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Query: UMLS:C0011881 (diabetic nephropathy)
10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necropsy of a patient who died of uremia complicating juvenile diabetes revealed selective calcification of the perineurial sheaths in the sciatic nerves. The calcium phosphate deposits were limited to the outer layers of the perineurium while the innermost lamellae were free. Structural analysis, including electron diffraction and X-ray microanalysis, showed electron-dense, spicular deposits, which were composed mainly of finely crystallized hydroxyapatite. The end-stage diabetic nephropathy of the patient was associated with an extremely high calcium phosphorus ion product known to favour metastatic calcification. The mechanism of the selective localization of the calcium phosphate deposits to the outer layers of the perineurial sheaths is discussed with reference to the structure and suggested barrier function of the perineurium in regard to phosphate ions.
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PMID:Calcification of the perineurium. A case report. 18 98

Out of 27 patients with advanced diabetic nephropathy accepted for renal transplantation. 11 had cardiac symptoms and 10 others had advanced neuropathy. The former group had a poor outcome with 100% mortality within one year, seven patients dying before transplantation. Neuropathy also indicated a poor prognosis. Early transplantation, before the stage of terminal uraemia, was at no advantage in this material.
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PMID:Factors influencing the prognosis in diabetic patients accepted for renal transplantation. 35 88

Abnormal glycosaminoglycan metabolism is involved in the onset of anatomo-functional derangements in diabetic nephropathy, and determines the loss of glomerular basement membrane anionic charges leading to albuminuria. Glycosaminoglycan administration was shown to increase the negative electrical potential of the vessel wall, inhibit mesangial cell proliferation, which is an anatomical hallmark of diabetic nephropathy, and slow down the progression to uremia in subtotally nephrectomized rats, a model that shares some pathogenetic key events with diabetic nephropathy. Based on these considerations, we verified the effect of exogenous glycosaminoglycans on renal involvement in streptozotocin diabetic rats. Long-term administration of two glycosaminoglycans (low-molecular weight heparin and dermatan sulphate) prevented glomerular basement membrane thickening, glomerular anionic charge reduction, as well as the onset of albuminuria without affecting glomerular filtration rate and metabolic control of the disease. Our data demonstrate that the long-term administration of glycosaminoglycans has a favorable effect on morphological and functional renal abnormalities in diabetic rats.
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PMID:Glycosaminoglycans prevent morphological renal alterations and albuminuria in diabetic rats. 132 49

Spontaneously hypertensive rats (SHR) were injected with streptozotocin (STZ-SHR) to induce diabetes. The effect of DP-1904, a thromboxane A2 synthetase inhibitor, on diabetic nephropathy was then studied by administering it for 5 months (1 or 10 mg/kg). DP-1904 did not affect renal 6-keto prostaglandin (PG)F1 alpha production in STZ-SHR, but markedly inhibited renal thromboxane (TX) B2 production, so that the 6-keto PGF1 alpha/TXB2 ratio was significantly increased (P less than 0.05). STZ-SHR showed significant uraemia and proteinuria, plus increases in urinary gamma-glutamyl-transpeptidase and urinary N-acetyl-beta-glucosaminidase. DP-1904 significantly decreased (P less than 0.01) the urinary changes. STZ-SHR also showed an increase in mesangial periodic acid-Schiff-positive substance and in relative renal weight, both of which were significantly inhibited by DP-1904 (P less than 0.05). Thus, DP-1904 inhibited both TXB2 production and the progression of renal damage in STZ-SHR.
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PMID:A thromboxane A2 synthetase inhibitor retards hypertensive rat diabetic nephropathy. 135 Sep 91

