Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunofluorescent studies have demonstrated that actomyosin (AMY) is present in the mesangium in a restrictive pattern, whereas fibroblast surface antigen (FSA) has a more extensive mesangial distribution. Antibody to glomerular basement membrane (GBM) is localized to the GBM. One hundred ninety-six tissue samples, including 17 from normal subjects, 94 from patients with primary renal diseases, and 85 from transplanted kidneys, were examined for changes in distribution of AMY, FSA, and GBM antigens. The distribution of AMY and FSA in the mesangium is markedly increased in width in patients with diabetic nephropathy, and the GBM is thickened. AMY and FSA are mildly increased in patients with glomerulonephritis and GBM is normal. Patients with membranoproliferative glomerulonephritis (MPGN) show a loss of all glomerular antigens. Increased mesangial AMY was found in 12 of 37 transplanted kidneys in diabetic patients vs 4 of 33 nondiabetics 0 to 4 years after transplantation (P < 0.025). This difference is more notable at 2 to 4 years, with 5 of 9 diabetics showing increased AMY vs 0 of 6 nondiabetic patients (P < 0.0005). In MPGN, 5 of 8 tissues showed decreased mesangial AMY vs 3 of 36 diabetic patients (P < 0.0005) and 1 of 32 patients with other glomerulopathies (P < 0.0005). GBM thickening is not associated with specific pretransplant diseases. In transplanted kidneys, the pattern of FSA is dissociated from that of AMY: over half of all patients have increased FSA, even when AMY is normal. Whether this unique finding in transplanted kidneys reflects an increase in the synthesis of FSA by mesangial cells or the failure to clear this (circulating) antigen from the mesangial matrix is unknown.
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PMID:The immunohistopathology of glomerular antigens. II. The glomerular basement membrane, actomyosin, and fibroblast surface antigens in normal, diseased, and transplanted human kidneys. 33 46

The present study describes 3 patients with the simultaneous occurrence of diabetic nephropathy and immune-complex mediated glomerulonephritis. Renal manifestation included proteinuria and hematuria which were preceded by or co-existent with an infectious process. Renal manifestation included proteinuria and hematuria which were preceded by or co-existent with an infectious process. Renal histology showed the characteristic change of diabetic nephropathy along with those of immune complex glomerulonephritis. Immunofluorescence studies showed a linear pattern with a superimposed granular pattern of IgG and C3 deposits. Renal function and urinary findings improved in the 2 patients who were followed up.
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PMID:Diabetes mellitus with immune complex glomerulonephritis. 37 11

Forty-eight patients with nephrotic syndrome were evaluated prospectively; the studies included inferior venacavagrams and ventilation perfusion lung scans. Eleven patients were found to have renal vein thrombosis (RVT). Eight of 21 patients with membranous glomerulonephritis (MGN) or membranoproliferative glomerulonephritis (MPGN) has RVT (38%). Clinical, laboratory, and pathological findings were not different among those patients with MGN and MPGN whether RVT was present or not. Patients with diabetic nephropathy or lupus nephritis did not have RVT. There was a high incidence of other thromboembolic phenomena as well as asymptomatic perfusion defects demonstrated by the lung scan, especially in patients with MGN or MPGN. These data suggest the disease process underlying the nephrotic syndrome may play a paramount role in the genesis of RVT or thromboembolic phenomena.
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PMID:On the incidence of renal vein thrombosis in the nephrotic syndrome. 84 51

During the years 1973, 1974 and 1975, the average annual rate of new ESRD patients was 50.4/million in a 7-county region of Southeastern Michigan. There were marked differences in the rate of new ESRD cases which paralleled the proportion of black individuals in the population. The ESRD rate for the black population was not significantly different in 3 districts within this region, ranging from 125.4 to 159.4/million. The ESRD rate for the white population ranged from 29.4 to 41.3/million, white individuals in Detroit having a significantly lower ESRD rate than white individuals in the area immediately adjacent to the city. The reason for this difference is not apparent. The data indicate that black individuals are more prone to develop ESRD from glomerulonephritis, hypertension, and diabetic nephropathy. In addition, racial factors are an important consideration in health care planning for ESRD treatment.
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PMID:Racial factors in the incidence and causation of end-stage renal disease (ESRD). 91 Mar 46

