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

The development of proliferative diabetic retinopathy was studied in three cohorts consisting of 292 patients with recent juvenile-onset, type I (insulin-dependent) diabetes who were followed 20-40 yr beginning in 1939, 1949, and 1959. The risk of this severe eye complication was almost nonexistent during the first 10 yr of diabetes, rose abruptly to its maximum level (approximately 30/100 person-years), and remained at that level for the next 25 yr. This pattern did not vary with sex, age at onset of diabetes, or level of glycemic control during the first 5 yr of diabetes. However, the risk of proliferative retinopathy was strongly related to the level of glycemic control during the several years preceding onset of this complication. This was a dose-dependent relationship, with patients in the highest quartile of the distribution of the index of frequency of hyperglycemia having a 10-fold higher risk than individuals in the lowest quartile. A virtually identical pattern was observed in patients who developed diabetes in 1959 as was observed in those who developed diabetes in 1949 or 1939. In contrast, diabetic nephropathy as evidenced by persistent proteinuria showed a lower incidence in the 1959 than in the 1939 cohort. In conclusion, these incidence data do not support the notion that the risk of proliferative retinopathy is mainly a function of duration of diabetes. Instead, the pattern of occurrence of this severe eye complication in type I diabetes suggests that the process leading to the development of proliferative retinopathy consists of two or more stages and that progression through each stage may be governed by different factors.
 ...
PMID:Risk of proliferative diabetic retinopathy in juvenile-onset type I diabetes: a 40-yr follow-up study. 376 14

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.
 ...
PMID:Declining incidence of persistent proteinuria in type I (insulin-dependent) diabetic patients in Denmark. 380 32

The effect of prolonged restoration of near-normoglycemia on the progression of diabetic nephropathy was evaluated in a controlled study in which 10 insulin-dependent (type 1) diabetic patients with clinical proteinuria were randomized to continue with conventional insulin treatment (CIT) or to undertake more intensive diabetic therapy using continuous subcutaneous insulin infusion (CSII). The patients, mean age 33 +/- 8 yr, mean duration of diabetes 15 +/- 4 yr, were studied before and during 12 months of either CIT or CSII therapy. Glycemic control was assessed by means of mean blood glucose (MBG) +/- Standard deviation (SD), urinary glucose excretion and glycosylated hemoglobin, while renal function was assessed by albumin, IgG and beta-2-microglobulin urinary excretion rates, serum creatinine and creatinine clearance. Blood glucose level, urinary glucose excretion and glycosylated hemoglobin fell significantly in the CSII group, while no differences were found in the CIT group after the 12 months observation period. Both groups showed a deterioration in all indices of renal function, as illustrated by an increase of protein excretion rates and of serum creatinine, and by a decline in creatinine clearance. Comparison of the rate of increase of urinary albumin and IgG excretion and of serum creatinine and of the rate of fall in creatinine clearance between CIT and CSII groups demonstrated that the rate of progression of diabetic nephropathy may be slowed by correction of hyperglycemia. Our study, with due reservations because of the small number of examined patients and differences in kidney function at the beginning of the trial shows that intensive diabetic care may play a role in the proteinuric stage of diabetes in slowing further destruction of residual glomerular structure and in delaying end stage renal failure.
 ...
PMID:Effect of long-term near-normoglycemia on the progression of diabetic nephropathy. 388 4

Approximately 40-45% of insulin-dependent diabetic (IDD) patients will develop, with time, clinical proteinuria, a forerunner of certain renal failure. Before this, however, up to 45% of IDD patients excrete supranormal amounts of protein in the urine, though still undetectable by dipstix test. This microproteinuria appears to be glomerular in origin, consists mainly of albumin and IgG, and is associated with poor glycemic control and marginal elevation of arterial pressure. Glomerular hemodynamic disturbances, and loss of charge selectivity of the glomerular membrane, are probably responsible for this microproteinuria, which appears reversible by correction of hyperglycemia and raised blood pressure. Once the dipstix test becomes positive (i.e. total urinary protein excretion exceeds 0.5 g/24h) and blood pressure rises into the hypertensive range, glomerular filtration rate (GFR) falls relentlessly. By the time GFR is as low as 20 ml/min/1.73 m2, more IgG relative to albumin is being filtered, giving rise to a low selectivity proteinuria, a condition consistent with changes in the size selectivity properties of the glomerular filtre. Glycemic control does not affect the decline in GFR, although blood pressure control and low protein diet can slow it, presumably by altering the self-perpetuating hemodynamic disturbances that occur in surviving glomeruli. The recent demonstration that IDD patients with microalbuminuria in excess of 30 micrograms/min have approximately a 20-fold increase in risk of developing persistent detectable proteinuria has provided a link between these two phases of diabetic nephropathy. The reversibility of the early microalbuminuria heralds a real chance of preventing the later irreversible phase of end-stage renal failure.
 ...
PMID:Genesis and evolution of proteinuria in diabetes mellitus. 388 40

