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

Uremia, the result of renal failure, is a serious clinical problem. Rising azotemia during gravidity significantly increases perinatal morbidity and mortality. This study presents the case of 34 years old patient with 27-year medical history of diabetes mellitus type 1 with diabetic nephropathy and chronic renal insufficiency. The patient got pregnant in the stage of preterminal renal failure. During the first trimester, she showed hypertension and proteinuria. In her 25th week of pregnancy, she was hospitalized with progressive proteinuria, almost uncontrollable hypertension and increased azotemia. Intensive conservative therapy led to a slight decrease of azotemia and proteinuria levels which, however, remained high. In fact, we considered using elimination methods several times. Due to severe hypoxia of the foetus, the gravidity was terminated by section at 30 weeks. After the parturition, the newborn had to be resuscitated. In the first days, the newborn showed increased azotemia which decreased spontaneously after several days. In a month after the termination of gravidity, N-substances increased again and the patient was enrolled in the chronic dialysis programme.
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PMID:[Chronic renal disease and gravidity--case study]. 1687 70

Until the early nineteenth century, diabetes mellitus was regarded as a disease of the kidney, in which there was an increase in the volume of urine and a wasting of the flesh. With the identification of glucose in blood and urine in the late eighteenth century, first it was re-framed as a disease of assimilation and only then became a metabolic disorder. Whilst these changing concepts were debated, it was noted in parallel that diabetics might show coagulable urine containing albumin, even before Bright and others had established this as a sign of kidney disease. Wilhelm Griesinger (1817-1868) was perhaps the first to suggest in 1859 that the diabetes might be causing the Bright's disease, with the latter as a 'complication'. During the next half-century the observation that as albuminuria appeared and increased, so glycosuria improved or might remit, with a parallel or subsequent evolution into uraemia. Glomerulosclerosis and arteriolosclerosis were described in occasional patients during the same period, but text-books of pathology ignored these observations. Thus it was only when diabetics began to survive longer using insulin treatment in the early 1920s that a diabetic nephropathy became widely recognized. After a few isolated descriptions which were ignored, the now famous paper of Paul Kimmelstiel and Clifford Wilson appeared in 1935 detailing nodular renal lesions in just 8 maturity-onset (48-68 year old) diabetics. They barely noted the association with diabetes however, and it was Arthur Allen in 1941 who clarified the association in 105 patients with diabetes, again all aged over 40. Despite the age of the patients in these early studies, diabetic nephropathy became thought of as a disease of young diabetics as a cohort of survivors of juvenile diabetes passed 15 years or more of disease and more than half developed nephropathy. In the 1950s the technique of renal biopsy was rapidly applied to the study of diabetics, and the early lesions defined using electron microscopy as well as optical methods. Then the role of diabetic nephropathy as a cause of renal failure changed: to begin with numbers of young insulin-requiring diabetics were small and infrequently referred for dialysis treatment or transplantation. Then in the 1970s and 1980s the proportion of such juvenile-onset diabetics developing renal failure gradually fell, but at the same time much larger numbers of older diabetics survived their vascular disease and required treatment for renal failure. World-wide, today diabetes accounts for 20-50% of patients entering established renal failure programs, and absolute numbers increase as greater longevity and western-style living has promoted an 'epidemic' of diabetes at all ages.
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PMID:The discovery of diabetic nephropathy: from small print to centre stage. 1687 18

A 64-year-old man was admitted because of abdominal fullness, edema and anorexia. He had come to our hospital for treatment of liver cirrhosis and diabetic nephropathy for 1 year. We started diuretics and human albumin intravenous administration. Although the edema disappeared and abdominal fullness improved a little, blood urea nitrogen (BUN) and serum creatinine became elevated, hepatic function deteriorated and he lost his appetite. We consequently started continuous ambulatory peritoneal dialysis (CAPD) in order to control ascites and uremia. Abdominal fullness, appetite and BUN and serum creatinine improved without hepatic function deterioration. It might be important to start CAPD to control ascites although serum creatinine levels might be slightly elevated.
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PMID:A case report of a diabetic nephropathy patient with cirrhotic ascites treated by peritoneal dialysis. 1730 79

