Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The value of polypeptide analyses in the diagnoses of diabetic nephropathy. Early diagnostic signs are rapidly gaining importance in the prevention and care of diabetic complications. The aim of this paper was to review the clinical significance of measurements of the serum and urine levels of beta-2-microglobulin, microalbuminuria and the plasma and urine levels of beta-thromboglobulin. We would like to emphasize their possible role in monitoring and prediction of the chronic sequelae of diabetes mellitus.
 ...
PMID:[The value of polypeptide analysis (beta-2-microglobulin, microalbuminuria, beta-thromboglobulin) in the diagnosis of diabetic nephropathies]. 147 8

Plasma and urinary concentrations of different amino acids were investigated during diabetic ketoacidosis (DKA) and 12, 24, 72 hours after initiation of therapy. In DKA, plasma concentration of glutamic acid, aspartic acid, valine, leucine and isoleucine significantly increased while that of asparagine and glutamine decreased compared to levels in well-controlled diabetic patients. The urinary excretion of branched-chain amino acids, histidine, serine and threonine was elevated while those of glutamic acid, glutamine, glycine and taurine were reduced. Among the different amino acids, histidine excretion had the highest variability. A strong correlation was found between the urinary excretion of several amino acids and that of the beta-2-microglobulin characterizing tubular dysfunction. Changes in the excretion of different amino acids reflect the altered metabolic state and renal function due to DKA.
Diabetes Res Clin Pract 1991 May
PMID:Changes in plasma and urinary amino acid levels during diabetic ketoacidosis in children. 190 67

We studied the possible association of the low serum uric acid level with incipient diabetic nephropathy in non-insulin-dependent diabetes mellitus (NIDDM). Of 201 NIDDM patients without a diminished glomerular filtration rate, 66 patients (32.8%) showed moderate hypouricemia of less than the mean-1 SD of 201 nondiabetic controls. Thirteen (6.5%) showed marked hypouricemia of less than the mean-2 SD. Hypouricemic patients showed normal daily urinary urate excretion with a markedly elevated urate clearance/creatinine clearance ratio. Most were under poor glycemic control, and presented either negative or intermittent clinical proteinuria. However, neither poor glycemic control, nor the presence of proteinuria or retinopathy alone significantly affected the serum uric acid level of the whole diabetic population. The glomerular filtration rate was determined in comparable groups of diabetic patients with hypouricemia and nonhypouricemic diabetic controls. The hypouricemic group showed a significantly higher endogenous creatinine clearance and lower serum beta-2-microglobulin levels than the nonhypouricemic group. These findings suggest that the hypouricemic group had a higher glomerular filtration rate. Long-term observation of up to 12 years of the above patients revealed that, in most patients, persistent hypouricemia was observed prior to the initial appearance of intermittent proteinuria. We hypothesize that glomerular hyperfiltration also occurs in NIDDM and that it lowers the serum uric acid by increasing the renal clearance of urate. Hypouricemia may also predict the future progression of incipient nephropathy in NIDDM.
 ...
PMID:Diabetic hypouricemia as an indicator of clinical nephropathy. 219 Apr 67

We examined the correlation between urinary GH, urinary albumin, and beta-2-microglobulin excretion to determine how the excretion of GH relates to markers of renal glomerular and tubular function. Urinary albumin and GH excretion was determined in timed daytime and nighttime urine collections obtained from both subjects with diabetes mellitus and subjects with short stature. For subjects with diabetes, urinary GH excretion rate correlated highly with urinary albumin concentration and excretion rate in both the range of 0 to 1.6 g/L (r = 0.75), P less than 0.001) and in the microalbuminuria range, 0 to 0.4 g/L (r = 0.53, P less than 0.001). Changes in GH and albumin excretion occurred in parallel in 71% of the subjects with diabetes and elevated albumin excretion. The mean GH excretion rate was higher in the group with elevated albumin excretion rate (AER) during both day and night compared to the group with microalbuminuria during the day and normal AER at night. For subjects with short stature, the mean albumin excretion rate was 0.7 +/- 1.3 micrograms/min (range 0.05-8.3 micrograms/min) using a sensitive enzyme-linked immunosorbent assay to measure albumin concentration. The correlation of GH and albumin excretion rates for the subjects with short stature was not statistically significant (r = 0.14, P less than 0.5). About half of the subjects with diabetes and elevated AER (greater than 10 micrograms/min) had a GH excretion rate within the range observed in subjects with short stature. The GH and albumin excretion rate were not correlated in this group. There was a positive correlation of both albumin and GH excretion rate with age in the subjects with diabetes. Urinary GH and beta-2-microglobulin excretion rates were determined in a larger group of subjects with diabetes and a separate group with short stature. Urinary GH and beta-2-microglobulin excretion were correlated both in subjects with diabetes (r = 0.46, P less than 0.001) and with short stature (r = 0.64, P less than 0.001). The association was present in urine collected either during the day or night. The mean GH excretion rate of the group with diabetes was greater than the group with short stature. In conclusion, there was an association of urinary GH and albumin excretion rate in subjects with abnormal glomerular function as indicated by elevated albumin excretion rate. An association of urinary GH and beta-2-microglobulin excretion was observed in subjects with normal tubular function.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Correlation of urinary albumin and beta-2-microglobulin and growth hormone excretion in patients with diabetes mellitus and short stature. 220 97

