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)

It is well known that urinary FDP is one of the parameters of intrarenal coagulation in renal disease. The measurement of urinary FDP, however, is not satisfactory enough, since it is not a quantitative and sensitive method. Latex photometric immunoassay has recently been developed as a quantitative and more sensitive method. Since fibrinogen reacts with FDP-E less than FDP, the measurement of urinary FDP-E is much better than that of urinary FDP in order to determine the presence of intrarenal coagulation and fibrinolysis of patients with renal diseases. The aim of this study is to clarify the clinical significance of urinary FDP-E measured by LPIA in the renal disease. The results were as follows: (1) Urinary FDP-E correlate with urinary protein, FDP, FDP-D, fibrinopeptide A (FPA), but not serum FDP-E. (2) The diseases which showed higher amounts of urinary FDP-E were diabetic nephropathy, amyloidosis and chronic glomerulonephritis. On the other hand, the diseases which showed smaller amounts of urinary FDP-E were minimal change, toxemia of pregnancy and lupus nephritis. All patients with higher amounts of urinary FDP-E showed marked renal dysfunction. But all the patients with the marked renal dysfunction did not always show higher amounts of urinary FDP-E. The urinary FDP-E showed a positive correlation to 1/serum creatinine. These results suggested that the measurement of urinary FDP-E is a useful method in determining the presence and degree of intrarenal coagulation and fibrinolysis in renal diseases.
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PMID:[Clinical significance of urinary FDP-E measured by latex photometric immunoassay (LPIA) in the renal disease]. 187 56

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

The results are available of combined examination of the kidneys in 84 patients with manifest nephrotic syndrome varying in etiology: 57 had glomerulonephritis, 18 amyloidosis, 9 diabetic nephropathy. The study covered lipid metabolism, immunological status, lifetime morphological investigation of the kidneys. The latter procedure proved advantageous over biochemical and immunological studies in deciding upon nosological diagnosis of nephrotic syndrome and its prognosis. Destruction of podocytic miner processes revealed in all the syndrome cases can serve a uniform morphological substrate underlying massive proteinuria.
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PMID:[Clinical, immunological and morphological evaluation of nephrotic syndrome]. 221 41

The urinary excretion of immunoglobulin light chains kappa and lambda, immunoglobulin G, transferrin, and beta-2-microglobulin was studied in 21 patients with nonimmunoglobulin-related amyloid nephropathy (secondary, type AA) associated with rheumatic disease and in 39 patients with glomerulopathy of nonamyloid origin, as well as in 22 patients with rheumatic disease without signs of nephropathy and in 15 healthy subjects. Patients with amyloidosis were found to have a higher ratio of excreted lambda/kappa light chains than patients with diabetic nephropathy or chronic glomerulonephritis. The increased lambda/kappa ratio was not dependent on the grade of proteinuria and was evident in patients with mild as well as heavy proteinuria. The ratio of lambda/kappa light chains in serum of patients with amyloidosis did not differ from that in healthy controls. The results suggest that amyloid deposition in the kidneys is associated with a selective alternation of the immunoglobulin light chain excretion in the urine.
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PMID:Urinary protein excretion patterns in reactive (secondary) systemic amyloidosis. 314 96

Renal histopathology in 87 patients, aged over 60, with nephrotic syndrome were studied. In 57 patients diagnosed as primary glomerular disease, membranous glomerulonephritis (MGN) was of the most common histologic type (52.6% of the cases), and mesangial proliferative glomerulonephritis (21.1%), membranoproliferative glomerulonephritis (12.3%) and minimal change (12.3%) were the other types of primary glomerular disease. In the remaining 30 patients, nephrotic syndrome resulted from secondary glomerular diseases including diabetic nephropathy and renal amyloidosis. In comparison with the nephrotic syndrome of younger age group (669 cases, younger than 60 years of age), the incidence of MGN, diabetes and amyloidosis were significantly higher in the elderly. In contrast with unfavorable prognosis of diabetic nephropathy and amyloidosis, most cases of MGN and minimal change recovered from the nephrotic state with steroid treatment even in the elderly. Thus, a statistical finding that the prognosis of senile nephrotic syndrome is unfavorable as a whole, appears to be ascribable to the increased incidence of secondary glomerular diseases rather than to "aging" itself. The present results that the incidence of diabetic nephropathy was high and the outcome of MGN was favorable in the elderly, taken together with the results from other studies in Japan, are fairly different from the results of similar studies in the Western world.
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PMID:Histologic studies on the nephrotic syndrome in the elderly. 343 83

Muzolimine is a diuretic with chemical features different from all other known diuretics, and its use seem to be particularly interesting in patients with chronic renal failure. In fact, similarly to furosemide, muzolimine presents a strong action on Henle's loop but with a slower and more lasting effect, as experimentally demonstrated in both animals and man. We used high doses muzolimine (240, 480, 720 mg/die) in 16 patients with chronic renal failure (creatinine clearance less than 20 ml/min) and clinical pattern of important hydrosaline retention (6 primitive glomerulonephritis, 3 interstitial nephrites, 1 vascular nephropathy, 1 diabetic nephropathy, 1 lupus nephritis, 1 amyloidosis, 1 polycystic nephropathy and 2 nephropathies of unknown diagnosis). Muzolimine diuretic action was compared with furosemide 500 mg/die. The schedule employed was: furosemide 500 mg/die for 5 days followed by 6 days of muzolimine treatment at increasing doses (240 mg on 1st and 2nd day, 480 mg on 3rd and 4th, 720 mg on 5th and 6th). In all patients (undergoing a diet constant in water, sodium, potassium and protein content) body weight, blood pressure, heart rate, serum and urinary electrolyte concentration, serum and urinary uric acid, BUN, creatinine clearance, glycaemia, hematocrit and hemoglobin were daily controlled. A clinical and laboratory investigation of the possible side effects was also assessed; in particular liver enzymes, bilirubin and total serum proteins were considered. In our study muzolimine increased the renal excretion of water, sodium and chloride in all cases. This effect is more evident during the treatment with the highest dose (720 mg/die) but already appears with the 480 mg/die dose and is higher than that obtained with comparable doses of furosemide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Muzolimine in chronic renal failure: a study in 16 patients. 400 86

