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)

Since their introduction in clinical practice in 1980, ACE inhibitors have been found useful in the treatment of hypertension and CHF. In hypertension, they are effective as monotherapy in 40% to 50% of the patients, and in combination with diuretics or calcium antagonists, they are effective in up to 85% of the patients. They are well tolerated, are not associated with depression, impotence, bronchospasm or metabolic derangements such as hypokalemia, hyperuricemia or hyperglycemia, and do not have adverse effects on the quality of life. As a result, they are preferred in hypertensive patients with CHF, left ventricular dysfunction, mental depression, older age, coronary artery disease, metabolic disorders, chronic destructive pulmonary disease, and peripheral vascular disease. In CHF they cause long-lasting hemodynamic and symptomatic improvement, improve exercise tolerance, and may lower mortality in certain patient subsets. Evolving new indications for ACE inhibitors include the diagnosis of renovascular hypertension, the prediction of surgical success, the treatment of scleroderma renal crisis, the reduction of proteinuria, renal protection, cardioprotection, the improvement of arterial compliance, in Bartter's syndrome and idiopathic edema, etc. ACE inhibitors are usually well tolerated but in some instances they may cause class-specific side effects such as hypotension; usually reversible azotemia or renal failure, especially in patients with renal artery stenosis or with CHF with low blood pressure; cough; angioedema; and hyperkalemia. Differences among ACE inhibitors are emerging and include chemical class (e.g., zinc ligand), biotransformation, potency, pharmacokinetics, prodrugs, tissue effects, additional pharmacologic properties, and drug interactions.
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PMID:Angiotensin converting enzyme inhibitors. II. Clinical use. 305 46

Persistent clinical proteinuria (i.e., urinary protein excretion greater than 0.5 g/24 h) is an ominous development in a person with diabetes. It eventually leads to a decline in the glomerular filtration rate and ultimately to end-stage renal failure or premature cardiovascular mortality. Progression of renal disease appears to be related to arterial blood pressure and protein intake and is primarily independent of the metabolic state. More sensitive immunoassays for detecting low concentrations of albumin in urine have led to recognition of subclinical increases in albumin excretion rates in nonclinically proteinuric diabetic patients, a phenomenon named microalbuminuria. Studies have shown that patients with microalbuminuria have a significantly increased risk for clinical proteinuria and cardiovascular mortality. Microalbuminuria is rarely found during the first 5 yr of a patient's diabetes, suggesting that it is a sign of early glomerular damage rather than a marker for susceptibility to it. In patients with non-insulin-dependent diabetes mellitus (NIDDM), an association has been found between microalbuminuria and coronary heart disease, but this relationship needs further investigation. In patients with insulin-dependent diabetes mellitus (IDDM), this subclinical form of proteinuria is associated with poor metabolic control and, more important, with marginal elevation of blood pressure. Correction of hyperglycemia by intensified insulin treatment might arrest progression to persistent clinical proteinuria; moreover, restricted protein intake and lowering of blood pressure have been shown to reduce the albumin excretion rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Etiology and prognostic significance of albuminuria in diabetes. 307 75

Table III compares metabolic and morphologic characteristics of different species of control and KK mice. The C57BL/6J demonstrates no significant metabolic, clinical or histologic abnormalities. Our two highly inbred Swiss albino groups I and II also do not show significant glomerular lesions, although we found striking intolerance to glucose, hyperinsulinism, and obesity among them. Thus a genetic predisposition may be necessary in addition to various environmental factors to produce microangiopathy in KK mice. The yellow AY mouse is included in this table, since it is strikingly hyperinsulinemic and obese without concomitant vasculopathy such as the other mentioned control strains have. In conclusion, the KK mice develop chemical diabetes preceded by a stage of prediabetes and also demonstrate renal, retinal and neurologic complications similar to those seen in human diabetes. Of particular interest is the development of mild to moderate glomerulosclerosis in the prediabetic stage; with progression to severe glomerulosclerosis and attendant proteinuria later in life. With proper back-crossing, both hyperglycemia and glomerulosclerosis can be transmitted to normal control mice, suggesting that a specific genetic background is necessary for the development of diabetes and diabetic-like microangiopathy. We therefore suggest that the KK mouse serves as an ideal genetic animal for the study of non-insulin-dependent diabetes mellitus and its complications for rational prevention and therapy.
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PMID:Hereditary diabetes in the KK mouse: an overview. 307 69