In 68 type I diabetics without permanent proteinuria, mean age 28 +/- 9 years, where diabetes was detected at the age of 14 +/- 7 years and persists for 14 +/- 8 years the urinary excretion of albumin and beta-2-microglobulin was assessed. The results were evaluated in relation to the persistence of diabetes, the blood pressure reading, family-history of diabetes and type of insulin therapy. In addition to microalbuminuria in 29% of the subjects which is a manifestation of glomerular damage, the authors detected in 58% elevated beta-2-microglobulin excretion indicating early changes of the proximal tubule. There was a relationship between microalbuminuria and "relative hypertension" which enhances albumin excretion and increases the risk of diabetic nephropathy. The relationship between microalbuminuria and a positive family-history of diabetes supports the hypothesis of a genetic background for the possible development of nephropathy. There was also a relationship with the duration of diabetes and the favourable effect of prolonged intensive insulin treatment. The clinical impact of beta-2-microglobulinuria in the diagnosis of the incipient stage of diabetic nephropathy must be tested in future investigations.
 ...
PMID:[Early diagnosis of nephropathy in type I diabetics]. 224 68

The nature of microproteinuria in the early years of insulin-dependent diabetes was investigated in a cross sectional study of 80 children with insulin-dependent diabetes and 40 normal children. Urinary excretion of three low molecular weight proteins: alpha-1-microglobulin, beta-2-microglobulin and kappa light chains was used as an index of proximal renal tubular function. The first urine samples of the morning were collected and excretion of proteins measured was expressed as ratio of protein to creatinine. There was a strong correlation between excretion of alpha-1-microglobulin and chi light chains and their excretion was significantly higher in diabetic children indicating decreased proximal tubular reabsorbtion. The excretion of beta-2-microglobulin was found to be an unsatisfactory index of proximal tubular function. Urinary albumin excretion was not significantly raised in diabetic children and did not correlate with urinary alpha-1-microglobulin or chi light chain excretion. Glycaemic control might influence proximal tubular function as both urinary glucose concentration and glycosylated haemoglobin showed correlations with urinary alpha-1-microglobulin excretion and with urinary chi light chain excretion.
 ...
PMID:Tubular dysfunction and microalbuminuria in insulin dependent diabetes. 245 77

There is evidence that increased excretion of urinary enzymes and low-molecular mass proteins indicate impaired tubular function. The excretion of N-acetyl-beta-D-glucosaminidase (NAG), lysozyme, and ribonuclease in Type I diabetic patients with (n = 19) and without (n = 17) persistent proteinuria (urinary protein excretion greater than 0.5 g/day) was investigated and compared with this excretion in 30 weight- and gender-matched nondiabetic subjects without renal disease. Urinary NAG excretion was significantly higher in diabetic patients with and without persistent proteinuria (1.16 +/- 0.09 and 3.19 +/- 1.2 Umol/L creatinine, respectively) compared to controls (0.37 +/- 0.03 Umol/L creatinine p less than 0.01). In addition, the urinary excretion of lysozyme and ribonuclease was significantly increased in diabetic patients. Urinary NAG was found to correlate positively with albuminuria and proteinuria (r = 0.95 and 0.93, respectively), as well as with ribonuclease and lysozyme (r = 0.93 and 0.60; p less than 0.01) in patients with persistent proteinuria. Furthermore, NAG excretion was significantly related to the duration of diabetes (r = 0.36; p less than 0.05). No relationship existed between urinary NAG and serum creatinine, beta-2-microglobulin, and degree of metabolic control (HbA7). The lysozyme excretion, but not NAG excretion, was significantly related to hypertension in patients with clinical proteinuria. In conclusion, our results suggest a relationship between the development of tubular dysfunction and the impairment of glomerular function in diabetic nephropathy. An increased excretion of NAG and low-molecular mass proteins may indicate early nephropathy
 ...
PMID:Further evidence for tubular dysfunction in insulin dependent diabetes. 252 61

