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
what is oedema, management?
Occurs due to the kidneys decreased ability to maintain sodium/fluid balance in CKD
- Restrict dietary sodium
- Restrict fluid intake
- Offload the fluid with diuretic therapy: thiazides less effective if CrCl <20ml/min; loop diuretics usually used in higher doses (e.g. furosemide)
- if medication ineffective? dialysis
- beware of medications that need a high fluid volume e.g. those with a high sodium or water content
what is hyperkalaemia, management?
CKD patients are less able to excrete potassium and can develop hyperkalaemia
Non-pharmacological options: potassium
restriction
Pharmacological options:
- Calcium resonium PO TDS or Lokelma
- IV calcium gluconate (stabilise heart)
- Actrapid insulin (push K+ into cells)
- Not working? Dialysis = last resort
what is severe hyperkalaemia, management?
Severe hyperkalaemia is an emergency! Firstly needs IV calcium gluconate to stabilise the cardiac tissue. Then insulin can be used to push potassium from the blood into the cells. If this still doesn’t work, then last resort would be to use dialysis.
management of hypertension?
Target blood pressure: 140/90 mm/Hg
Treatment usually with ACEI or ARB; titrate to maximum tolerated dose RENOPROTECTIVE IN CKD
If ACEI or ARB unsuitable then doxazosin is a common option
what is mineral and bone disorder?
Hormones & minerals are essential to grow and rebuild bones
The kidneys play an essential role in this by balancing levels of phosphorus and calcium in the blood
The four constituents involved in MBD are:
Calcitriol (active vitamin D)
Calcium
Phosphorus (Phosphate)
Parathyroid hormone
what is the significance of calcitriol?
Healthy kidneys activate a form of vitamin D into calcitriol, the active form of the vitamin
Calcitriol maintains blood calcium levels
Healthy kidneys also remove excess phosphorus/phosphate
what happens to calcitriol in CKD?
- production of calcitriol stops
- this causes a reduction of calcium in the blood
- phosphorus/phosphate levels in the blood rise
=> vitamin D deficiency + hyperphosphataemia + hypocalcaemia
the process of hyperparathyroidism
vitamin D deficiency + hyperphosphataemia + hypocalcaemia = hyperparathyroidism
The high phosphate in CKD then stimulates calcium to be released from the bones.
The low calcium also activates parathyroid hormone release (PTH) which stimulates calcium to also be released from the bones to try to correct the low calcium levels.
Therefore the high phosphate and low calcium with high PTH leads to the breakdown of bones.
Happens slowly over time and asymptomatic, so may not seen the bone changes for many years.
CKD patients may end up with hyperparathyroidism too due to the continuous low calcium activating the PTH to be released to correct the low calcium.
treatment of MBD
Calcitriol deficiency
- alfacalcidol (activated vit D)
Hyperphosphataemia
- phosphate binders e.g. sevelamer or lanthanum carbonate & restricted phosphate diet
Hyperparathyroidism
- if we correct Calcitriol deficiency
and Hyperphosphatemia, do you think that PTH release stops?
High parathyroid – in theory, correcting the first two issues should lead to normal calcium levels, but since it has been constantly stimulated, there are now issues where PTH release doesn’t stop anymore
describe and give treatment of Hyperparathyroidism
?
continued stimulation of the parathyroid gland results in it becoming enlarged and continues to release PTH despite correcting vitamin D/phosphate levels
- continued PTH levels will still result in hypercalcaemia
cinacalcet or parathyroidectomy
Uraemia in CKD.
In CKD the kidneys are less able to excrete waste products such as urea and other nitrogenous compounds
Build up of urea – can lead to encephalopathy or coma.
No drugs to treat this, only option is dialysis to remove waste products.
summary of typical CKD medication regimen
Acidosis -> sodium bicarbonate 1g TDS
Renal anaemia -> ferrous fumarate 210mg OD
Renal anaemia -> S/C or IV ESA
Dyslipiademia -> atorvastatin 20mg ON
Fluid overload -> diuretics, usually high doses of furosemide (BD)
Hyperkalaemia -> calcium resonium TDS / lokelma as hospital txt
Hypertension -> antihypertensive e.g. ramipril OM or doxazosin OM
Vitamin D deficiency -> alfacalcidol up to OD
Hyperphosphataemia -> sevelamer (or lanthanum) TDS with meals
Hyperparathyroidism -> cinacalcet OD
what are some factors to consider with diabetes and CKD?
Diabetes and CKD are often seen together due to nephropathy in diabetics (microvascular complication).
In a pt with normal kidney function, your first line drug is metformin, but if you have CKD, metformin in contraindicated if CrCL <30ml/min due to risk of lactic acidosis.
Renal clearance of drugs is different so need to be careful with what you can recommend, for example gliclazide as a second line may need to be started at much lower doses than usual.
what are some factors to consider with hypertension and CKD
ACEIs / ARBs are renoprotection in CKD but nephrotoxic in AKI
Any other options for hypertension?
Calcium channel blockers are safe in renal failure BUT they cause/exacerbate fluid overload
what are some factors to consider with Pain management and CKD
Paracetamol is usually still fine but what if we’re following the WHO ladder?
Codeine, tramadol, morphine -> accumulate in renal failure!
Other options? Oxycodone, fentanyl patch, buprenorphine patch
