- CRF
- CRF
- GFR has fallen to 10% of normal function (20ml/min)
- ESRD
- GFR falls below 5% of normal function (10ml/min)
- Causes include DM, HT, GN, PCKD
- Sodium balance
- CRF can be associated with Na⁺ retention, depletion or normal Na⁺ balance and is influenced by diuretic use
- Most have Na⁺ and water retention while extra cellular fluid remains isotonic.
- Potassium balance
- Adaptive processes increase K⁺ secretion in the distal nephron and also in the gut
- In acidosis, the serum K⁺ will rise 0.5mmol/L for every 0.1 unit decrease in pH
- Acidosis
- A common feature of ESRD. There is inability to excrete protons and buffers and there is little reserve to counter acute acidosis caused by sepsis
- Calcium, PO4ˉ, PTH and osteodystrophy
- Plasma concentration of Ca²⁺ is reduced in CRF. Renal production of calcitrol (1,25-(OH)2D3) declines causing decreased intestinal absorption of calcium. Phosphate excretion is reduced and as concentrations increase, calcium phosphate is deposited in soft tissues, further lowering Ca²⁺. The low Ca²⁺ stimulates PTH leading to secondary hyperparathyroidism, which increases osteoclasts activity
- Normochromic normocytic anaemia is common due to low epo and uraemia reduced red cell life. Chronic GI loss is also a problem. Compensatory increases in 2,3 DPG moves the curve to the right
- Coagulopathy occurs despite normal PT, APTT and platelet numbers. It is multifactorial but rapid improvements in coagulation require the use of cryo, DDAVP (enhances VWf release)
- Wait about 4-6hrs post dialysis for fluid compartment equilibration and heparin to clear
- Pharmacokinetics
- Hypoalbuminaemia and acidosis increase free drug availability of highly bound drugs.
- Elimination of ionised or water soluble drugs is reduced
- The loading dose duration of action depends more on redistribution
- Lipid soluble drugs metabolised in the liver can have active water soluble metabolizes eg morphine, or significant S/E eg (nor-pethadine)
- Metabolism of sevoflurane produces fluoride ions and their use in prolonged cases should be avoided
- Excretion of anticholinergics and Anticholinesterases is prolonged
- Duration of action of LA is reduced and doses should be reduced by 25% due to reduced protein binding and lower seizure threshold
- Endocrine
- Glucose tolerance is impaired but the insulin required is less due to reduced metabolism by the failing kidney.
- CNS
- Myoclonus, encephalopathy, seizures, personality changes and peripheral neuropathy can all occur. Dialysis dementia can occur after years of dialysis due to aluminium toxicity.
- Gut
- Anorexia, nausea and vomiting contributes to malnutrition. Delayed gastric emptying. PUD is common.
- Immune system
- Sepsis is the leading cause of death due to inhibition of cell mediated immunity
- CV and pulmonary changes
- HT occurs in 80% but less so in sodium wasting nephropathies such as PCKD. HT may need Rx with β-blockers, ACE(I), α-antagonists and vasodilators.
- CVD is a common cause of mortality due to decreased triglyceride clearance, HT, fluid overload.
- Decreases in surfactant leads to atelectasis
- CEACCP
Link:ceaccp.oxfordjournals.org/content/3/5/130.full.pdf