The serum and urine level of beta-2-microglobulin was examined by the authors in different stages of nephropathy of 250 patients suffering from diabetes mellitus (I type 178 pts, II type 72 pts). Beta-2-microglobulin values measured in diabetic patients without renal microangiopathy did not show any difference compared with that of the controls. In patients with freshly discovered diabetes mellitus significantly decreased beta-2-microglobulin levels were found, probably due to the increased glomerular filtration rate. Increasing beta-2-microglobulin values indicating an early glomerular lesion--were observed in incipient diabetic nephropathy. These values were significantly higher compared with that of healthy individuals and diabetic patients without renal microangiopathy. In the IV stage of disease the serum and urine beta-2-microglobulin levels were equally found to be elevated, indicating an impaired function of proximal tubuli beside the vascular lesions. The most expressed beta-2-microglobulin value elevations were observed in the stage of nephropathy. The authors emphasize the importance of determination and common evaluation of 24 hours protein excretion and serum urine beta-2-microglobulin values the earliest diagnosis of incipient renal lesion. According to their results, the introduction of this method may be very useful for early indication and follow-up of specific renal complications in diabetes mellitus patients.
 ...
PMID:[Possibility of early diagnosis of diabetic nephropathies]. 264 49

We carried out sonographic examination of 160 type I diabetics measuring the renal volume, the parenchyma/renal pelvis index and the brightness of the parenchyma. Creatinine and beta-2-microglobulin in the serum, creatinine clearance and albumin excretion by urine were determined as functional parameters. In contrast to existing results, we were unable to find significant changes in kidney size or function in newly diagnosed diabetics (duration of diabetes up to 6 months). Both the parenchyma/renal pelvis index and the kidney parenchyma were unchanged compared to control persons of the same age. It was only if diabetes lasted from 6 months to 5 years, that the renal volume was 19% larger (192 +/- 37 cm3/1.73 m2) than that of recently diagnosed patients (p less than 0.01). The index had increased by 15%, whereas the creatinine clearance had increased by 18% to 121 +/- 27 ml/min as a result of increased perfusion. The renal volume decreased continuously over a five-year period of duration of diabetes. Initially, microalbuminuria became manifest, followed some time later by a decrease in creatinine clearance and a corresponding increase in creatinine and beta-2-microglobulin in serum. No change in parenchyma brightness was noted. Diabetics with moderate renal insufficiency (creatinine 1.2 to 2 mg/dl) compared to diabetics without insufficiency developed larger kidneys (207 cm3/1.73 m2; p less than 0.01). Only in case of severe insufficiency (creatinine greater than 2 mg/dl) did the kidneys did shrink significantly (121 cm3/1,73 m2, n = 8, p less than 0.01). The temporary enlargement of the kidneys could be a prognostically unfavourable sign pointing towards a developing diabetic nephropathy.
 ...
PMID:[Sonographic changes in the size of the kidneys in type I diabetes as a method of early detection of diabetic nephropathy]. 307 Jul 48

Renal Kallikrein, an enzyme of the distal tubule acting through kinin liberation, may participate to the control of renal circulation and blood pressure. To study if an impairment of its secretion may exist in diabetics, a cross-sectional study was carried out on 40 non-hypertensive and 29 hypertensive diabetics, compared to 30-age related controls. Urinary Kallikrein Activity (UKA) was measured by its kininogenase activity with and without trypsin preincubation. Compared to UKA in controls (86 +/- 9 micrograms lysyl-bradykinin [LBK] produced per minute of incubation), UKA was significantly reduced either in non-hypertensive diabetics (59 +/- 8 micrograms LBK. min.-1; p less than 0.05) and in hypertensive diabetics (26 +/- 6 micrograms LBK. min.-1; p less than 0.001). The ratio of total/active urinary kallikrein was similar in diabetics and in controls. The decline of UKA in diabetics was related to the duration of their disease (r = -0.38; p less than 0.05) and to their stage of retinopathy (r = -0.46; p less than 0.001). UKA values were proportional to creatinine clearance in diabetics (r = 0.58; p less than 0.001). The lowest UKA values were found in patients with a high urinary excretion of albumin (above 500 mg/day): 8 +/- 2 micrograms LBK. min-1 (p less than 0.001) and beta-2-microglobulin (above 382 micrograms/day): 12 +/- 4 micrograms LBK. min-1 (p less than 0.001). These findings support that an impaired secretion of renal kallikrein in diabetics can be related to the duration of diabetes and to the severity of microangiopathy.
 ...
PMID:[Reduction of urinary kallikrein in hypertensive diabetics]. 309 98


1 2 3 Next >>