14/10/2024 Flashcards
(22 cards)
How to calculate urea:creatinine ratio?
Urea divided by (creatinine / 1000)
How to interpret urea/creatinine ratio?
If >100:1 its a pre-renal cause as urea absorption is increased
40-100:1 = normal or post-renal
<40:1 = renal as kidneys are failing to absorb urea
What can cause hyaline casts in urine?
Normal after exercise, during fevers or with loop diuretics
What are hyaline casts?
They consist of uromodulin (Tamm-horsfall proteins)
At what eGFR can CKD cause anaemia?
Usually <35
Suspect a different cause if eGFR is still >60
What can anaemia in CKD predispose you to?
Left ventricular hypertrophy
Causes of anaemia in CKD?
reduced erythropoietin levels - the most significant factor in CKD causing anaemia. CKD is associated with a decrease in the production of erythropoietin, a hormone produced by the kidneys that stimulates erythropoiesis in the bone marrow. reduced erythropoietin levels → diminished red blood cell production
reduced absorption of iron - hepcidin is an acute-phase reactant. in CKD, hepcidin levels are often increased due to inflammation and reduced renal clearance. elevated hepcidin levels lead to decreased iron absorption from the gut and impaired release of stored iron from macrophages and hepatocytes, reducing the iron available for erythropoiesis. additionally, metabolic acidosis, a common condition in CKD, can inhibit the conversion of ferric iron 3+ to its absorbable form, ferrous iron 2+, in the duodenum → reduced iron absorption.
reduced erythropoiesis due to toxic effects of uraemia on bone marrow
anorexia/nausea due to uraemia
reduced red cell survival (especially in haemodialysis)
blood loss due to capillary fragility and poor platelet function
stress ulceration leading to chronic blood loss
Target haemoglobin for anaemia in CKD?
100-120
Tx of anaemia caused by CKD?
determination and optimisation of iron status should be carried out prior to the administration of erythropoiesis-stimulating agents (ESA).
oral iron should be offered for patients who are not on ESAs or haemodialysis. If target Hb levels are not reached within 3 months then patients should be switched to IV iron
patients on ESAs or haemodialysis generally require IV iron
ESAs such as erythropoietin and darbepoetin should be used in those ‘who are likely to benefit in terms of quality of life and physical function’
Pathophysiology of nephrotic syndrome?
Damage to GBM and podocyte increases permeability to proteins
This causes albumin loss which leads to a decreased oncotic pressure = oedema
Why does nephrotic syndrome predispose a pt to VTEs?
As it causes loss of antithrombin-III, protein C, protein S and there is an increase in fibrinogen
What should you start any pt with diabetes and an ACR >=3 on?
ACEi
ARB if black African or afrocarribean
Causes of a raised anion gap metabolic acidosis?
Increased production of acids such as lactic acidosis (shock, hypoxia), ketoacidosis (DKA or alcoholic)
Decreased excretion of acids e.g. in renal failure increase urate
Ingestion of toxins e.g. methanol, ethylene glycol, salicylate overdose
Starvation ketosis
Chronic paracetamol use
Why does CKD lead to low vitamin D?
As the kidneys are where 1 alpha hydroxylation of 25-hydroxycholecalciferol usually occurs = can’t active vitamin D
Why does CKD lead to increased phosphate?
As kidneys usually excreted phosphate so when damaged cannot remove it as well
Why does CKD cause osteomalacia?
Low vitamin D
Why does CKD cause low calcium?
Due to the kidneys being less able to make active vitamin D which is required for calcium absorption
Why does CKD cause secondary hyperparathyroidism?
Defect in the activation of vitamin D in the kidneys due to CKD leads to hypocalcemia and hyperphosphatemia, resulting in a compensatory increase in parathyroid gland cellularity and parathyroid hormone production and causing secondary hyperparathyroidism
= low or normal Ca, high phosphate, low vitamin D< elevated PTH
Management of mineral bone disease caused by CKD?
Decrease dietary phosphate intake
Phosphate binders e.g. calcium carbonate or sevelamer
Vitamin D e.g. alfacalcidiol or calcitriol
Parathyroidectomy in some cases
What is the difference between calcitriol and alfacalcidol?
Calcitriol is the active form of vitamin D so when ingested it does not require any further metabolism
Alfacalciol is a synthetic analogue of vitamin D that requires 25 hydroxylation by the liver but is already hydroxylated at the 1α position
(Importantly both bypass the 1 alpha hydroxylation by the kidneys!)
Outline vitamin D metabolism in the body?
Vitamin D is produced in the skin when 7-dehydrocholesterol is exposed to ultraviolet (UV) light from the sun.
Vitamin D can also be obtained from the diet: Ergocalciferol (Vitamin D2) is found in plant sources and cholecalciferol (Vitamin D3) is found in animal products.
Cholecalciferol (D3) is transported to the liver, where it is converted to 25-hydroxycalciferol (25(OH)D). This form of vitamin D is considered slightly active and is commonly measured in the blood to assess vitamin D status.
The 25-hydroxycalciferol (25(OH)D) is then converted in the kidneys to 1,25-dihydroxycalciferol (1,25(OH)₂D).
This is the most active form of vitamin D, and it is approximately 1000 times more active than 25(OH)D.
What will be seen in urine in interstitial nephritis?
White cell casts