Proteinuria was diminished by concomitant oral administration of sorbinil, an aldose reductase inhibitor to streptozotocin-induced diabetic rats. Animals were placed in one of three groups: control, diabetic, sorbinil-treated diabetic. For a period of 10 weeks, 24-hour urine samples were analyzed weekly for volume, glucose, ketone, total protein (Pesce-Strande) and individual protein components having molecular weights between 15,000 and 120,000 daltons. The latter were examined by polyacrylamide gel electrophoresis and quantitated by laser densitometric analysis. Results indicated that controls excreted albumin (68,000 daltons) and low-molecular weight proteins between 15,000 and 20,000 daltons. Throughout the 10-week period of diabetes, there was a 7- to 12-fold increase in total urinary protein excreted in 24 h. Diabetic-induced proteinuria primarily resulted from excretion of newly detected proteins having molecular weights of 30,000-100,000 daltons and an increase amount of albumin. Sorbinil treatment prevented approximately 70% of the increase in total protein excretion despite persistent hyperglycemia, glycosuria and ketonuria. Laser densitometric analysis indicated that the aldose reductase inhibitor decreased by 70% the excretion of newly detected proteins and albumin while maintaining the 15,000- to 20,000-dalton proteins. These results suggest that the polyol pathway is implicated in diabetic-induced proteinuria and inhibition of aldose reductase may represent a therapeutic approach for management of diabetic nephropathy.
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PMID:Diminished proteinuria in diabetes mellitus by sorbinil, an aldose reductase inhibitor. 308 Jul 63

Sorbinil, an aldose reductase inhibitor, was examined as a therapeutic agent to arrest and/or reverse proteinuria in 'type 1' insulin-dependent BB rats having spontaneous diabetes mellitus. Prior to sorbinil treatment, diabetic rats exhibited hyperglycemia and increased urinary excretion of urobilinogen, glucose and protein. To assess proteinuria, 24-hour urine samples were analyzed for both total protein and individual components between 30,000 and 100,000 daltons. Daily oral administration of sorbinil (20 mg/kg body weight) was initiated and the aforementioned parameters reevaluated after 1, 2 and 4 months. Results indicated that after 1 month of sorbinil treatment, urobilinogen was normalized in all diabetic BB rats (n = 12), whereas urinary protein excretion was either diminished (67%) or remained constant (16%), despite persistence of hyperglycemia and glycosuria. These therapeutic effects were sustained after 2 months of sorbinil treatment. After 4 months, protein excretion was normalized (6.56 +/- 3.34 mg/24 h), despite persistence of hyperglycemia and glycosuria (n = 12); in marked contrast, 6 untreated rats continued to exhibit proteinuria (17.76 +/- 2.59 mg/day). Sorbinil diminished albumin and a series of urinary proteins between 30,000 and 100,000 daltons, suggesting that sorbinil may represent a therapeutic approach to manage diabetic nephropathy as indicated by diminution of proteinuria.
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PMID:Reversal of proteinuria by sorbinil, an aldose reductase inhibitor in spontaneously diabetic (BB) rats. 312 36

Clinical risk factors for nephropathy were assessed in a population-based study of Rochester, Minnesota, residents with diabetes mellitus initially diagnosed between 1945 and 1969 (incidence cohort). The 1031 Rochester residents with non-insulin-dependent diabetes mellitus (NIDDM) were followed through their complete medical records in the community to 1 January 1982. The prevalence of persistent proteinuria was 8.2% at the diagnosis of NIDDM. Among those initially free of persistent proteinuria, the subsequent incidence was 15.3/1000 person-yr. Twenty years after the diagnosis of diabetes, the cumulative incidence of persistent proteinuria was 24.6%. A proportional hazards model identified the following risk factors for persistent proteinuria in NIDDM: elevated initial fasting blood glucose (P less than .01); older age at onset of diabetes (P less than .01); male gender (P = .05); and presence of macrovascular disease (P = .05), diabetic retinopathy (P = .05), or glycosuria (P = .07) at the diagnosis of diabetes. Separate analyses controlling for attained age indicated no association between duration of NIDDM and the incidence of persistent proteinuria. Stratified analysis of the two most significant risk factors (fasting blood glucose and age) indicated that hyperglycemia was a stronger risk factor for proteinuria in younger diabetic subjects, perhaps because of a competing risk of death in the elderly diabetic patient. In contrast to a recently described decreasing secular trend of proteinuria in Danish insulin-dependent diabetes mellitus patients, there was no decrease over the past 40 yr in proteinuria risk in this NIDDM incidence cohort.
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PMID:Epidemiology of persistent proteinuria in type II diabetes mellitus. Population-based study in Rochester, Minnesota. 337 84

