10.5 Key Concepts in Chronic Kidney Disease (CKD) Flashcards
Is CKD a disease?
No. it is a state, a syndrome, just like AKI/ARF
What is the diagnostic criteria for CKD/the minimum timeframe?
- GFR less than 60 for >= 3 months
OR: - Signs of kidney disease (albuminuria, haematuria of no other cause, pathological abnormalities) for >=3 months
It is estimated that __% of people with CKD know they have it
10% (!!!!)
List, from more to less common, some causes of CKD
- Diabetes
- Glomerulonpehritis (2° to IgA nephropathy, nephrotic syndrome, lupus etc.)
- Hypertension
- Polycystic kidney disease
- Cancer
What are some common presenting symptoms of CKD? What is an important qualifier to this?
- Common symptoms include nausea/vomiting (metabolic imbalance), oedema (low albumin), itchy skin (uraemia), SOB (acidosis + hypoalbuminuria), changes to urination
- However, we are thought to be able to lose up to 90% kidney function without experiencing symptoms, so patients may be asymptomatic
Predialysis, non-lifestyle treatment methods for CKD are…
- BP control (reduce damage)
- Reduce proteinuria
- Smoking cessation (reduce damage)
- Correct acidosis (symptomatic relief)
- Glycaemic control (prevent damage/UTI, which would worsen it)
- Treat any complications of kidney failure (symptomatic relief)
Lifestyle modifications for CKD include…
- Dietary sodium restriction (prevent fluid retention)
- Weight reduction
- Smoking cessation
- Avoid over the counter NSAIDs
What therapies might we consider in end-stage renal disease?
- Transplantation (preferred for QOL)
- Dialysis
Explain, in terms of calcium and phosphate, how CKD affects the bones, and what the consequence of this is called
- Decreased GFR means phosphate is retained in blood
- High phosphate suppresses vit D3 production
- This causes less calcium to be absorbed, thus weakening the bones
- This is called osteodystrophy
List 6 clinical consequences of CKD
- Anaemia (decreased EPO, uraemia kills RBCs faster)
- Hypertension ()dec perfusion compensation by JGA)
- Chronic uraemia (decreased GFR)
- Metabolic acidosis (decreased acid clearance)
- Hyperkalaemia (decreased potassium clearance
- Osteodystrophy (high phosate [dec GFR] suppresses Vit D3)
What are some clinical consequences of hyperkalaemia?
- Arrythmias (disrupted cardiomyocyte resting membrane potential)
- Muscle weakness (lowered membrane potential)
- Neurologic signs such as confusion (altered neuron membrane potential)
Differences between CKD and ARF/AKI
- AKI is more likely reversible
- AKI treatment is to reverse cause and support kidneys, CKD treatment is to slow damage as much as possible
What are the broad principles of management of CKD?
- Manage hypertension
- Manage anaemia (such as recombinant EPO)
- Improve hypocalcaemia and hyperphosphataemia
- Dietary restrictions (decreased sodium, weight loss etc.)
- Consider transplant/dialysis in end-stage patients
What pathologic changes can chronic hypertension creates in the kidneys? What is this called, as a unified disease process?
- Ateries: arteriosclerosis, wall thickeining, lumen narrowing, smc hyperplasia
- Glomerulus: glomerulosclerosis
- Tubulointerstitial: interstitial fibrosis
(Collectively, this is called benign nephrosclerosis)
What pathologic changes can malignant hypertension creates in the kidneys? What is this called, as a unified disease process?
- Arteries: acute necorsis due to extreme endothelial damage, “onion skinning” concentric, latered thickening of the arterioles, narrowed lumen & dec perfusion
- Glomerulus: necrosis, microthrombi formation, ischaemic glomerulosclerosis
- Tubules: acute tubular necrosis
(Collectively, this can be referred to as malignant nephrosclerosis)