Chronic Kidney Disease Flashcards
What is chronic kidney disease?
Permanent + progressive kidney damage - manifested by abnormal albumin excretion or decreased kidney function that persists for more than 3 months
Why is chronic kidney disease normally irreversible?
Renal tissue is replaced by extracellular matrix in response to damage
How is chronic kidney disease measured?
eGFR
Primary causes of chronic kidney disease
Directly affect kidneys
- Polycystic kidney disease
- Acute tubular necrosis
- Recurrent pyelonephritis (regular infections)
- Glomerulonephritis
Secondary causes of chronic kidney disease
Diabetes mellitus (diabetes nephropathy)
Hypertension
Renovascular disease
Autoimmune
Presentation of CKD
- most are asymptomatic
- oedema
- foamy urine
- pruritus
- hypertension
- loss of appetite
- pallor (due to anaemia)
Investigations of CKD
- eGFR
- ACR
- urinedipstick + microscopy
- USS KUB
- HbA1c
- blood pressure
- lipid profile
- bone profile
What investigations could you do to work out the cause of CKD?
- urinalysis (protein/blood)
- USS KUB
- kidney biopsy
- HbA1c - diabetes
- ANCA - vasculitis
- anti-GBM + ANA - lupus
- blood pressure
How do you stage chronic kidney disease?
using eGFR
- stage 1: >90
- stage 2: 60-89
- stage 3a: 45-59
- stage 3b: 30-44
- stage 4: 15-29
- stage 5: <15 (kidney failure)
How do you stage chronic kidney disease using ACR?
Albumin-creatinine ratio
- stage 1: <3
- stage 2: 3-30
- stage 3: >30
Why are the kidneys smaller in kidney damage?
Loss of kidney tissue (cortex)
Management of CKD
- treat underlying disease
- treat complications e.g. EPO, dietary advice, vitamin replacement
- ACEi/ARBs - hypertension + proteinurai
- offer statin to reduce CVD risk
- weight loss advice + exercise
- smoking cessation
- plan for future - discuss options for if they reach ESRF (RRT)
How do we control blood pressure in chronic kidney disease?
Patients with CKD will almost always mean hypertension
- antihypertensives e.g. ACEi, angiotensin receptor blockers
- diuretics
- fluid restriction
Complications of chronic kidney disease
- anaemia: EPO not produced by kidneys
- fluid overload + oedema
- metabolic acidosis
- bone mineral disease: lack of active form of vit D > reduced calcium absorption
- non-bone calcification
- uraemia > uraemic pericarditis + encephalopathy
- hyperphosphatemia + hypocalcaemia (secondary hyperparathyroidism)
- hypertension
- accelerated atherosclerosis | cardiovascular disease
Why is anaemia a complication of CKD?
- decreased EPO produced by kidneys
- decreased erythropoiesis
- decreased RBC production
Treatment of anaemia in CKD
EPO injection
Iron supplements
Target Hb levels (10-12g/dL)
Why is bone mineral disease a complication of CKD?
- decreased active vitamin D
- less calcium reabsorption > lower plasma [Ca2+]
-
hypocalcaemia
. - decreased phosphate excretion
- increased plasma [PO4]
-
hyperphospatemia
. - stimulates parathyroid glands
- hyperparathyroidhormone
- increases parathyroid hormones
- increases bone resorption (bone breakdown by osteoclasts)
- bone mineral disease
Management + treatment of bone mineral disease in those with ESRD
- phosphate binders to control the amount of phosphate in blood
- vitamin D supplements: suppresses PTH production + increases calcium absorption
- calcimimetic agents: enhances sensitivity of parathyroid gland to calcium > reducing PTH secretion
- regular monitoring of calcium, phosphate + PTH levels
What is uraemia?
Raised levels of urea in blood
Symptoms of ureamia
- muscle cramps
- itch
- stroke
- swelling
- high BP
- nausea + vomiting
- anaemia
- easy bleeding
- constipation + diarrhoea
What is end stage renal failure?
When death is likely without renal replacement therapy
eGFR <15
When is renal replacement therapy needed?
When renal function declines to a level no longer adequate to support health
eGFR 8-10
Types of renal replacement therapy
Haemodialysis
Peritoneal dialysis
Renal transplant
Relationship between calcium and phosphate
Inversely proportional
If one goes up, the other goes down
How does renal function affect calcium and phosphate levels?
What does this cause?
- decreased active vitamin D
- less calcium reabsorption > lower plasma [Ca2+]
-
hypocalcaemia
. - decreased phosphate excretion
- increased plasma [PO4]
-
hyperphospatemia
. - stimulates parathyroid glands
- hyperparathyroidhormone
- increases parathyroid hormones
- increases bone resorption
- bone mineral disease
Describe hyperfiltration in diabetes mellitus
- blood is filtered
- blood glucose remains elevated as the SGLT2 transporters are all occupied
- sodium reabsorbed coupled with glucose
- less Na+ delivered to macula densa
- RAAS is activated
- more Na+ absorbed > increased BP
- afferent arteriole vasodilation
- increased GFR > increased glomerular capillaries
What do you want the normal systolic BP to be in a patient with a normal albumin:creatinine ratio compared to a patient with a high AC ratio?
Normal: <140
High: <130
Why is uraemia a complication of CKD?
Damage to filtration > can’t excrete in urine properly
Presentation of polycystic kidney disease
- 30-40 years
- hypertension
- loin pain
- haematuria
- bilateral palpable kidneys
- large kidneys with yellow fluid filled cysts
- recurrent UTIs
Inheritance of polycystic kidney disease
Autosomal dominant (more common)
Autosomal recessive
How does polycystic kidney disease present with macroscopic haematuria?
- cysts can form in childhood
- cysts fill with blood following trauma
- cysts burst > haematuria + abdominal pain
What can polycystic disease cause?
Hypertension
CKD
How does high levels of PTH cause bone resorption?
Activation of oestoclasts causes increased bone breakdown
Extra renal manifestations of autosomal dominant polycystic kidney disease
- mitral regurgitation
- cerebral aneurysms
- colonic diverticula
- hepatic, splenic, pancreatic, ovarian + prostatic cysts
When is autosomal recessive polycystic kidney disease often noticed?
On antenatal scans with oligohydramnios
Management of polycystic kidney disease
- antihypertensives
- analgesia
- antibiotics
- drainage by aspiration or surgery
- dialysis or renal transplant for end stage renal failure
- avoid contact sports to reduce risk of rupture
- avoid NSAIDs + anticoagulants
- MR angiography to screen for cerebral aneurysms
What drug can be used in management of autosomal dominant polycystic kidney disease + why?
tolvaptan - vasopressin receptor antagonist
- slows development of cysts + progression of renal failure
What should people with polycystic kidney disease avoid?
- contact sports due to risk of rupture
- NSAIDs
- anticoagulants
Follow ups for CKD
- frequency of monitoring depends on the stage of disease + individual risk factors for progression
- measure GFR + ACR
- FBC
- bone profile
