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Guideline [Progression factors for chronic kidney disease. Secondary prevention] 2008
García de Vinuesa S. · Hospital General Universitario Gregorio Marañón, Madrid. · Nefrologia. · Pubmed #19018733 No free full text.
Abstract: The natural history of most chronic kidney diseases (CKD) indicates that glomerular filtration gradually declines over time, progressing to more advanced stages of kidney failure. Since the publication of the first studies by the Modification of Diet in Renal Disease (MDRD) Study Group, numerous factors have been identified that can accelerate this progression. Some are dependent on the etiology, but other are common to all and may accelerate progression of kidney disease: Non-modifiable progression factors for CKD: - Etiology of kidney disease - Degree of initial kidney function - Gender - Age - Ethnicity/Other genetic factors - Birth weight Modifiable progression factors for CKD: - Proteinuria - High blood pressure - Poor glycemic control in diabetes - Smoking - Obesity - Metabolic syndrome/Insulin resistance - Dyslipidemia - Anemia - Metabolic factors (Ca/P, uric acid) - Use of nephrotoxic drugs. Therapeutic intervention on these factors has shown that it reduce the rate of progression of CKD (Strength of Recommendation A).There is no clear evidence that correction of these factors slows CKD (Strength of Recommendation C), although it has been shown to have a beneficial effect on cardiovascular risk at other levels.
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Article [Calciphylaxis: fatal complication of cardiometabolic syndrome in patients with end stage kidney disease] free! 2008
Verdalles Guzmán U, de la Cueva P, Verde E, García de Vinuesa S, Goicoechea M, Mosse A, López Gómez JM, Luño J. · Servicio de Nefrología, Hospital General Universitario Gregorio Marañón, Madrid. · Nefrologia. · Pubmed #18336128 links to free full text
Abstract: Calciphylaxis characterized by schemic skin ulceration due to subcutaneous small arterioles calcification, is a rare disease but usually fatal. Disorders of calcium metabolism and vascular calcifications are common in dialysis patients but calciphylaxis prevalence is low in patients with end stage renal disease. So we proposed other emergent factors implicated in calciphylaxis development. METHODS: We studied retrospective 8 patients who developed calciphylaxis in our service from january 2001 to december 2006. RESULTS: All patients were female with mean age at diagnosis 68.5+/-6.7 years. All patients were receiving hemodialysis therapy and 6 patients had been receiving hemodialysis less than four months. Six patients had diabetes mellitus type II and all patients were obese (BMI >25 kg/m2). All patients had metabolic syndrome (APTIII) with bad control hypertension and 6 (75%) were receiving anticoagulation therapy with warfarin. Patients didn t have severe alterations of calcium metabolism, all had product calcium-phosphorus <55. All patients developed low blood pressure at the beginning of dialysis treatment (98.3+/-22.7/60+/-18,29 mmHg). 7 patients present proximal lesions in fatty regions like abdomen and thighs. Histopathologic examination reveals calcium deposits in arteriole-sized and small vessels with vascular thrombosis. Prognosis was poor, seven patients died secondary to a sepsis originated in infected cutaneous ulcers. CONCLUSIONS: calciphylaxis is a disease with poor prognosis and high mortality, without specific treatment actually. Female gender, obesity associated with diabetes mellitus and cardiometabolic syndrome, anticoagulant therapy with warfarin and low blood pressure associated with hemodialysis therapy, are risk factors to develop calciphylaxis, in absence of severe disorders of calcium metabolism. In these patients is important to avoid hypotension episodes during dialysis, dialysis hypotension appears to be an important risk factor who promotes ischemia of subcutaneous adipose tissue.
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