Glycosuria, hyperglycemia, and nephrotic-range proteinuria developed in a 68-year-old patient after clonidine was added to a stable antihypertensive regimen, which included metoprolol, of three years' duration. He later became glucose-intolerant with fasting hyperglycemia. Clonidine has been reported to transiently impair glucose tolerance. Persistent diabetes in a previously normoglycemic patient following clonidine has not been reported, and it supports the possibility that clonidine and metoprolol may have additive effects in suppressing endogenous insulin secretion.
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PMID:Nephrotic-range proteinuria and hyperglycemia associated with clonidine therapy. 351 63

To evaluate the efficacy of conventional diabetes care in a rural area, metabolic control and the presence of late complications were studied in 622 diabetic patients treated by general practitioners beyond the reach of diabetic centers. Seventy-three (12%) of the patients were classified as type I diabetics (age, 38.0 +/- 16.1 yr; duration of diabetes, 12.8 +/- 9.3 yr) and 549 as type II diabetics (age, 67.0 +/- 10.8 yr; duration of diabetes, 7.3 +/- 5.8 yr). Fifty-eight percent of type I diabetic patients administered insulin once daily and 42% twice daily, whereas most (83%) type II diabetics on insulin received only one insulin injection per day. Treatment of type II diabetic patients consisted of sulfonylureas (58%), diet alone (22%), insulin (18%), and biguanides or a combination of sulfonylurea with biguanides (2%). Poor therapeutic efficacy was observed in all patients, and postprandial hyperglycemia (blood glucose greater than 160 mg/dl) was predominant both in type I diabetics (86%) and in type II diabetics on insulin (80%) as well as off insulin (55%). HbA1c above normal (greater than 5.8%) was seen in 96% of type I and in 90 and 73% of type II diabetics with or without insulin therapy, respectively. Accompanying glucosuria was present in type I (73%) and in type II diabetics (on insulin, 71%; off insulin, 33%). Mean prevalence of late diabetic complications was greatest for insulin-treated patients (type I, type II with, and type II without insulin treatment: retinopathy, 41, 56, 22%; proteinuria, 13, 14, 3%; peripheral neuropathy, 21, 51, 12%), whereas macroangiopathy (16, 53, 31%) predominated in type II diabetic patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diabetes care in rural area: clinical and metabolic evaluation. 353 76

A 2-month-old, well developed, healthy boy, weighing 5.55 kg, was fed 200 ml of bottle-milk containing 65 ml of sake. So-called kanzamashi (sake boiled in the evening and remaining in a bottle overnight,) was mistaken for yuzamashi (water boiled and left to cool), and used to prepare a 15% formula milk. About 10 minutes later, the baby became flushed, began to breath hard, and lose consciousness, and an alcoholic odor was noticed. He was brought to our clinic, where gastric lavage and parenteral fluid therapy were started. On admission, his main physical signs were, whole body had become red, unconsciousness, alcoholic odor, tachycardia and tachypnea, without low body temperature, while his remarked laboratory findings were metabolic acidosis, hyperglycemia, and high A/G ratio. Moreover, a transient proteinuria, alternately followed by a transient glycosuria, appeared within the course. About 10 hours later, he showed an obvious improvement in both physical and laboratory findings. As an explanation of these changes in his condition due to alcohol ingestion, we speculated that a metabolic acidosis with hyperglycemia caused the disturbed reabsorption in his renal tubulus, which revealed alternating proteinuria and glycosuria.
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PMID:Acute alcohol intoxication in a two-month-old baby. 357 10

Muscle capillary basement membrane width is a sensitive marker for the presence of diabetic microangiopathy. Studies have indicated that genetic factors and alterations in glucose metabolism influence muscle capillary basement membrane width. To define the role of these factors we have measured muscle capillary basement membrane thickness in controls, insulin dependent diabetics, and individuals with diabetes secondary to the ingestion of Vacor, a rat poison, which results in hyperglycemia. Hemoglobin A1 concentrations were increased in both diabetic groups, but hemoglobin A1 levels and the duration of diabetes were similar in the two diabetic groups. The muscle capillary basement membrane width was increased to a similar extent in the insulin-dependent diabetics (control, 1,781 +/- 46 vs. IDD, 2,287 +/- 144 A, P less than 0.001) and in the Vacor diabetic group (2,320 +/- 149 A, P less than 0.001). In the insulin-dependent diabetic group, 63% of the patients had a muscle capillary basement membrane width greater than two standard deviations above the mean of the controls, while in the Vacor diabetic group this figure was 56%. Despite the relatively short duration of diabetes (6.2 +/- 0.3 yr), 44% of the Vacor diabetic patients had retinopathy and 28% had proteinuria. The present study provides strong evidence that even in the absence of genetic diabetes mellitus, hyperglycemia or some other abnormality related to insulin lack can cause microvascular changes.
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PMID:Muscle capillary basement membrane width in patients with vacor-induced diabetes mellitus. 372 72


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