Chronic kidney disease Flashcards
What is chronic kidney disease?
Gradual and irreversible deterioration in renal function due to progressive loss of functioning nephrons.
Kidney damage, as indicated by persistent proteinuria, haematuria or structural abnormality.
What are the risk factors of chronic kidney disease?
Primary causes of CKD worldwide are:
Hypertension.
Diabetes mellitus.
Increasing prevalence in the UK can be attributed to:
Ageing population.
Increasing rates of obesity.
Increasing ethnic diversity.
How can progression of kidney disease be slowed?
Blood pressure control.
Glycaemic control.
Reducing proteinuria.
What is the link between chronic kidney disease and hypertension?
Cardiovascular disease is most common cause of death in patients with CKD.
Large body of evidence demonstrating benefits of strict BP control in slowing the progression of CKD.
Inhibitors of RAAS are the treatment of choice in:
Patients with diabetes and ACR > 3mg/mmol.
Patients without diabetes and ACR > 30mg/mmol.
ACE inhibitors and A2RBs preferentially reduce intra- glomerular pressure and lower proteinuria.
Monitor SCr and potassium level before and 1 to 2 weeks after initiation or dose change.
Discontinue if SCr increases to > 30% above baseline, or potassium level > 6 mmol/L within first 2 months.
What is the link between chronic kidney disease and diabetes?
Hyperglycaemia is an independent risk factor for CKD.
Diabetic nephropathy is caused by haemodynamic and metabolic changes to glomerular basement membrane.
Recommended HbA1c target to prevent or delay development of microalbuminuria is 7.0% (53 mmol/mol).
ACE inhibitors and A2RBs have renoprotective effects in early and late nephropathy caused by type 2 diabetes.
Consider addition of SGLT2 inhibitors if ACR > 30mg/mmol.
What are the symptoms of chronic kidney disease?
Accumulation of uraemic toxins leads to anorexia, nausea, vomiting, pruritis, fatigue, weight loss, neurological changes, constipation, GI bleeding.
Renal medullary damage and the osmotic effects of uraemia initially leads to polyuria and nocturia.
Inability to excrete sodium & water adequately leads to peripheral, pulmonary or cerebral oedema, ascites.
Proteinuria results from glomerular leakage & failure of renal tubules to reabsorb protein.
Hyperkalamemia.
Sodium disorders.
Metabolic acidosis.
How would you manage uraemia?
Reduced dietary protein intake may improve symptoms.
Gastrointestinal symptoms (nausea, vomiting, constipation) are treated with conventional antiemetics and laxatives.
Pruritis may be caused by imbalances in calcium, phosphate and PTH – treat with sedating antihistamines, or gabapentin.
Muscle cramps may respond to oral quinine preparations.
How would you manage fluid retention?
Restrict fluid intake to 1 – 3 litres per day.
Reduce dietary sodium intake and avoid sodium-containing medicines where possible.
Control is best achieved with dialysis, but loop diuretics can be useful to relieve symptoms.
Higher doses are needed in patients with advanced CKD (eGFR < 30ml/min) due to diminished tubular secretion.
How would you manage metabolic acidosis?
Managed with oral sodium bicarbonate 1 – 6g daily.
Benefits seen with respect to bone health, nutritional status, and delaying CKD progression.
Sodium load may aggravate oedema and hypertension.
Severe or persistent acidosis will require dialysis.
What is the link between chronic kidney disease and anemia?
Primarily due to failure of peritubular cells of the kidney to synthesise or secrete erythropoietin.
Also caused by iron deficiency, shortened red cell survival, and impairment of erythropoiesis by uraemic toxins.
Traditionally, managed with repeated blood transfusions.
Introduction of erythropoiesis-stimulating agents (ESAs) has maintained efficacy but improved safety of treatment.
What are erythropoiesis-stimulating agents?
Erythropoiesis-stimulating agents are medications which stimulate the bone marrow to make red blood cells. They are used to treat anemia.
Initially available as epoietin-α and epoietin-β, given 2 to 3 times weekly by IV or SC injection.
May cause hypertension.
What is hyperphosphataemia?
Phosphate excretion is reduced, leading to initial compensatory rise in PTH.
PTH stimulates the kidney to excrete more phosphate.
Ability of kidney to respond to PTH diminishes, and phosphate levels increase.
How would you manage hyperphosphataemia?
Limiting dietary phosphate intake from phosphate-rich foods (e.g. dairy products, oily fish) is essential.
Phosphate-binders reduce gastrointestinal absorption of dietary phosphate (taken with food for maximum effect):
Calcium containing phosphate binders and non-calcium containing phosphate binders.
Choice of treatment depends on calcium level, side effect profile, daily tablet burden, and patient preference.
When would you prescribe calcium containing and non-calcium containing phosphate binders?
Calcium containing binders:
E.g. calcium acetate, calcium carbonate.
Recommended first line treatment (low cost!).
Useful for correcting hypocalcaemia.
Non-calcium containing binders
E.g. aluminium hydroxide, sevelamer, lanthanum.
Preferred in hypercalcaemia or patients at risk of vascular calcification.
Aluminium reserved for refractory hyperphosphataemia due to risk of accumulation and toxicity in renal failure.
How is vitamin D metabolised?
1α-hydroxylase activity is reduced in CKD and from effects of hyperphosphataemia.
Production of calcitriol (active vitamin D3) is reduced.
Intestinal absorption of calcium is reduced, leading to hypocalcaemia.