Diabetic nephropathy is currently the leading cause of new patients requiring dialysis in the United States. Management of the diabetic patient with ESRD is complicated by the frequent coexistence of complications affecting other organ systems, including retinopathy, cardiovascular disease, peripheral neuropathy, or autonomic neuropathy, manifested as gastroparesis, diarrhea or obstipation, cystopathy, or orthostatic hypotension. Associated clinical syndromes must be followed and treated, if possible, while preparing the patient to receive renal replacement therapy. Both the clinical condition and the psychosocial environment are key factors in choice of ESRD therapy for an individual patient. Rehabilitation data are best for patients who undergo kidney transplantation, but these data are confounded by the fact that the healthiest patients are referred for this treatment modality. Living, related kidney transplant is the preferred initial choice for the diabetic patient with kidney disease. At most centers, both in the United States and abroad, the cadaveric transplant is the second choice for uremia therapy. At the appropriate institution, the patient with type I diabetes may also be considered for a simultaneous cadaveric pancreas transplant. While awaiting cadaveric transplantation, or if contraindication to transplantation is present (chronic infection, recent malignancy, or severe cardiac disease), diabetic patients with severe impairment of the glomerular filtration rate (less than 10-15 ml/min) are referred for vascular access placement and/or insertion of a peritoneal catheter. The decision regarding the choice of CAPD vs. hemodialysis must be made on an individual basis. Rehabilitation and survival data for these therapies are similar, although technique survival rates for CAPD decline dramatically as time progresses because of infectious complications. In-center hemodialysis has the worst survival and rehabilitation profile, but the sickest, most debilitated patients with the highest number of comorbid conditions tend to be referred for that therapeutic modality. Most studies of rehabilitation were performed before use of recombinant human erythropoietin, and comparison between ESRD treatment modalities will have to be reevaluated now that the drug is routinely used.
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PMID:Diabetic nephropathy. Management of the end-stage patient. 139 19

Diabetic nephropathy typically presents more than a decade after diagnosis of diabetes and correlates with the duration of poorly controlled disease. Diabetic nephropathy begins as glomerular hypertension and hyperfiltration, followed by microalbuminuria and the development of hypertension, overt proteinuria, nephrotic syndrome, and a progressive decline in the glomerular filtration rate. Increasing expansion of the glomerular mesangium correlates with loss of function, resulting in uremia. This process eventually leads to the need for dialysis or renal transplantation in 30 percent of patients with insulin-dependent diabetes. By lowering intraglomerular pressure through enhanced glycemic control, inhibition of angiotensin and limitation of protein intake, severe nephropathy may be prevented, delayed or even partially reversed. Treatment must stress control of hypertension.
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PMID:Diabetic nephropathy: early detection, prevention and management. 155 42

Diabetic nephropathy is now the leading cause of renal failure in patients referred for uremia therapy. The diabetic patient is a complicated treatment problem from the first detection of microalbuminmuria, at which time decisions regarding choice of antihypertensive and strictness of metabolic control assume increasing importance. At present, our policy is to advocate strict control of blood pressure, aiming for a systolic blood pressure of less than 140 mm Hg and a diastolic blood pressure of less than 80 mm Hg. We attempt to maintain hemoglobin Alc levels at less than 8%, if the patient does not develop frequent episodes of hypoglycemia. We extend these recommendations to the patient with frank proteinuria, nephrotic syndrome and early uremia, understanding that strict metabolic control may be impossible as patients lose GFR. In addition, we recommend avoidance of a high protein diet in the early nephropathic diabetic, with diet of approximately 1 gm/kg/d. As renal failure progresses, we embark on an analysis of the patient's abilities, lifestyle, and social support. At a GFR of approximately 10 mL/min, we initiate preparations for uremia therapy. If a willing and appropriate living related kidney donor is available, the patient is referred for cardiovascular evaluation and kidney transplantation performed subsequently. If no donor is immediately available, we refer the patient for vascular access placement and/or insertion of a Tenckhoff peritoneal catheter, if preferred. Most of these predialysis patients also undergo screening for placement on the cadaveric kidney transplant list, including cardiac work-up as is done for the patients who receive living-related renal transplants. Because of the long waiting list in Brooklyn, and the universal shortage of organ donors, many of these patients eventually end up on dialysis for some period of time. Other extrarenal problems (urologic, ophthalmologic) are addressed at initial referral and followed up, in hopes of maintaining the patient in optimal physical shape as uremia progresses. The care of the diabetic patient with ESRD ideally involves a consortium of caregivers. We include a nurse-educator familiar with options for uremia therapy, a podiatrist, a cardiologist, and often a urologist, an endocrinologist, and a gastroenterologist. In addition, a social worker is helpful to assess psychologic difficulties in adjustment to uremia, socioeconomic considerations, and rehabilitation status. Finally, the nephrologist, as coordinator of this team works with the vascular or transplant surgeon, to facilitate the transition to ESRD and its therapy.
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PMID:Care of the diabetic patient with end-stage renal disease. 219 Feb 84

