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

The qualitative features of the proteinuria in diabetic nephropathy was studied by carrying out tests of clearance quotient of IgG and albumin in diabetic patients. Diabetic patients with micro and macroalbuminuria showed a major selectivity of proteinuria in relation to normoalbuminuric patients; this suggests a loss of anions at glomerular level.
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PMID:[Qualitative study of proteinuria in diabetic nephropathy]. 193 90

The prevalence of hypertension was evaluated in 479 white subjects with diabetes, according to the type of diabetes and the presence of persistent proteinuria as a marker for diabetic nephropathy. Hypertension was uncommon in 178 insulin dependent diabetic subjects without proteinuria (5%) (mean age 25.0 +/- 12.5 years), but occurred in 23% of 58 patients with proteinuria (mean age 28.9 +/- 14.1 years) and in 90% with azotaemia (P less than 0.00001). Among patients with non-insulin-dependent diabetes hypertension was found in 25% of 170 without renal disease (mean age 48.0 +/- 10.3 years) and in 53% of 53 (mean age 51.4 +/- 13.0 years) with proteinuria (P = 0.0002). We conclude that the prevalence of hypertension among subjects with diabetes depends on the type of diabetes, age, and the presence and severity of diabetic renal involvement.
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PMID:Hypertension, proteinuria and azotaemia in diabetes. 194 96

Overall 42 normotensive patients suffering from type I diabetes mellitus without proteinuria were examined for the effect of hyperfiltration on renal glomerular function and for changes in glomerular function seen during medicamentous treatment of hyperfiltration. Glomerular function was evaluated from the basal level of glomerular filtration (GF), the status of filtration reserves (i. e. according to the dynamics of the GF level in response to oral protein administration), and from the magnitude of albuminuria. Three groups of diabetes mellitus patients were distinguished: with filtration reserves, with decreased filtration reserves, and with no reserves. All the three groups did not differ in the age, diabetes standing or the degree of carbohydrate disorders compensation (HBA1c). Still, the patients with no filtration reserves significantly differ from the other groups with a high level of GF and albuminuria. In 9 patients, a study was made of the effect produced by captopril (an inhibitor of the angiotensin-transforming enzyme) on filtration reserves and albuminuria. After 3 to 6 months of the treatment five patients with no filtration reserves manifested a fall of the basal level of GF down to normal, the recovery of filtration reserves, and a decline of albuminuria. It is assumed that elimination of hyperfiltration due to the treatment with the inhibitors of the angiotensin-transforming enzyme may be an effective means of diabetic nephropathy prevention.
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PMID:[The recovery of the kidney filtration functional reserve in diabetes mellitus patients on captopril treatment]. 194 47

Recent data suggest genetic contributions to the microvascular complications of Type 1 (insulin-dependent) diabetes mellitus. Most research has focused on the HLA region, and the potential role of other genetic loci has not been adequately explored. We examined the possible relationship between DNA polymorphisms in the region 5' to the insulin gene on chromosome 11 and diabetic nephropathy. This was done by comparison of those diabetic patients homozygous for class 1 alleles at the 5' insulin gene polymorphism locus to 1/3 heterozygotes in a well-characterized series of 324 insulin-requiring diabetic patients from the Wisconsin Epidemiologic Study of Diabetic Retinopathy. Proteinuria (defined as greater than or equal to 0.3 g protein/l urine), was used as suggestive evidence for diabetic nephropathy. Hypertension, a frequent associated finding in diabetic patients with nephropathy, was defined as a blood pressure greater than 140/90 or a history of previous treatment of hypertension. The two genotypically defined groups did not differ from each other in regard to sex ratio, age at diagnosis, age at examination, duration of diabetes, body mass, HbAlc or C-peptide. The 1+1 group had a higher prevalence of proteinuria, 29% as compared to 16.2% in other genotypes (p less than 0.05). There was no significant difference in the frequency of hypertension between the two genotypic groups. This finding suggests that the 5' insulin gene polymorphism may be associated with risk for nephropathy, but the pathophysiologic mechanism remains unclear.
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PMID:The 5' insulin gene polymorphism and the genetics of vascular complications in type 1 (insulin-dependent) diabetes mellitus. 195 2