Chronic kidney disease (CKD) has become a major health-care problem of global proportions. Progression to end-stage renal disease (ESRD), the need for renal replacement therapy, and the high annual death rate of dialysis patients are the most noticeable outcomes of CKD. Less appreciated, however, is the fact that most patients with CKD actually die mainly from cardiovascular disease, rather than progress to ESRD. Coronary artery calcification (CAC), a surrogate marker of atherosclerosis, is common in dialysis and CKD patients. Coronary artery calcium scores, as measured by ultrafast computed tomography, is an independent predictor of future cardiac events. Using this technique, several studies have documented extensive calcification in dialysis patients, a subject of several exhaustive reviews. Unfortunately, much less attention has been paid to calcification in nondialyzed patients with CKD. In this review, I will emphasize the fact that CVC is common in patients with CKD not yet on dialysis, develops early in the course of CKD, and worsens with the decline in renal function particularly among diabetics who progressed to ESRD. I will also discuss the pathogenesis of CVC in CKD patients and highlight the lack of a major role for abnormalities of mineral metabolism in the pathogenesis of calcification in CKD patients. In addition to the high prevalence of traditional risk factors for CAD, the presence of proteinuria, reduced renal function, diabetic nephropathy, and the rate of progression to ESRD may represent the main uremia-related factors that increase the risk for calcification in CKD. Finally, I will review the protective role of inhibitors of calcification in CKD.
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PMID:Cardiovascular calcification in nondialyzed patients with chronic kidney disease. 1737 87

A prediabetic state is defined as a higher than normal blood glucose level but not yet high enough to meet the diagnosis of overt diabetes mellitus. While patients with advanced diabetic nephropathy are vulnerable to hypoglycemia, we believe that there is sufficient evidence that uremic nondiabetic patients are susceptible to hyperglycemia, which calls for more attention that uremia is a prediabetic state. It is, therefore, intriguing to identify these uremic factors which lead to prediabetes. Such a study may have significance to improve uremic patients' outcomes. To raise the awareness of the uremic prediabetic state, this review will, therefore, elaborate on the analysis of factors important in the development of prediabetes in uremia and will delineate whether their modification leads to an improved patient outcome.
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PMID:Evidence for increased risk of prediabetes in the uremic patient. 1808 72

Acute movement disorder associated with reversible bilateral basal ganglia lesions is an increasingly recognized syndrome in patients with end-stage renal disease, especially in the setting of concurrent diabetes mellitus. We report an elderly man with end-stage diabetic nephropathy treated by daily automated peritoneal dialysis who developed subacute symptoms of gait disturbance, dysarthria, dysphagia and lethargy. Computed tomography and magnetic resonance imaging of the head revealed bilateral symmetrical basal ganglia lesions. Repeat imaging 3 weeks later showed that these lesions had regressed spontaneously. However, his neurological symptoms improved slowly. These findings were similar to 23 other cases in the literature. Review of these cases shows that clinical features were predominantly bradykinesia, gait disturbance and concurrent metabolic acidosis (observed in 90% of cases). The pathogenesis of this condition has not been clearly defined, but uraemia may be an aggravating factor in predisposed patients, particularly in the presence of diabetic microvascular disease. There is no specific treatment for this condition; supportive measures are the mainstay of management. In the majority of patients, neurological improvement lags behind regression of basal ganglia lesions seen with neuroimaging, and the long-term outcome is variable.
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PMID:Bilateral basal ganglia lesions in patients with end-stage diabetic nephropathy. 1819 7

