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)

The renal microvasculature was examined stereoscopically after intraarterial injection of silicone rubber. Specimens studied were: 29 cases of normal kidney, 4 cases of sclerotic kidney, 10 cases of acute renal failure, and 10 cases of chronic renal failure from the final stage of chronic glomerulonephritis, malignant nephrosclerosis, diabetic nephropathy, and cortical necrosis. The following were common evidences for chronic renal failure: much reduction and wide deficiencies of filling in the cortex, increased filling of vasa recta, narrowing and spiralling of interlobular arteries and cortical afferent arterioles, appearance of giant glomeruli, rarefaction of the peritubular capillary plexus, and relative preservation of glomeruli in the juxtamedullary zone and vasa recta in the medulla may be the major pathway, after the interlobular arteries and afferent arterioles in the subcapsular cortex are destroyed, and these vascular architectural changes may be intimately related to the pathophysiology of chronic renal failure.
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PMID:Renal microvasculature in chronic renal failure. 106 90

With the aim of determining the relative prevalence of the diseases underlying chronic renal failure (CRF) in a large homogeneous black tropical population, the autopsy records of the Obafemi Awolowo University Teaching Hospital over a four year period were studied. Out of a total of 702 cases coming to autopsy during this period, 66 (9.4%) died as a result of CRF. The highest number of cases of CRF fell within the 31-40 year age group with a male/female ratio of 1.28:1. Chronic glomerulonephritis was responsible for 40.9% of cases, malignant nephrosclerosis 16.6%, benign nephrosclerosis 7.6% while endstage renal disease (ESRD) was responsible for 15.4%. A miscellaneous group of diseases was responsible for 19.7%, about half of which was due to chronic pyelonephritis. Rarer causes of CRF were diabetic nephropathy, multiple myeloma, systemic lupus erythematosus and analgesic nephropathy.
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PMID:The pathological basis of chronic renal failure in Nigerians. An autopsy study. 149 21

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

Camostat mesilate, a developed derivative of gabexate mesilate for oral use, was administered in a daily dose of 600 mg for 4 weeks to 17 patients with heavy proteinuria due to various nephropathies. Five patients had glomerulonephritis (3 patients with IgA nephropathy, one each with membranoproliferative GN and membranous nephropathy) and 3 had systemic vasculitis. These patients had been treated with glucocorticoid, cyclophosphamide, anticoagulants, and dipyridamole. Five patients had diabetic nephropathy and had been treated with conventional therapy including angiotensin converting enzyme inhibitors. Two cases with benign nephrosclerosis, one with Alport syndrome, and the rest with end-stage renal failure of undetermined cause were also included in this study. Urinary protein decreased promptly within 2 weeks (from 5.2 +/- 0.7 to 3.5 +/- 0.5, mean +/- SE, p less than 0.005), and serum total protein and albumin levels increased significantly. Serum creatinine levels did not change. Decreases in urinary protein excretion of more than 50% were observed in five out of eight patients with glomerulonephritis or systemic vasculitis, two out of five with diabetic nephropathy, and one with chronic renal failure. However, urinary protein excretion values remained at the same level in two patients with benign nephrosclerosis and a patient with Alport syndrome. We suggest that camostat mesilate caused a change in glomerular capillary permeability for macromolecules through its inhibitory effects on the kallikrein-kinin system, complement system, coagulation system, and platelet function, which contributed to the treatment of the various nephropathies.
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PMID:Effect of camostat mesilate on heavy proteinuria in various nephropathies. 279 62

Disorders of fluid and electrolyte metabolism in elderly diabetics were studied. High frequency of hyperkalemia (20.8%), hypomagnesemia (14.6%), hypocalcemia (13.7%), hyperphosphatemia (8.6%), hyponatremia (8.1%) and hyperchloremia (7.2%) was observed among 332 elderly diabetics. Furthermore, hyperkalemia, hyperphosphatemia, hyponatremia, hyperchloremia, hypercalcemia and hypermagnesemia were more frequent in diabetics with renal insufficiency (serum Cr greater than or equal to 1.5 mg/dl) than in diabetics with normal renal function (serum Cr less than or equal to 1.4 mg/dl). In addition, statistically significant negative correlation were observed between plasma glucose levels and serum levels of sodium and chloride in diabetics with normal renal function. These results clearly demonstrated that the most important causal factor of electrolyte disorders in elderly diabetics might be the renal dysfunction due to diabetic nephropathy and/or nephrosclerosis. Moreover, glucose intolerance is also one of the causal factors for hyponatremia and hypochloremia. Disorders of fluid and electrolyte metabolism were manifest in 31 diabetic patients with hyperosmolar non-ketotic coma. The frequency of patients with abnormally elevated serum levels of sodium, potassium and chloride, and patients with abnormally lowered serum levels of calcium was high in this morbid state. Water and sodium deficit, examined in 11 cases of hyperosmolar non-ketotic coma, was 4780 +/- 2100 ml (107 +/- 43 ml/kg body weight) and 290 +/- 170 mEq (6.8 +/- 4.2 mEq/kg body weight), respectively. However, no significant deficit of potassium was observed in the patients. Statistically significant positive correlations between water deficit and serum Cr levels and with serum effective osmolarity were observed. However, there were no significant correlations between water deficit and plasma glucose levels, serum sodium levels and serum osmolarity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Disorders of fluid and electrolyte metabolism in elderly diabetics]. 279 74

