Chronic Kidney Disease

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Presentation transcript:

Chronic Kidney Disease

Normal Physiology of the Kidney Hormones – EPO, RAAS, 1-alpha-hydroxylase Metabolic – excretion of urea/creatinine etc. Homeostasis – acid base balance, electrolyte levels

Chronic Kidney Disease A progressive decline in renal function Present for at least 3 months Marked by increased serum creatinine and a fall in GFR

Aetiology Diabetes is the most important precursor to CKD. Consider the different disease processes: Vascular: increases in pressure, vasculitis Immunological: glomeruonephritis Infection: pylonephritis, UTI Congenital: polycystic disease Obstruction

Clinical features Pallor and malaise – due to anaemia Pruritis – accumulation of urea + other metabolites Polyuria, nocturia Bone pain – metabolic bone disease Sleep reversal, restless legs

Staging

Management Aggressive BP control Prevent hyperlipideamia ACEi, ARB, CCB Aim <140/90 Prevent hyperlipideamia Statins Vit D supplements

Management of ESRD Renal replacement therapy: *Transplantation HD PD Haemodialysis: blood taken from patient and put through dialyser Peritoneal dialysis: tube inserted into peritoneal cavity and dialysate run through *Transplantation HD PD Requires hospital visit each time Requires trained staff Less frequent (3x week) Need strict diet and fluid intake More flexible Patient is able to be home based Less dietary restrictions Body image problems More prone to infection Frequent (1x at least per day) Associated with DM

Questions 1. Describe how CKD can lead to metabolic bone disease (5 marks).

Reduction in vitamin D means less Ca can be absorbed from gut This stimulates parathyroid gland PTH released Stimulates Ca resorption from bone Bones become weak, less crystalloid formation

Thanks for listening. Any questions just email: K. Tomlinson@warwick Thanks for listening! Any questions just email: K.Tomlinson@warwick.ac.uk