Genetic predisposition to essential hypertension, as indicated by increased maximal velocity of Na+/Li+ countertransport in red cells, has been suggested as a marker for the risk of developing diabetic nephropathy. To evaluate the validity of this concept in non-insulin-dependent diabetics, we measured the maximal velocity of Na+/Li+ countertransport in red cells in 18 male diabetics suffering from proteinuria due to biopsy proven diabetic glomerulosclerosis (GFR: 51 [range 27 to 146] ml/min/1.73 m2), 17 male diabetics with normoalbuminuria, and in 18 sex-, age-, and body mass index-matched healthy control subjects. Na+/Li+ countertransport was identical in patients with and without diabetic nephropathy, 0.43 (0.24 to 0.92) versus 0.44 (0.20 to 0.83) mmol/(liter cells x hr), but was elevated compared to control subjects, 0.32 (0.09 to 0.73; P less than 0.05). Arterial blood pressure was elevated in patients with nephropathy (162/92 +/- 21/9 mm Hg) compared to normoalbuminuric patients (132/82 +/- 15/7) and control subjects (133/83 +/- 14/7 mm Hg; P less than 0.001). Our study does not support the hypothesis that the risk of diabetic nephropathy in non-insulin-dependent diabetes is associated with a genetic predisposition to hypertension. Diabetes per se seems to enhance Na+/Li+ countertransport activity.
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PMID:Red cell Na+/Li+ countertransport in non-insulin-dependent diabetics with diabetic nephropathy. 200 27

We analyzed the components of urinary proteins in 58 diabetic patients with either short duration or long-standing disease using sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis (SDS-PAGE), in comparison with 21 healthy volunteers. It was found that the percentage of protein with a molecular weight (Mr) of 140 kDa was greater in diabetics with normal renal function and negative clinical proteinuria (less than 100 mg/24 h) than in normals. In patients with clinical proteinuria (greater than 100 mg/24 h), the percentage of protein with an Mr of 67 kDa (presumably albumin) was predominantly increased, while the percentage of lower Mr proteins was considerably decreased. A positive correlation existed between the total urinary protein excretion and the percentage of 67 kDa protein in diabetics without clinical proteinuria (r = 0.487, p less than 0.01), but not in normal subjects. Recovery of glycemic control led to a decrease of urine proteins with an Mr lower than 67 kDa, while deterioration of the control resulted in an increase in these proteins. The present data confirm the idea that analysis of the components of urine proteins by SDS-PAGE represents a useful approach to understanding the glomerular and tubular functions in diabetic patients. Additionally, this investigation appears to provide biochemical evidence that dysfunction of the glomerular permselectivity to plasma proteins might already have occurred in diabetic patients without clinical evidence of diabetic nephropathy.
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PMID:Analysis of urinary protein in diabetics; its clinical implications as a predictor of nephropathy. 203 31

Haemostatic activation was measured in patients with either non-diabetic chronic renal failure (CRF) or diabetic nephropathy. We have investigated the relationship between these haemostatic markers and the rate of progression of renal failure. When compared with age- and sex-matched healthy controls, both patient groups showed significantly elevated plasma concentrations of D dimer, von Willebrand factor antigen (vWFAg), and C-reactive protein (CRP) (all P less than 0.001), as well as an increase in spontaneous platelet aggregation (P less than 0.01). Plasma concentration of platelet factor 4 was slightly but not significantly increased. Serum thromboxane was subnormal (P less than 0.01). Multiple regression analysis showed that in non-diabetic CRF proteinuria and serum TxB2 were independently related to the rate of progression of renal failure; in diabetic nephropathy proteinuria and vWFAg were independently related to the rate of progression. In both groups the relationship was stronger with proteinuria (standardised regression coefficients 0.56 and 0.45 respectively) than with serum TxB2 (0.29) or with vWFAg (0.37). We have found haemostatic activation in both non-diabetic and diabetic progressive renal failure. Proteinuria, and also in this study serum TxB2 and vWFAg, appear to be determining factors in the progression of renal failure, and their measurement may have prognostic value.
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PMID:Haemostatic activation and proteinuria as factors in the progression of chronic renal failure. 205 12

Although glomerular damage plays a well-established and important role in the pathomechanism of diabetic nephropathy, it alone does not fully explain the progression of renal complications in long-term diabetes mellitus. We discuss experimental evidence showing involvement of the postglomerular microvessels (peritubular capillaries and venules) in diabetic microangiopathy. This involvement is manifest in increased permeability of these vessels to plasma proteins and in highly augmented lymphatic drainage of the extravasated proteins from the renal interstitium. We suggest that in the advanced phase of diabetic nephropathy, proteinuria (corresponding to excess leakage of proteins through the glomerular capillary wall) indicates the probability that postglomerular microvessels have also allowed leakage of plasma proteins. As long as lymphatic drainage is capable of removing the increased quantity of extravasated plasma proteins from the interstitium, renal function should not be deleteriously affected. However, if the excess amount of extravasated proteins exceeds the capacity of lymphatic drainage, increases in interstitial volume and pressure are unavoidable with detrimental consequences for glomerular filtration and tubular reabsorption. Under these conditions, a potential positive-feedback loop can be visualized that involves increased extravasation of plasma proteins leading to increased interstitial pressure that through dilation of the afferent and efferent arterioles results in a further increase in protein extravasation. These conditions combined with glomerular damage should lead to the eventual collapse of renal function.
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PMID:Role of postglomerular microvessels in pathophysiology of diabetic nephropathy. Assessment and hypothesis. 206 Jul 15

