week 2- Clinical manifestations & treatment of CKD+ Dialysis & Nephrotoxicity Flashcards
what are the clinical manifestations for CKD?
-urinary symptoms
-Proteinuria
-fluid retention
-uraemia
-anaemia
-electrolyte disturbance
-Hypertension
-Muscle dysfunction
-Renal bone disease (renal
osteodystrophy)
what are the urinary symptoms in CKD?
– Very early stages only – Polyuria – Medullary damage – Osmotic effect of urea (>40 mmol/l) – Loss of ability to concentrate urine – Nocturia
what are the Proteinuria symptoms in CKD?
-IF PROEIN IS FOUND IN URINE 24HR SAMPLE IS COLLETED. – Degree of proteinuria occurs in all CKD – Proteinuria >2g in 24 hr glomerular disease – >5g in 24hrs severe disease = Nephrotic Syndrome
what are the fluid retention symptoms in CKD?
– As CKD progresses, GFR decrease very low levels – Kidneys unable to excrete Na+ & water – leading to peripheral & pulmonary oedema & ascites – 80% of CKD patients will have volume dependent HT
what are the uraemia symptoms in CKD?
-greater than 50mmol/l – Measurement of level of “toxins” in blood – Often used to decide when to start dialysis – Symptoms: • anorexia • N&V • constipation • foul taste • skin discoloration (gets deposited in the skin) • pruritis
what are the anaemia symptoms in CKD?
– Due to failure of kidney to produce the hormone erythropoetin – Regulates red blood cell proliferation in the bone marrow – Symptoms: • fatigue & lethargy • breathlessness • angina
what are the Electrolyte
disturbances symptoms in CKD?
– Hyperkalaemia • due to kidneys inability to remove K+ • >7mmol/l leading to medical emergency & risk of cardiac arrest – Acidosis • due to kidneys inability to remove H+ • leads to decrease plasma bicarbonate
what are the hypertension symptoms in CKD?
-80 of ppl with CKD have hypertension – Vast majority of CKD patients will have HT – Mainly due to circulatory volume expansion due to Na+ retention – HT can also increase the rate of decline of renal function
what are the Muscle dysfunction symptoms in CKD?
– Cramps & restless legs – Especially at night – General nutritional deficiencies & electrolyte disturbances
what are the different processes for Renal bone disease (renal
osteodystrophy)?
– Cholecalciferol (inactive precursor of Vitamin D)
absorbed from GI tract & produced in skin due to
sunlight
– Production of active vitamin D - 1,25-
dihydroxycholecalciferol (calcitriol) requires
hydroxylation in 25 position by liver and 1
position in kidney (does not occur in renal
failure)
– lead to Vitamin D deficiency
– lead to Defective bone mineralisation
– lead to Osteomalacia (bone softening)
– low Vitamin D
– leads to low calcium absorption from gut
– leading to Hypocalcaemia
–Hypocalcaemia due to lack of vitamin D is made worse by Hyperphosphataemia due to failure to excrete phosphate via kidneys
– leading to Hypocalcaemia because phosphate
ions sequester calcium as calcium phosphate in bones which would decrease calcium levels even more
– Hyperphosphataemia leading to pruritis (deposition of the phosphates)
– Metabolism of calcium & phosphate
controlled by parathyroid hormone (PTH)
produced by the parathyroid glands
– Kidney unable to respond to PTH by increased renal
calcium reabsorption
– leading persistent hyperparathyroidism &
hyperplasia of thyroid glands (may require
removal)
– Hyperparathyroidism leading disturbance in
normal bone architecture
– leading Osteosclerosis (bone hardening)
– leading to Bone pain
what is the treating of chronic kidney disease?
there are two broad areas
-conservative= diet and drugs (hat would treat the manifestations)
aim is to treat symptoms and decrease the decline in renal failure
-renal replacement therapy= dialysis and transplantation
what is often the treatment for end stage renal failure?
the 3 D’s
diet, drugs and dialysis
What is the propose of drugs, dialysis and transplant?
- drugs used to treat the manifestations and symptoms
- dialysis and transplant is to cure the underlying cause
what kind of drugs are used to treat hypertension in CKD?
- Diuretics
- ß- blockers
- Calcium channel blockers
- ACEIs
- Angiotensin II inhibitors
- alpha - blockers
- Vasodilators
what are some main facts about diuretcis?
– Only LOOPs (e.g. furosemide) – Only occasionally used for HT - mainly for oedema – Thiazides (except metolozone) ineffective at CrCl<25ml/min – Potassium sparing risk of hyperkalaemia
what are some main facts about beta-blocker?
– Cardioselective – E.g. Metoprolol, atenolol – Metoprolol cleared through liver – Start with low dose and titrate up
what are some main facts about CCB?
– Can produce oedema
(especially Nifedipine)
– LEADS TO confusion with
symptoms of fluid overload
what are some main facts about ACEI’s/Angiotensin II
inhibitors?
– Can cause decline in renal function but not an issue in ESRF (although increased risk of other side-effects) – C/I: Renal artery stenosis (where blood flow to kidney relies upon Angiotensin II vasoconstriction)
what are some main facts about alpha-blocker?
– E.g. Doxazosin
– Cleared through liver
what are some main facts about vasodilators??
– E.g. Hydralazine, Minoxidil – reserved when HT inadequately controlled by others – S/E: • Reflex tachycardia (use with ß- blocker) • Fluid retention (use with diuretic) • Minoxidil leading to excess hair growth!!
what is Bp target for most patients?
<140/90
if type 1 diabetic <130/80
what is oedema as a consequence of CKD?
Mainly pulmonary • Best controlled with dialysis • Loop diuretics in pre-dialysis stage • Furosemide - up to 2g daily (500mg tablet) • Fluid & sodium restriction • Stop when dialysis starts
what is hyperkalaemia as a consequence of CKD?
• >7mmol/l dialysis imperative due to risk of cardiac arrest
• Emergency treatment:
– Calcium gluconate [10ml 10% iv over 5-10mins]
– Improves myocardial stability
– Insulin (20 IU soluble) + Glucose (50ml 50% iv)
– Insulin stimulates intracellular K+ uptake
– Glucose to prevent hypoglycaemia
– Calcium Resonium [15-30g powder orally or
enema]
– ion exchange resin binds to K+ in GI tract &
releases Ca2+ in exchange
– Always give with lactulose 10ml for each 15g dose
as very constipating
