CKD Flashcards
DEFINE
“abnormalities of kidney function or structure present for more than 3 months, with implications for health”
describe
Very common, usually exists with other conditions such as CVD or diabetes. Rare to have CKD by itself. Patients with CKD may be older as well so may be more complex.
Early stage CKD is asymptomatic therefore sometimes they can be late referrals which increases the risk of mortality and morbidity. This risk increases with age. There are different stages of CKD ranging from mild to severe.
Risk increases with age
Costly disease to NHS, especially dialysis
how does it progress
In CKD, we look at eGFR but measured against the albumin:Cr ratio. (ACR).
As CKD progresses and worsens, the kidney structure breaks down and becomes more “leaky”, and not as tight, so large moleules like proteins (such as albumin) start to leak out of the blood and into the urine. Albumin is normally in low concentrations in the urine as they do not pass through the kidneys, but when CKD is more severe, the albumin leaks through and the albumin is cleared from the body. Therefore ACR is measured.
To measure ACR, a urine sample and dipstick is done, to compare the amount of albumin that has leaked out, to the Cr. The higher the albumin to Cr ratio, the more severe the CKD.
staging of ckd
There are 5 stages of CKD – stages 1 – 3, the kidneys can still filter waste, but stages 4 – 5 are more severe and the kidneys may stop working completely.
risk factors?
Diabetes – nephropathy
Hypertension – high BP pushing the kidneys so more likely to be damaged
AKI - especially if treated late or poorly managed, can become CKD or if repeated AKIs, may lead to permanent damage.
Infections - especially UTI or recurrent infections, especially pyelonephritis which damages the kidney itself
Medications – e.g. lithium, NSAIDs
diagnosing ckd?
Establish Cr level and ACR via dipstick.
Check if there is any blood in the urine and there is no reason for this.
Or could be a result of imaging e.g. US or biopsy
Functions of the kidneys; so what if they stop working?
3 main functions of the kidney – kidney problems, it affects these functions.
Homeostasis – filtration, absorption, secretion, getting rid of waste products like Urea, regulating pH, removal of K+, regulating BP
Hormone function – Renin release (see 2nd year lectures) + Epoetin (later slides) + activation of Vit D to the active form
Metabolic function – removal of drugs from body
Therefore if you know the functions of the kidney, you will know what is affected in CKD
clinical complications of ckd, name
Acidosis – kidneys can’t regulate hydrogen ions anymore so blood becomes acidic as can’t get rid of H+
Anaemia – either lack of EPO or lack of iron
Dyslipidaemia – abnormal lipid metabolism
Fluid overload – kidneys can’t regulate BP or water or sodium ions as it used to, so less excreted meaning more accumulation – may get oedema in hands or legs
Hyperkalaemia – can’t clear potassium as much so raised K+
Hypertension – can’t regulate BP as before
Mineral + bone disorder – regarding vitamin D, calcium, phosphate
Uraemia – less able to excrete urea so builds up
ACIDOSIS, management, treatment and SE
Inability of kidneys to maintain blood pH
CKD progresses - kidneys are less able to excrete H+ and reabsorb HCO3-
kidneys can’t regulate hydrogen ions anymore so blood becomes acidic as can’t get rid of H+
patients with CKD are put on long-term PO sodium bicarbonate (1g TDS)
- acute treatment of metabolic acidosis = IV sodium bicarbonate
- secondary increase in sodium so beware of fluid retention
renal anaemia
when the quality or quantity of red blood cells are below normal
Anaemia – red blood cells low OR quality of red blood cells below normal.
Renal anaemia = 2 causes. Lack of circulating iron or lack of EPO.
why is lack of circulating iron one of the most common causes in CKD?
Many reasons: may be on Haemodialysis / more blood tests, so constant samples = Increased blood loss
Dietary inadequacy -> many patients are on a renal diet to restrict phosphate intake
Poor iron absorption due to uraemia or use of phosphate binders
Reduced or impaired erythropoiesis due to lack of erythropoietin or iron
what is the management for lack of circulating iron?
pre-dialysis patients
- oral iron usually for 3 months maximum
- if no improvement in oral iron, give IV iron
- examples: ferrous sulphate or ferrous fumarate
- side effect of PO iron = GI irritation, black stools
- note recent change to oral iron dosing – now mostly OD
Dialysis patients
- give IV iron
- given after a dialysis session
- many different types of IV iron but usually Ferinject
how can a lack of erythropoietin lead to renal anaemia?
Erythropoietin (EPO) is a naturally occurring hormone produced by the kidneys
EPO stimulates the bone marrow to produce red blood cells
Therefore in CKD, less EPO is made, therefore less RBCs, leading to renal anaemia.
treatment for erythropoietin?
Multiple treatment options known as erythropoietin stimulating agents (ESA)
- Eprex: recombinant human EPO
- Aranesp: novel erythropoiesis stimulating protein; longer t1/2 than Eprex
- Mircera: longest t1/2 that provides continuous activity
What is dyslipidemia, treatment?
clinical complication of CKD, abnormal lipid metabolism. High rate of cardiovascular disease in patients with CKD
NICE: atorvastatin 20mg OD
