Laboratory 10 15 November 2017 End stage renal disease
Pathology-focus on end-stage renal disease Outline of todays talk Pathology-focus on end-stage renal disease urea and creatinine-what are they and how do they end up in the blood blood plasma urea and creatinine versus urinary urea and creatinine Contributing pathologies and parameters types 1 and 2 diabetes-glucose management atherosclerosis-lipids and lipoproteins hypertension body fat-contributing to 3 above pathologies platelet reactivity contributing to 3 above pathologies nutrient intake
End stage renal disease (ESRD) Pathology inability to produce waste products, maintain fluid and electrolyte balance, and produce hormones
ESRD Pathology End-stage renal disease-associations diabetes (types 1 and 2)-poor glucose management- upsets lipids and lipoproteins and dumps excess glucose into the renal tubules causing damage to their function and ultimately ESRD atherosclerosis-upset lipids and lipoproteins which may be caused by diabetes -atherosclerosis may also cause hypertension hypertension-may be caused by diabetes and hence atherosclerosis or atherosclerosis without diabetes hypertension can damage the glomerular membrane resulting in renal tubule damage due to proteins and other molecules not normally found beyond minimal amounts in the renal tubules
ESRD Pathology End-stage renal disease-associations body fat-particularly so abdominal fat which can trigger type 2 diabetes, atherosclerosis, hypertension, and hence chronic kidney disease platelet reactivity is less in ESRD-why?
ESRD Pathology End-stage renal disease-associations all above pathologies contribute to ESRD risk
Nutrient intake management with ESRD Dietary: Fluid limited-why? Sodium limited-why? Potassium limited-why? Carbohydrate management-why? Calcium-why? Phosphorous-why?
Management with ESRD Also want to control plasma triglycerides, cholesterol, HDL-c, LDL-c, blood pressure BMI to control atherosclerosis and hence further hypertension- this can be done by diet pre- and post- ESRD onset