Chronic Kidney Disease Flashcards
Diagnosis
GFR <60ml/min for >3 months with or without evidence of kidney damage OR
Evidence of kidney damage with or without decreased GFR for >3 months (albuminuria, haematuria, pathological abnormalities, anatomical abnormalities)
- kidney function test, blood test for eGFR creatinine
- test for albuminuria, urine test for albumin/ creatinine ratio (ACR)
- test for hypertension, check bp
Stages
3a- 45-59, 3b- 30-44, moderately reduced kidney function. Prevent mineral bone disease, electrolyte disturbances and malnutrition
4- 15-29, severely reduced plan for end stage renal failure
5- <15, very severe or end stage kidney failure. Look for treatment choices
Manage HTN, nausea, fluid balance, prevent anaemia and acidosis
Causes
Diabetes Glomerulonephritis Hypertension PKD Other
Pathophysiology of CKD
Initial and ongoing insults: diabetes, HTN, age, drugs, vascular disease, obesity, proteinuria
Damage to nephron
Hyperfiltration and hypertrophy of residual nephrons, increases glomerular capillary pressure
Progressive renal dysfunction
Phosphate and calcium in CKD
Decreased phosphate excretion leads to hyperphosphataemia or decreased hydroxylate vit D decreases calcitrol
Leads to hypocalcemia
Leads to hyperparathyroidism
Leads to increased calcium absorption from gut and kidney and calcium loss from bones
Causes extracellular calcification including vascular calcification and or metabolic bone disease CKD MBD
Management of CKDMBD
Based on assessment of phosphorous, calcium and PTH levels
Decisions about phosphate lowering treatment should be based on progressively or persistently elevated serum phosphorous
Lowering elevated phosphorous levels towards the normal range
Restricting the dose of calcium based phosphate binders
Limiting dietary phosphate intake in the treatment of hyperphosphataemia alone or in combination with other treatments
Avoid hypercalcaemia
Use of calcitrol and vit D analogs for patients with CKD and with sever and progressive hyperparathyroidism
