increase the frequency of normal glucose levels without undue hypoglycemia.
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PMID:Parameters of good control in diabetes mellitus. 699 74

To determine whether insulin-like growth factor I (IGF-I) affects kidney function in patients with end-stage chronic renal failure, we administered recombinant human IGF-I (rhIGF-I) (100 micrograms/kg body wt subcutaneously twice daily) to nine individuals with baseline inulin clearances below 21 ml/min/1.73 m2. Four patients were treated for four days (short-term treatment) and five for periods between 13 and 27 days (long-term treatment). Administration of rhIGF-I increased inulin clearance, p-aminohippurate (PAH) clearance and the percent tubular reabsorption of filtered phosphate, and decreased plasma creatinine, blood urea nitrogen (BUN) and plasma phosphate during short-term administration. Kidney volume was unchanged in patients receiving the growth factor. rhIGF-I did not cause weight gain, proteinuria or hypoglycemia. Inulin clearance was not increased significantly above baseline after 13 or 20 days of IGF-I administration. PAH clearance remained elevated after 13 days, but not after 20 days of IGF-I. Levels of total circulating IGF-I were elevated above basal levels during the entire course of long-term IGF-I administration. In contrast, levels of circulating IGF binding protein 3 (IGFBP3) declined over time. Side effects related to IGF-I forced discontinuation of its use in two of five patients undergoing long-term treatment, and side-effects possibly related to IGF-I prompted discontinuation of its use in two others. We conclude that rhIGF-I can enhance glomerular filtration rate and renal plasma flow when administered short-term to humans with end-stage chronic renal renal failure. Further studies will be required to define its efficacy and usefulness long-term.
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PMID:Effects of IGF-I on renal function in end-stage chronic renal failure. 793 38


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