CKD Flashcards
Define Chronic Kidney Disease
abnormal kidney structure and/or function which is present for >3 months
Name 3 congenital causes of CKD
- polycystic kidney disease
- medullary cystic disease
- congenital obstructive uropathy
Name glomerular causes of CKD
primary glomerular disease - FSGS
secondary glomerular disease - lupus, amyloidosis, accelerated HTN, haemolytic uraemic syndrome, sickle cell disease, diabetic glomerulosclerosis
Name 3 vascular causes of CKD
- hypertensive nephrosclerosis
- renovascular disease
- diabetic nephropathy
Which are the 2 most common causes of CKD?
- Diabetes
2. Hypertension
in which ethnic group is CKD more common?
Afro-caribbeans
Describe the stages of CKD
- kidney damage with normal/increased GFR (≥90)
- GFR 89-60
3a. GFR 59-45
3b. GFR 44-30 - GFR 29-15
5 - GFR ≤15
What is end stage kidney disease defined by (symptoms or GFR)?
Symptoms!
When do symptoms in CKD typically appear?
when there is significant uraemia (>40mmol/L)
Describe symptoms of uraemia
- malaise
- characteristic metallic taste
- anorexia and weight loss
- mild cognitive decline > confusion > myoclonic jerks > seizure > coma
- insomnia
- impaired concentrating ability > polyuria and nocturia
- pruritis
- parasthesia
- bone pain
- salt and water retention
- hypertension
- anaemia
Describe clinical signs indicative of uraemia
- short stature (if hx of CKD in childhood)
- pallor
- increased photosensitive pigmentation
- signs of fluid overload
- glove and stocking sensity loss
- encephalopathic flap
Which tests are useful in the investigation of CKD
- urinalysis
- urine microscopy
- urine biochemistry (urine osmilarity; electrophoresis (paraprotein)
- serum biochemistry (U&E, eGFR, creatinine, blood glucose and HbA1c)
- imaging
- USS to establish renal size and exclude hydronephrosis
- CT for investigation of calculi and obstruction
- MR - vascular disease
- Renal biopsy
Name complications of CKD
- Anaemia
- CKD bone disorder
- Cardiovascular disease
- Pruritis
- Gout
- Hyperparathyroidism
Why does anaemia occur in CKD?
- EPO deficiency
- retention of Bone Marrow toxins
- red cells have a shortened lifespan in uraemia
Describe the pathophysiology of CKD bone disorder
- impaired production of active Vitamin D > reduced absorption of calcium from GI tract and kidney filtrate
- phosphate accumulation due to impaired renal excretion
- PTH released in order to increase serum calcium - increased osteoclast activation
Why is the risk of CVD raised in CKD?
- Hypertension
- Diabetes (commonest cause of CKD)
- uraemia can lead to dyslipidaemia
- raised serum Ca and phosphate + uraemia increases risk of coronary artery calcification
Describe how CKD can cause secondary and tertiary hyperparathyroisism
- Lack of vitamin D conversion and inadequate phosphate excretion leads to increased PTH secretion to promote renal excretion of phosphate (but has no effect)
- raised PTH unable to increase phosphate excretion, but it stimulates osteoclasts, raising Ca and phosphate further - positive feedback leading to more PTH secretion
- Eventually, secondary hyperparathyroidism can lead to tertiary hyperparathyroidism
What are the general measures used to manage CKD
- address any underlying modifiable cause
- address CV risk factors
- avoid nephrotoxic drugs
- reduce dose of any renally excreted drugs
- salt restriction
- Exogenous EPO and calcium suppliments
- restrict dietary phosphate and give phosphate binder
- calcium receptor analogue - ciacalet
- sodium bicarbonate
- restrict dietary potassium
What is used as renoprotection for CKD
- maintain BP <120/80
- achieve proteinuria <0.3
- ACEi/ARBs
- must monitor K+
- loop/thiazide diuretic
- statins
- good diabetic control
What factors should warrant consideration for starting dialysis
- eGFR 5-7
- inability to control volume status leading to fluid overload
- inability to control BP
- acid-base/electrolyte abnormalities
- cognitive impairment/impact of symptoms of uraemia on daily living
Which nephrotoxic drugs should be avoided in CKD?
- tetracyclines
- gentamycin
- NSAIDs
- potassium sparing agents