Since 1981, the Korean Society of Nephrology began annual report on renal replacement therapy in Korea. The annual number of new patients receiving dialysis treatment in 1986 increased to 957 patients (23.3 per million population) from 825 patients (20.4 per million population) in 1985. And the total number of patients on replacement therapy increased from 1,508 patients (37.3 per million population) to 2,534 patients (61.7 per million population). 1,340 patients (32.6 per million population) of these patients were on hemodialysis, 573 patients (13.9 per million population) on continuous ambulatory peritoneal dialysis (CAPD) and 621 patients (15.1 per million population) on functioning renal graft as of December 31, 1986. The common causes of renal failure of new patients were chronic glomerulonephritis (41.6%) followed by diabetic nephropathy (12.6%), nypertensive nephrosclerosis (7.8%), chronic pyelonephritis (2.5%) and others. The annual mortality rate decreased from 21.9% in 1981 to 13.5 in 1986. The common causes of death in patients on dialysis therapy were cardiac (32.8%), vascular (14.7%), infective (14.7%) and social problems (11.2%) in the order of frequency. Recently, the number of patients requiring dialysis is rapidly increasing due to expanded medical insurance support for dialysis and improved economic status of our country. Therefore, it is necessary to draw up counterplan for a rapid growth of the number of new patients.
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PMID:Multicenter report on dialysis and transplantation in Korea, 1986. Korean Society of Nephrology. 307 56

The progression of renal failure was analyzed in 108 patients with mild to moderate renal impairment, none of whom had received any form of dietary protein, phosphate restriction or immunosuppressive treatment. The reciprocal of plasma creatinine was plotted against time using a minimum of six plasma creatinine values taken over at least six months (mean 13 values over 41 months). Plots indicated there was linear deterioration in 70 patients, non-linear deterioration in 15 and stable renal function in 24. Progressive renal failure was common in patients with glomerulonephritis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease. Most patients with hypertensive nephrosclerosis, analgesic nephropathy and renal impairment following acute renal failure were stable. Among those with progressive impairment the mean rates of deterioration were significantly faster for patients with glomerulonephritis and diabetic nephropathy compared to those with chronic pyelonephritis, polycystic kidney disease and undiagnosed renal disease (p less than 0.01). Hence the underlying renal pathological changes appear to be important in determining progression of renal failure and also the subsequent rate of deterioration. For those with linear progression of renal failure there was a significant correlation between 24-h urinary protein excretion and the rate of deterioration. This relationship held for glomerulonephritis and chronic pyelonephritis as separate diagnostic groups only. Proteinuria, therefore, may be a useful prognostic index for the rate of progression of established renal failure. Calcium phosphate product correlated poorly with the rate of deterioration. We were unable to demonstrate a relationship between spontaneous protein intake and deterioration of renal function. However, patients prescribed high protein diets were not included in dietary analysis and we cannot, therefore, exclude the possibility that a high dietary protein intake may accelerate renal failure. Similarly we were unable to show a significant relationship between blood pressure and progression of renal failure although there were weak correlations between mean arterial pressure and rate of deterioration for chronic pyelonephritis and glomerulonephritis.
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PMID:Renal pathology and proteinuria determine progression in untreated mild/moderate chronic renal failure. 320 6