Events in the natural history of diabetic nephropathy (including the onset of persistent proteinuria and end-stage renal failure) were studied in a cohort of 292 patients with juvenile-onset type I diabetes who were followed for 20 to 40 years. The risk of persistent proteinuria increased rapidly between the fifth and 15th years of diabetes and declined thereafter. This pattern suggests that susceptibility to this complication was limited to a subset of patients and was exhausted over time. Patients with the most frequent severe hyperglycemia (the highest quartile) during the first 15 years of diabetes had a risk of persistent proteinuria that was four and a half times higher than that for those with the least frequent hyperglycemia (the lowest quartile). Patients whose diabetes was diagnosed in the 1930s had twice the risk of persistent proteinuria as those in whom the condition was diagnosed in later decades. Once persistent proteinuria appeared, progression to renal failure almost always followed. Half reached this stage within 10 years, and the interval for progression did not vary according to sex, frequency of hyperglycemia, or calendar year of diagnosis of diabetes. This period, however, was significantly shorter (eight versus 14 years) for patients whose diabetes was diagnosed after puberty than for those who were younger at onset. In conclusion, the development of diabetic nephropathy consists of at least two stages. The onset of proteinuria, although related to the level of exposure to hyperglycemia, appears to be influenced by genetic and/or environmental factors. The second stage, progression to renal failure, seems to be influenced by processes related to maturation or aging.
 ...
PMID:The changing natural history of nephropathy in type I diabetes. 399 59

Light and electron microscopic studies were performed on renal glomeruli of diabetic mutant and age-matched normal mice and correlated with alterations in urinary excretion. The glomeruli of young (prediabetic) mutants and their normal littermates were normal and identical. With increasing age, the glomeruli of normal control mice were characterized by mesangial prominence and increased thickness and nodular densities of the peripheral basal lamina. These alterations were also observed in the diabetic mutant mice but more frequently and to a greatly exaggerated degree. The diabetic mutants were polyuric and excreted a quantity of protein identified by agarose and inmunoelectrophoresis as a serum protein. The excretion of this protein preceded the recognition of the morphologic alterations and did not increase in magnitude with the progression of glomerular changes. This report challenges the theoretic concept of genetically controlled diabetic glomerular lesions and discusses possible relationships between the glomerular alterations, the presence of proteinuria and the presence of hyperglycemia.
 ...
PMID:Studies in the diabetic mutant mouse. VI. Evolution of glomerular lesions and associated proteinuria. 500 70

Diabetic nephropathy has evolved into the single most prevalent cause of uremia among patients sustained by the United States End Stage Renal Disease program. Clarification of the natural history of kidney involvement and insufficiency in Type I and II diabetes has improved substantially over the past 5 years. However, it remains a poorly understood and relatively underreported morbid entity. This report reviews the problem, then reconstructs the natural history of diabetic nephropathy by studying the course of 50 Type I and Type II uremic diabetics treated with hemodialysis at The Long Island College Hospital. It traces the various stages from hyperglycemia to proteinuria to renal failure, and then reports morbidity, including cardiac, eye, stroke, and amputation complications. A new paradox is herein reported--the unpredictable insulin requirement, including new insulin need for the first time once hemodialysis was begun, in 8 of 50 patients studied.
 ...
PMID:The natural history of diabetic nephropathy: unpredictable insulin requirements--a further clue. 636 68

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.
 ...
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

The levels of glycosylated hemoglobin (Hb AI), intermittent glycemia and glycosuria over 24 hr, Mw index, fasting serum cholesterol and triglycerides, and 24-hr proteinuria were determined in 20 healthy subjects and 88 diabetics representing different clinical types of diabetes mellitus. In each of the subjects all the tests were carried out on a single day. The other investigations included endogenous creatinine clearance, ECG and ophthalmoscopic examination of the eye-fundus. The mean Hb AI levels in the "A" control group (up to 40 yr of age) and in the "B" control group (41-60 yr) were mean +/- SD = 6.8 +/- 0.65% and mean +/- SD = 6.49 +/- 0.99% of the total hemoglobin concentration, respectively. A significant increase in Hb AI concentration was found in all the diabetic patients. The increase, independent of the subject's age, clinical type of diabetes and the therapy employed, was related to the degree of hyperglycemia. In Type I diabetes there was no positive correlation between Hb AI concentration on the one hand and fasting glycemia, the 24-hr profile of glycemia, glycosuria and Mw index on the other. The latter indices of diabetes mellitus control seem thus to differ in value and significance. In Type II diabetes, both newly-diagnosed and of long duration, treated with the sulfonylurea derivatives, a marked correlation was found between Hb AI level and fasting glycemia, the mean value of 8 glycemia determinations over 24-hr, Mw index and 24-hr glycosuria. In Type II diabetes treated with insulin a correlation was established between Hb AI and other findings, except fasting glycemia.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Glycosylated hemoglobin (Hb AI) as an indicator of therapy effects in different clinical types of diabetes. 664 47

Increased capillary permeability to large molecular weight plasma proteins is an early phenomenon in diabetes that affects the microvasculature of the kidney, eye, brain, and many other peripheral tissues such as skin and muscle. This widespread vascular leakiness is related to the metabolic disturbance of diabetes and associated changes in blood flow and intravascular pressure. Correction of hyperglycemia and increased blood flow reduces and often normalizes the excessive leakage. The relevance of increased small vessel permeability to eventual organ and tissue damage remains largely speculative. However, recent experimental evidence has suggested that certain levels of subclinical elevated urinary albumin excretion rate strongly predict the onset of Albustix-positive proteinuria, a certain precursor of renal failure. Hemodynamic factors in the genesis of diabetic microangiopathy are discussed, and a hypothetic sequence of events leading from increased capillary permeability to end stage organ or tissue failure is suggested.
 ...
PMID:Increased capillary permeability in diabetes mellitus and its relationship to microvascular angiopathy. 667 94


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>