Erythrocytes are involved in the transport of oxygen and carbon dioxide in the body. Since pH is the influential factor in the Bohr-Haldane effect, pHi is actively maintained via secondary active transports Na(+)/H(+) exchange and HC(3) (-)/Cl(-) anion exchanger. Because of the redox properties of the iron, hemoglobin generates reactive oxygen species and thus, the human erythrocyte is constantly exposed to oxidative damage. Although the adult erythrocyte lacks protein synthesis and cannot restore damaged proteins, it is equipped with high activity of protective enzymes. Redox changes in the cell initiate various signalling pathways. Plasma membrane oxido-reductases (PMORs) are transmembrane electron transport systems that have been found in the membranes of all cells and have been extensively characterized in the human erythrocyte. Erythrocyte PMORs transfer reducing equivalents from intracellular reductants to extracellular oxidants, thus their most important role seems to be to enable the cell respond to changes in intra- and extra-cellular redox environments.So far the activity of erythrocyte PMORs in disease states has not been systematically investigated. This review summarizes present knowledge on erythrocyte electron transfer activity in humans (health, type 1 diabetes, diabetic nephropathy, and chronic uremia) and hypothesizes an integrated model of the functional organization of erythrocyte plasma membrane where electron pathways work in parallel with transport metabolons to maintain redox homeostasis.
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PMID:Electron Pathways through Erythrocyte Plasma Membrane in Human Physiology and Pathology: Potential Redox Biomarker? 1966 14

Although diabetes is clearly linked to macro- and microvasculopathy in multiple organs resulting in cardiovascular and cerebrovascular catastrophic diseases, blindness, and limb amputations, it is the relentless progression of diabetic nephropathy toward becoming the major cause of end-stage renal disease (ESRD) that now challenges budgets and treatment facilities providing hemodialysis, peritoneal dialysis, and kidney transplantation. Nephrology, as a specialty, is now dominated by the necessity to address geriatrics and endocrinology to cope with the tidal wave of elderly ESRD patients suffering from uremia caused by diabetes. On the brighter side, emergence of effective renoprotective regimens now slow the incidence rate of ESRD in those with diagnosed diabetes. There is bona fide reason to hope that within a decade, kidney failure attributable to diabetes will be transformed into a preventable complication of a disease that has dominated and directed our heritage.
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PMID:Diabetic nephropathy in the elderly. 1976 87

Cancer is an important cause of mortality in patients on hemodialysis and kidney transplant recipients. Immunodepression and the genotoxic action of uremia are critical pathogenic agents. A 59-year-old man, ex-smoker, who had been on hemodialysis for seven months because of uremic degeneration of diabetic nephropathy, underwent a combined kidney-pancreas transplant in 1991, complicated by slow-resolution CMV infection. In 1993, after kidney graft failure due to chronic rejection, hemodialysis treatment was restarted with good pancreatic function. Steroid therapy was interrupted and azathioprine and cyclosporine immunosuppressive therapy maintained. In September 2007 the patient was diagnosed with two neoplasms of the oral mucosa: a well-differentiated squamous carcinoma and a spinocellular carcinoma associated with field cancerization. The tumors were resected, followed by laser treatment. Histological examination revealed squamous cell carcinoma without lymph node involvement. Azathioprine was interrupted. In January 2008 adjuvant radiotherapy to the surgical areas of the oral mucosa and neck was started. In February a verrucous nevus on the patient's chest turned out to be a spinocellular carcinoma in situ. In May 2008 recurrence of keratinizing squamous carcinoma of the oral mucosa was found, this time with nodal involvement. Cyclosporine administration was interrupted and after consultation with the oncology committee it was decided to continue with supportive therapy only, until the patient's death in August 2008.
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PMID:[Recurrent multifocal cancer lesions in a patient on hemodialysis after kidney pancreas transplant failure]. 2054 24

Glycemic control via the use of exogenous insulin injections in diabetic patients is incomplete, resulting in multiple long-term complications, such as retinopathy, neuropathy, vasculopathy, and nephropathy. The goal of whole-pancreas and kidney transplantation is to achieve long-term insulin independence and correct uremia. The proposed benefits of pancreas and kidney transplantation are improved quality of life, prevention of recurrent diabetic nephropathy, freedom from exogenous insulin, stabilization or improvement in secondary complications, and improved mortality. No other regimen of insulin delivery or renal replacement besides pancreas and kidney transplantation can achieve this level of physiologic regulation.
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PMID:Current state of combined kidney and pancreas transplantation. 2122 75


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