Aspect Of Haemodialysis In The Treatment Of Renal Failure

The haemodialysis apparatus consists of medicine (which houses the dialysate composition and delivery systems) the dialyser (artificial kidney) the blood delivery system and water purification equipment.


The dialyser provides interface for the exchange of diffusible solution between the blood and dialysate compartments within the dialyser. Two forms of dialysers are in use, namely, the hollow fibre and parallel plate. The hollow fibre dialyser is more common type and has the advantage s of smaller priming volume and ease of refuse. The semi permeable membrane providing the exchange is of four categories, namely; cellulose (e.g. cuprophane), substituted cellulose (e.g. cellulose acetate), cello-synthetic and synthetic (e.g. polysulphone, polyacrylonitile).

While the new synthetic membranes are more expensive they offer the best bio-compatibility while the un-substituted cellulosoic membrane is bio- incompatible eliciting complement activation.

Dialyser reuse not only reduces the cost of each dialyser but also may inadvertently reduce complement activation and the first use syndrome.


The dialysis machine forms the dialysate using the water and preformed concentrate. The dialysis concentrate employs either the acetate or bicarbonate buffer system which when mixed with the water constitutes the dialysate, the bicarbonate buffer though more expensive is more tolerable than acetate. The water for dialysis must be treated by filtration through activated charcoal, softening, deionization and reverse osmosis in other to effect decontamination from chemical and microbiological agents. The composition of the dialysate is shown on the table below:

Table 1: Concentration of solute in a Dialysate

SoluteConcentration mmol/L
Sodium135 – 145
Potassium0 – 4.0
Chloride99 – 101
Calcium1.0 – 1.5
Magnesium0.25 – 0.35
Glucose0 – 10
Acetate25 – 40
Bicarbonate35 – 40


Patients with renal failure have varying degree of loss of renal function manifesting as decreased glomeruler filtration rate with retention of nitrogenous waste products in the blood. While the forms of renal impairment may be asymptomatic requiring only conservative methods of treatment, patient with advanced renal failure require renal replacement therapy. The available type of renal replacement therapy includes dialysis, Continuous Forms of Renal Replacement Therapy (CRRT) and transplantation. Whereas the patient with acute renal failure (ARF) are managed mostly conservatively, some will require temporary dialysis in other to prevent life threatening effects of complications of ARF and support life until renal failure reverses. On the contrary, patients with End Stage Renal Disease (ESRD), the most advance stage of chronic renal failure will have to be supported indefinitely with dialysis until they can undergo renal transplantation; which is not a treatment option for ARF.

Dialysis treatment can either be by haemodialysis (home or centre based) or peritoneal dialysis can choose between continuous cyclic peritoneal dialysis, and continuous ambulatory peritoneal dialysis.

Continuous renal replacement therapies like the haemodialysis are extra corporeal technique for treating renal failure and they include continuous arterio-venous (a-v), veno-venous (v-v) haemodia-filtration continuous a-v/v-v haemo-filtration. CRRT and haemo-perfusion are preferred over haemodialysis in acutely and haemodynamically unstable patients. Vascular access is also less problematic in CRRT. In haemoperfusion, blood is passed through cartridge. It is particularly useful in acute poisoning with protein bound drugs and poison.


 A successful haemodialysis treatment requires a properly functioning vascular access, which may be temporary or permanent. The temporary access involves the insertion of venous catheters (as single or double luemen) into the large vein e.g. subclavian, internal jugular or femoral veins or the construction of A-V shunts with the Scribner shunt from an artery to a vein. The permanent vascular preferred for long-term haemodialysis are either A-V fistula (e.g. Cimino Breschia) or A-V graft.


 The absolute indication for commencing dialysis include the presence of the ureamic syndrome (anorexia, nausea, vomiting, pericarditis, cardiac temponade, asterixis confusion, comma etc) acute haemodialysis is anlso indicated in patients with drug poisoning hyperkalaemia in excess of 6.5µmol per litre and fluid over load. Acidosis resistant to medical treatment will benefit from haemodialysis. Patient with chronic renal failure may delay the onset of symptoms of uraemia by vigorous protein restriction but this is at the price of developing malnutrition, which is associated with increased morbidity and mortality. It is recommended that dialysis should be initiated once creatinine clearance falls to 10ml/min per 1.73 metre square body surface.


The dose of haemodialysis is determined by the duration of treatment, solute clearance of dialyser, and the type of membrane employed. There is evidence suggesting improved patient survival by increasing the duration of dialysis beyond the average 3-4 hrs, thrice weekly treatment commonly prescribed worldwide. Adequate dialysis determined by urea reduction ration greater than 70% and urea kinetic modelling Kt/V greater than 1.2 is associated with reduced morbidity (including anaemia and malnutrition) improved quality of life and reduced mortality of patients on chronic haemodialysis {K-urea clearance rate (sum of dialysis and renal clearance of urea) V-Urea distribution volume, t-time spent on dialysis}.


The most frequent encountered complication during haemodialysis is hypotension. The risk of hypotension may be related to excessive ultra-filtration, a large extra corporeal circulation, automatic neuropathy and food indigestion, impaired cardiac reverse, use of anti-hypertensive drugs prior to the dialysis session and use of warm dialysis. Bicarbonate dialysis is likely that acetate to precipitate hypotension. Repeated episode of hypotension are deleterious to the preservation of the renal reserve of the patient. The underlying cause of the hypotension should be identified and corrected, but emergency measures will include infusion of saline and reducing ultra-filtration.

Muscle cramps occurring during dialysis may be related to excessive fluid removal, hypotension or use off dialysate of low sodium content, avoid excessive ultra-filtration and administration of quinine sulphate.

Nausea and vomiting occur more frequently during acetate dialysis than bicarbonate dialysis vomiting and may be associated with hypotension or may be an early sign of the disequilibrium syndrome. Hypotension should be corrected and an antiemetic administered.

The first use syndrome type A is believed to be an anaphylactoid response to the ethylene oxide employed as a sterilizing agent in new dialysers manifesting as dyspnoea and urticaria. The type B is non-specific with symptoms of chest and back pains.

Dysequilibrium can occur during or soon after dialysis manifesting as nausea, headache, restlessness and seizures. It is thought to be as a result of cerebral edema precipitated by the rapid clearance of solute from the plasma during dialysis thereby leaving the brain cells hypertonic to plasma necessitating the brain cells to accumulate water. Rapid pH chages brought about by dialysis have also been implicated.

Avoiding rapid solute clearance, use of high sodium high glucose content dialysate, bets prevents dysequilibrium. Mannitol may be of benefit in treating severe dysequlibrim.

Other acute complications of haemodialysis include arrhythmias, haemorrhage, haemolysis, and air embolism. Chronic complications of haemodialysis include the increased cardiovascular mortality when compared to patients on peritoneal dialysis. Myocardial infarction in these patients may be associated with uncontrolled hypertension, hyperlipidemia, coronary calcification and hyperhomocysteinaemia. Dialysis dementiacan occur in patients on long-term haemodialysis with poorly treated water causing aluminium toxicity.

Dialysis amyloidosis can manifest as dialysis arthropathy, carpal tunnel syndrome, amyloid associated bone disease and gastro-intestinal bleeding. Haemodialysis with cellulosonic membranes fails to clear B-2 microglobin. This coupled with complement activation, which leads to increased production of the protein are the underlying causes of dialysis related amyloidosis.


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