Successful pancreas transplantation can result in the longterm normalization of glucose metabolism. Since most pancreas recipients already have severe diabetic complications, and the observation period after transplantation is rather short, an assessment of the effect of complete glucose normalization on these diabetic changes is problematic. It has, however, been shown that the development of diabetic nephropathy can be prevented, peripheral microcirculation improved, and autonomic and peripheral neuropathy and retinopathy stabilized. These positive effects are, possibly, in part due to the elimination of uremia, since most patients receive both a pancreas and a kidney. The aim must be to perform pancreas transplantation in an early stage of diabetes, even though remarkable improvements have also been reported in terminal stages of the disease, and the quality of life of these patients has been significantly improved.
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PMID:[Pancreas transplantation in Type I diabetic patients]. 227 7

In patients with insulin-dependent diabetes, antihypertensive treatment has a beneficial effect on the rate of progression toward uremia of overt diabetic nephropathy (albumin excretion rate [AER] greater than 300 mg/24 hour). The influence of hypertension on the progression of "incipient" nephropathy (AER ranging between 30 and 300 mg/24 hours) is not well defined, particularly in patients with noninsulin-dependent diabetes. In this study, 21 patients with noninsulin-dependent diabetes and hypertension (11 with normoalbuminuria and 10 with microalbuminuria), who were comparable for age, duration of diabetes and hypertension, were treated with indapamide, 2.5 mg once daily, and followed up for 24 months. Blood pressure, glomerular filtration rate (GFR), albumin excretion rate and subclass 4 of urinary immunoglobulin G (IgG4) were indicated. In normoalbuminuric patients, blood pressure was significantly reduced, whereas AER, IgG4 and GFR did not show any variation throughout the study. In microalbuminuric patients, blood pressure, AER and IgG4 were significantly reduced, and GFR remained unchanged. In patients with noninsulin-dependent diabetes, antihypertensive treatment, which is begun during incipient diabetic nephropathy, may have a beneficial effect on the progression of the disease, although a long-term follow-up study is needed to confirm this.
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PMID:Efficacy of antihypertensive treatment with indapamide in patients with noninsulin-dependent diabetes and persistent microalbuminuria. 233 Sep 7

The effect of early antihypertensive treatment on survival of patients with diabetic nephropathy was evaluated by studying two cohorts of Type 1 (insulin-dependent) diabetic patients developing persistent proteinuria in I: 1957-1973 (late treatment group n = 49) and II: 1979-1983 (early treatment group n = 71). At onset of nephropathy, the two cohorts were comparable with regard to age (29(8) vs 30(8) years, mean (SD], duration of diabetes (16(6) vs 18(7) years), blood pressure (132(16)/85(11) vs 134(16)/86(8) mm Hg), proteinuria (0.8(0.5-1.2) vs 0.8(0.6-1.2) g x 24 h-1, median (quartiles] and serum creatinine (87(14) vs (85(16) mumol x 1(-1]. The patients were followed frequently at the outpatients' clinic until death or for a median duration of 8 years. In the first cohort antihypertensive treatment was seldom used, whereas, in the second cohort antihypertensive treatment was started when blood pressure reached 144(18)/93(7) mm Hg. The probability of survival with a functioning kidney for more than 8 years was 48% in the first cohort and 87% in the second cohort, p less than 0.001. The improvement of survival was due mainly to a decreased mortality from uraemia. Early antihypertensive treatment is the most likely explanation for this improvement.
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PMID:Improved survival in patients with diabetic nephropathy. 261 60


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