We compared the glomerular filtration rate (GFR) response to amino acids in patients with glomerular disease and polycystic kidney disease. The GFR response to infusion of amino acids (75 g/12 h), of dopamine (2 micrograms/kg per min), or their combination was evaluated in nine healthy probands and in patients with two types of renal diseases at various degrees of renal function: 15 patients with ADPKD and 11 patients with glomerular disease (IgA glomerulonephritis or diabetic nephropathy). Steady-state inulin infusion technique was used. In healthy subjects amino acids increased median C(in) in response to amino acids was not found in glomerular disease. In contrast in most ADPKD patients median C(in) increased after amino acids (+6.0 ml/min; range -4 to +68), (P less than 0.05). The response to amino acids was not modified by dopamine. The results demonstrate that amino acid-induced acute changes of glomerular filtration differ in polycystic kidney disease compared with glomerular disease. These observations may have implications with respect to mechanisms of progression.
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PMID:The response of GFR to amino acids differs between autosomal dominant polycystic kidney disease (ADPKD) and glomerular disease. 133 69

Dipeptidyl peptidase IV (EC 3.4.14.5) and angiotensinase A (EC 4.4.11.7) were purified to homogeneity from pooled urine concentrate of patients with renal damage, using ultrafiltration, ammonium sulphate precipitation, lectin affinity chromatography, FPLC-ion-exchange(Mono-Q-)chromatography, and FPLC-gel filtration (Superdex). Based on the specific enzyme activity of the starting material, dipeptidyl peptidase IV was enriched 1629 fold, angiotensinase A 1183 fold. The relative molecular masses, Michaelis constants and isoelectric points were determined. Negative staining of the purified enzymes revealed globular proteins (5-7 nm). Antisera raised against dipeptidyl peptidase IV and angiotensinase A reacted specifically with tubular and, in the case of anti-angiotensinase A sera, with tubular and glomerular structures. In addition, urinary membrane vesicles of proximal tubule origin were eluted with the void volume (Superdex-gel filtration), indicating heavy epithelial cell disintegration. Both soluble tissue enzymes (dipeptidyl peptidase IV, angiotensinase A) and vacuolar blebs shed from epithelia contribute to proteinuria, as was shown in patients with glomerulonephritis, interstitial nephritis, diabetic nephropathy and, for angiotensinase A, in patients with essential arterial hypertension.
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PMID:Biochemical and immunological properties of urinary angiotensinase A and dipeptidylaminopeptidase IV. Their use as markers in patients with renal cell injury. 136 94

A case-control study was undertaken to investigate the possible role of chronic hydrocarbon exposure and tobacco and alcohol consumption in the causation of primary glomerulonephritis. Exposure to hydrocarbons and the consumption of tobacco and alcohol were assessed blindly by telephone interview and questionnaire in 55 patients with end-stage renal disease due to biopsy-proven primary glomerulonephritis in whom there had been no evidence of systemic disease. This was compared with 55 normal subjects matched for age, sex, social class and residential area and a comparable internal control group of 45 patients with end-stage renal disease secondary to systemic disease, diabetic nephropathy or chronic pyelonephritis. Hydrocarbon exposure scores derived from the results of the questionnaires were significantly higher (p < 0.001) in the patients with primary glomerulonephritis than in the normal subjects and the internal control group. Moreover, more detailed assessment of the type of hydrocarbon exposure showed significantly greater exposure of patients with glomerulonephritis to petroleum products (p < 0.001), greasing/degreasing agents (p < 0.01) and paints/glue (p < 0.05), and a resulting estimated relative risk of developing glomerulonephritis with each type of hydrocarbon exposure of 15.5, 5.3 and 2.0. Those patients with heavy hydrocarbon exposure (hydrocarbon score > 25,000) had a significantly higher serum creatinine at presentation than those with mild to moderate exposure, suggestive of more advanced renal disease. However, there was no significant difference in tobacco and alcohol consumption among subjects in different groups. We conclude that occupational exposure to hydrocarbon is likely to play a role in the pathogenesis of primary glomerulonephritis and that the risk of developing glomerulonephritis is greatest in those subjects exposed to petroleum products.
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PMID:Primary glomerulonephritis and hydrocarbon exposure: a case-control study and literature review. 143 76