Autopsies of all uraemic patients in Leningrad for three years, and materials of the City Nephrological Service have demonstrated that the structures of nephrological diseases in their early and terminal stages were different. Chronic glomerulonephritis has been noted in patients with normal renal function just as often as chronic pyelonephritis but the former prevails considerably among the causes of uraemia. The proportion of polycystic kidney disease, amyloidosis, and diabetic nephropathy increases in patients with chronic renal failure. Due to these changes and the difference in the death age of patients with various diseases the majority of patients suitable for treatment with long-term dialysis suffer from chronic glomerulonephritis and only 14.89-20.5% from chronic pyelonephritis.
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PMID:Epidemiology of chronic renal diseases. 622 4

Tenascin (TN), a large oligomeric glycoprotein, is a recently described component of the extracellular matrix (ECM). Previous reports focusing largely on the role of TN in nephrogenesis have documented the strong expression of TN in embryonic kidney tissue and implied an important role for TN in nephrogenesis. However, the expression of TN in normal and pathologic kidneys in adults has not been systematically evaluated. In this study immunohistochemical staining for TN was applied to 184 renal specimens diagnosed as: normal kidney (23 cases); minimal change disease and its variants (8); mesangial proliferative glomerulonephritis (GN) including IgA nephropathy and mesangial proliferative lupus nephritis (9); endocapillary proliferative GN including membranoproliferative GN, lupus nephritis, and post-infectious GN (25); crescentic GN (11); membranous GN (19); focal segmental sclerosis (15); thrombotic microangiopathy (8); amyloidosis (5); diabetic nephropathy (9); primary tubulointerstitial nephritis (14); transplant rejection (14); and ischemia (24). It was found that: (a) there was unequivocal global diffuse staining limited to the mesangium in normal kidney; (b) regardless of the etiologies and the morphologic types of glomerular disease, whenever there was expansion of the ECM, whether in the mesangial, endocapillary, or extracapillary spaces, there was a concomitant and proportional in situ increase in the TN staining; (c) globally sclerotic glomeruli, regardless of causes, showed diffuse, strong staining, especially in the subcapsular fibrous deposition seen in ischemic sclerosis; (d) non-sclerotic glomeruli showing early ischemic change uniformly displayed a marked decrease or complete loss of staining; (e) in cases of thrombotic microangiopathy, there was segmental or global staining of the capillary wall, probably corresponding to the enlarged lamina rara interna; (f) all nodular lesions in diabetic glomerulosclerosis showed strong staining, but in several of them this staining was much more pronounced in the periphery than in the center of the lesion. Our study proves that TN is probably a component of the normal mesangial matrix, that TN is an ubiquitous component of the expanded glomerular ECM in pathologic conditions regardless of morphologic subtypes, and that further studies on the cell types and mechanisms responsible for TN synthesis may provide a new venue for the understanding of the process of glomerular sclerosis.
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PMID:Tenascin is an important component of the glomerular extracellular matrix in normal and pathologic conditions. 751 Mar 49

The results of ultrasound (US)-guided renal parenchymal cutting needle biopsies in 101 consecutive patients were reviewed. The biopsies were done with the automated Biopty device mounted with a 2.0-mm needle. One or 2 needle passes yielded sufficient material for histologic analysis in 94% (95/101). Three or more passes were required in 6% (6/101) to obtain an adequate specimen. Mesangioproliferative glomerulonephritis, IgA-nephropathy, nephrosclerosis, diabetic nephropathy, secondary amyloidosis, lupus nephritis, minimal change glomerulonephritis and interstitial nephritis accounted for 79% of the final histologic diagnoses. The high quality and quantity of the tissue specimens yielded a definitive histologic diagnosis in renal parenchymal diseases of unknown etiology. Four major complications occurred, but no deaths or loss of kidney function were recorded. US proved useful as a guide to suitable biopsy site and in the detection of clinically significant complications. Prebiopsy screening of coagulation variables did not seem to prevent complications. Special attention should be paid to post-biopsy clinical observation.
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PMID:Diffuse renal disease. Diagnosis by ultrasound-guided cutting needle biopsy. 830 66

Senile Nagoya, Shibata, Yasuda (NSY) mice developed amyloidosis and died from renal failure as a result of amyloidosis. NSY mice were first reported as experimental congenital diabetic mice by Shibata et al. in 1980. This study questioned whether NSY mice died from diabetic nephropathy. The authors of the present study investigated the life span and cause of death in these mice. The life span of NSY mice was found to be 618.7 +/- 72.5 days. NSY mice that lived for more than 400 days showed rising blood urea nitrogen and large amounts of amyloid deposits in the glomerulus of the kidneys. NSY mice died of renal amyloidosis. Immunological methods revealed that AApoAII was evident in the amyloid deposits of NSY mice. Apart from the kidneys, amyloid deposition was also found in the tongue, esophagus, stomach, small intestine, large intestine, rectum, lung, heart and adrenal glands. Amyloid deposits were found to a slight degree in the liver and the spleen. The most dominant amyloid deposition in NSY mice was seen in the glomerulus of the kidneys. From the point of view of amyloid depositional distribution, NSY mice were unique compared with other spontaneous amyloid mice.
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PMID:Spontaneous amyloidosis in senile NSY mice. 832 7


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