It is well known that blood access is essential for long-term hemodialysis treatment. Arteriovenouos fistula (AVF) is the most widely used method. However, this method of access frequently fails (access failure) as a result of stenosis. We attempt simple femoral vein puncture (FV-method) instead of AVF in such patients and have experienced 12 patients who were undergoing hemodialysis treatment using the FV-method, three times a week for more than one year. We devised special needles (18- and 19-gauge) for the FV-method. Generally, we use a 19-gauge needle with 4 side holes. We discuss here the results of 12 patients consisting of 4 males and 8 females with a mean age of 57.9 years, a mean duration of dialysis of 10.0 years, and a mean duration of FV-method of 3.5 years. Their underlying diseases were chronic glomerulonephritis (9 patients), diabetic nephropathy (2 patients) and nephrosclerosis (1 patient). Before the use of the FV-method, AVFs were attempted a man of 3.8 times and an artificial graft, 4 times in 3 patients. Ten patients were outpatients and 2 were inpatients. As for the indications of the FV-method, 11 patients had access failure and another had suffered from heart failure resulting from an over flow of blood through AVF. KT/V, PCR and TACBUN were measured monthly and were within the normal range in almost all of the patients. Concerning complications of the FV-method, hematoma formation after detachment of the needle at the end of dialysis and pain at needle puncture were sometimes noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term hemodialysis treatment using femoral vein puncture method (FV-method) as blood access in 12 patients]. 747 9

The study of the current status of renal replacement therapy in Japan is based on the analysis of data from the registry reports for regular dialysis therapy and kidney transplantation. The total number of patients receiving regular dialysis therapy was 123,926 at the end of 1992: 117,809 (95.1%) on hemodialysis and 6,117 (4.9%) on peritoneal dialysis. The primary diseases of newly accepted patients were chronic glomerulonephritis (42.2%), diabetic nephropathy (28.4%), nephrosclerosis (5.9%), polycystic kidney disease (2.7%), chronic pyelonephritis (1.6%), and others. The number of kidney transplant patients in Japan was 8,384 at the end of 1991: 6,154 (73.4%) received a living donor transplantation and 2,230 (26.9%) received a cadaver donor transplantation. Overall 5-year survival rates of dialysis patients were 60.4%: 69.7% for chronic glomerulonephritis, 41.7% for diabetic nephropathy, 39.6% for nephrosclerosis, 73.6% for diffuse polycystic kidney disease, and 66.6% for chronic pyelonephritis. The causes of death of dialysis patients were heart failure (31.1%), cerebrovascular accident (13.6%), infectious diseases (11.3%), malignancies (7.1%), cachexia/uremia (6.7%), myocardial infarction (5.8%), and others. The gross mortality rate of dialysis patients was increased in cases of less than 4 hours of the average length of each dialysis session, less than 4% and more than 9% of the average weight loss during each dialysis session, less than 1.0 of Kt/V, and less than 0.9 and more than 1.7 g/kg/d of protein catabolic rate. Overall 5-year patient and graft survival rates of kidney transplant patients since 1964 were 82.7% and 60.3%: 84.4% and 65.0% in living donor cases, and 77.4% and 46.2% in cadaver donor case, respectively. Those since 1983 were 90.1% and 68.2%: 91.3% and 72.6% in living donor cases, and 87.8% and 59.3%, respectively. Graft survival rates were superior in cases treated with combined steroid, cyclosporine and azathioprine or mizoribine, to those treated with other immuno-suppressive regimens, and they decreased as the number of HLA-A, -B and -DR increased.
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PMID:Current status of renal replacement therapy in Japan. 781 May 20

Diabetic nephropathy is characterized by excessive glomerular matrix accumulation, basement membrane thickening and sclerosis. Although it is clear that systemic metabolic disturbances precipitate such renal changes, the signals and pathways involved in this process are not fully elucidated. Recent evidence suggests that growth factors/cytokines are intimately involved in the pathogenesis of diabetic nephropathy. Because of its prosclerotic properties, transforming growth factor-beta (TGF-beta) is a prime candidate mediator of diabetic nephrosclerosis. We examined perfused kidney tissues isolated from spontaneously diabetic, non-obese diabetic mice (NOD) for TGF-beta content. By using murine isotype specific TGF-beta probes, we demonstrate that within 5 to 10 days of hyperglycuria renal TGF-beta 2 mRNA and protein content increases. By immunohistochemical analysis, de novo TGF-beta immunoreactivity was detected within both glomeruli and the interstitium. In order to determine the signals involved in promoting kidney TGF-beta content in vivo, TGF-beta regulation was examined in renal mesangial cells in vitro. Murine mesangial cells stimulated with glycosylated protein secrete bioactive TGF-beta and demonstrate a disproportionate increase in the steady state levels of TGF-beta 2 mRNA. These data suggest that a major early renal response in NOD mice to hyperglycemia or to glycosylated proteins is characterized by increases in TGF-beta.
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PMID:Renal TGF-beta regulation in spontaneously diabetic NOD mice with correlations in mesangial cells. 799 97


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