End-stage renal disease (ESRD) treatment rates in the United States have increased steadily since 1973. Decreasing selection against elderly patients with a poor prognostic primary cause of ESRD (i.e., diabetic nephropathy) may partly account for this increase in rates. To test this hypothesis, we calculated log ESRD treatment incidence (ESRDI) rates by four major primary causes of ESRD (diabetic nephropathy (DN), hypertensive nephropathy (HN), glomerulonephritis (GN), and cystic kidney disease (PC); two age groups (old (O), greater than 65 and young (Y), 15 to 44 yr of age) for black and white, male and female, new ESRD patients from 1978 to 1987. As predicted, summary log ESRDI slopes (produced by analysis of covariance) occurred in the following decreasing order, ODN (0.19), OGN = OHN = YDN (0.134). YHN = YPC = YGN (in white patients) = slope not significantly different from 0. Log ESRDI slopes for young black males and females with GN increased significantly between 1978 and 1987, possibly as a result of an increased incidence of GN. In conclusion, decreasing selection may be a factor in the continuing increase in the U.S. ESRD population.
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PMID:Rate of change of end-stage renal disease treatment incidence 1978-1987--has there been selection? 160 Jan 22

Renal pathological changes of diabetes include thickening of all renal extracellular basement membranes and the mesangial matrix and, to a lesser extent, mesangial cell expansion. Two renal lesions appear critical in diabetic nephropathy. Mesangial expansion out of proportion to the size of the glomerulus is related to proteinuria, hypertension, and declining GFR. Arteriolar hyalinosis is related to global glomerulosclerosis, and both are correlated with the clinical features of nephropathy. By the time renal dysfunction is clinically detectable, these lesions tend to be advanced. Interstitial volume may be increased in insulin-dependent diabetes mellitus, particularly in areas containing sclerotic glomeruli or marked tubular atrophy. Parallel findings were documented for type I membranoproliferative glomerulonephritis in which the increased mesangial volume fraction was related to decreased GFR, increased glomerular permeability to protein, and hypertension. As in diabetes, the cortical interstitial volume fraction is correlated with functional abnormalities in type I membranoproliferative glomerulonephritis. Thus, in both of these chronic glomerular disorders, mesangial expansion and interstitial expansion are associated with disordered renal function. Thus, it is not true that glomerular structural changes correlate poorly with glomerular function. Whether it is the glomerular or interstitial pathology or both that is causally responsible for the dysfunction requires further study.
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PMID:Renal structure and function in insulin-dependent diabetes mellitus and type I membranoproliferative glomerulonephritis in humans. 160 Jan 34

The concentrations of two components of the complement system (C1q and C3) were measured in the urine and blood in 10 normal subjects and 134 patients with primary and secondary glomerulonephritis by using a highly sensitive enzyme immunoassay. The values of urinary excretion of C1q and C3 were well correlated to the ratios of fractional clearance of these complement proteins to that of neutral dextran of 55 A, which was used to minimize the influences of glomerular sieving because of their comparable molecular size to these complement components. The rate of renal tubular reabsorption of C1q and C3 were at least 89.2 and 93.4% of filtrated C1q and C3, respectively. Urinary C1q and C3 were excreted significantly in cases of membranoproliferative glomerulonephritis (MPGN), membranous glomerulonephritis, IgA nephropathy with both mesangial and capillary immune complex (IC) deposit and also in case of active lupus nephritis. On the other hand, the concentrations of these complement components were low in case of minimal lesion nephrotic syndrome, mild proliferative glomerulonephritis, inactive lupus nephritis and diabetic nephropathy without any immune staining. There was a significant correlation between the urinary excretion of C1q or C3 and intraglomerular IC deposition, especially IC deposition along the glomerular capillary wall. However, the degree of the excretion of these proteins was not correlated to the degree or permselectivity of proteinuria. The correlations between urinary C1q and C3 were observed in cases of IgA nephropathy with both mesangial and capillary deposit and MPGN, although we couldn't see the correlation in the other glomerular diseases. It is suggested that urinary excretion of such complement components represents the fixation of complement by deposited intraglomerular IC. The measurement of urinary concentration of these complement components provides a new clue to investigation or diagnosis of glomerular diseases.
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PMID:Significance of urinary complement components in various glomerular diseases. 169 33


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