For the early diagnosis of diabetic nephropathy, it is best to use the albumin excretion rate (AER). However, it is a complicated test to perform in the outpatient setting, and it is sometimes affected by inaccurate urine collection. Therefore, we have used the albumin/creatinine ratio, which is measured simply with randomly collected urine, for evaluation of microalbuminuria and found it to be of equal diagnostic value to the AER. The AER, albumin/creatinine ratio, and creatinine excretion rate were measured in 86 patients with NIDDN who were negative for proteinuria. Urine was obtained after bed rest and in the outpatients department (without rest). 1) The reproducibility of time-restricted urine sampling was investigated using the rate of creatinine excretion. The mean coefficient of variation was found to be 42%, and inaccurate urine sampling appeared to cause variation in the AER. 2) The AER and albumin/creatinine ratio obtained in the outpatient setting were higher than those after bed rest, and urine collection at the time of outpatient examination was considered to be more useful than that after bed rest. To check variations in urine collection at the time of outpatient examination, the albumin/creatinine ratio in random urine samples was superior on the basis of the correlation coefficients to urine obtained after bed rest. 3) The urinary creatinine excretion rate showed a significant sex difference (males: 0.823 +/- 0.152 mg/g. creat., females: 0.577 +/- 0.194 mg/g. creat) (p less than 0.001), but there was no significant difference for BMI and age. The relationship between each level of microalbuminuria and the creatinine excretion rate did not change significantly. 4) The following formula was used to calculate the albumin/creatinine ratio corresponding to the AER. Albumin/creatinine ratio formula; (see text) An AER of 30 micrograms/min thus corresponds to an albumin/creatinine ratio of 36 mg/g. creat. for males and 51 mg/g. creat. for females. 5) The percentage of positive results for microalbuminuria in patients with NIDDM showed that the albumin/creatinine ratio and the AER were equal as diagnostic criteria, when the sex difference was taken into consideration. Thus, the albumin/creatinine ratio is equal to the AER for evaluation of microalbuminuria, and it is a simple and convenient test to use in daily clinical practice.
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PMID:[Clinical evaluation of the albumin/creatinine ratio in outpatients with diabetes]. 206 14

Sera from 305 consecutive patients in a renal biopsy series were analyzed for the presence of anti-entactin antibodies by ELISA. Of these patients, 59% had primary glomerulonephritis, 21% had secondary glomerulonephritis, while 20% had other nephropathies (noninflammatory conditions like amyloidosis, diabetic nephropathy, nephrosclerosis, etc.). Forty-one of these patients (13.4%) were positive for IgG/IgM antibodies against entactin: 60% of them had primary glomerulonephritis, 35% had secondary glomerulonephritis, while the remaining 3 patients had other nephropathies. Fifteen (70%) of the 23 patients with primary glomerulonephritis had proliferative glomerulonephritis (PGN), whereas 13 (87%) of the 15 patients with secondary glomerulonephritis were due to systemic connective tissue diseases (SCTD): 7 due to SLE, 4 due to SLE like SCTD and two due to other SCTD. There was a peak of incidence corresponding to the group aged 18 to 30 years. A majority of these patients (12 of the total 17) had primary glomerulonephritis and were associated with nephrotic or subnephrotic grade proteinuria, poorly or nonresponsive to immunosuppressive treatment and associated, in several cases, with progressive deterioration of renal function. In addition, there was a tendency to another peak in the age group 51 to 60 years. Most of these patients (6 of the total 8) had glomerulonephritis secondary, mainly, to SLE or SLE like SCTD with milder degree of proteinuria and better preserved renal functions. Anti-entactin antibodies were not found in certain glomerulonephritides like IgA nephropathy and those secondary to systemic vasculitides and in control subjects (healthy subjects, and patients with a variety of non-renal disorders including inflammatory diseases).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circulating anti-entactin antibodies in patients with glomerulonephritis. 206 16


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