Dialysis Solutions

Dialysis Solutions

Drug Nomenclature

Date of monograph revision: 09-May-1997; 17-Jun-1998; 28-Sep-1999; 31-Oct-2001; 29-Nov-2003; 18-May-2004; 21-Apr-2005; 27-Apr-2005; 24-May-2006; (last modified: 04-Jun-2006)
Pharmacopoeias:

In Eur. (see Go to European Pharmacopoeia Convention Signatories), which includes separate monographs for solutions for haemodialysis, haemofiltration and haemodiafiltration, and peritoneal dialysis.

Dialysis and Haemofiltration

Dialysis and filtration solutions are solutions of electrolytes formulated in concentrations similar to those of extracellular fluid or plasma. They always contain sodium and chloride and bicarbonate or a bicarbonate precursor. In addition, they often contain calcium and magnesium, and rarely potassium. Glucose may be added as an osmotic agent. These solutions allow the removal of water and metabolites and the replacement of electrolytes.

In haemodialysis, the exchange of ions between the solution and the patient's blood is made across a semi-permeable membrane, primarily by diffusion. Excess fluid is removed by ultrafiltration achieved by a pressure gradient. Membranes are either derived from cellulose (e.g. cuprophane) or are synthetic. Bicarbonate rather than a bicarbonate precursor is increasingly preferred as the bicarbonate source in haemodialysis since the problems of precipitation of calcium and magnesium have been overcome by changes in dialysis technique. Acetate is still used in some dialysers, but is thought to have vasodilator and cardiodepressant actions, and may not be converted to bicarbonate fast enough for high-flux haemodialysis or in patients with liver disease. Haemodialysis solutions are provided in a sterile concentrated form for dilution with water before use; this water need not be sterile.

In peritoneal dialysis, the exchange is made across the membranes of the peritoneal cavity primarily by diffusion. Excess fluid is removed by ultrafiltration achieved by the use of osmotic agents such as glucose. The problems of calcium bicarbonate precipitation have not yet been overcome, and lactate is generally used as the bicarbonate precursor. Peritoneal dialysis solutions must be sterile and apyrogenic.

In haemofiltration, blood is filtered rather than dialysed. Metabolites are removed by convective transport, and excess water by hydrostatic ultrafiltration. Fluid and electrolytes are replaced by direct intravenous infusion. Most haemofiltration solutions use acetate or lactate as the bicarbonate source. Haemofiltration solutions must be sterile and apyrogenic.

Adverse Effects

Adverse effects occurring during haemodialysis include nausea, vomiting, hypotension, muscle cramps, and air embolus. Effects related to vascular access include infection, thrombosis, and haemorrhage. Adverse effects occurring during haemofiltration are similar to those for haemodialysis.

The most common adverse effects associated with peritoneal dialysis include peritonitis, hernias, hyperglycaemia, protein malnutrition, and catheter complications.

Long-term complications in dialysed patients, some of which may relate to renal failure itself, include haemodialysis-related amyloidosis, acquired cystic kidney disease, and accelerated atherosclerosis. Dialysis dementia is a special hazard of aluminium overload. Long-term peritoneal dialysis results in progressive structural changes to the peritoneal membrane ultimately resulting in dialysis failure.

References.

  1. 1. Himmelfarb J. Hemodialysis complications. Am J Kidney Dis 2005; 45: 1122–31. PubMed

Aluminium overload.

Accumulation of aluminium in patients on dialysis may result in dialysis dementia, anaemia, and aluminium-related bone disease (see also Go to Adverse Effects, Treatment, and Precautions). Sources of aluminium include the water used for preparation of dialysis fluids and aluminium-containing phosphate binders used in treating renal osteodystrophy (Go to Renal osteodystrophy). It is therefore important that water used for the preparation of dialysis fluids has a low aluminium concentration; Ph. Eur. 5.5 specifies a limit for aluminium of 10 micrograms/litre. Non-aluminium-containing phosphate binders such as calcium acetate or calcium carbonate may be preferred for long-term therapy. Aluminium overload in patients on dialysis has been treated with desferrioxamine (Go to Aluminium overload.).

Copper toxicity.

Liver and haematological toxicity has occurred as a result of absorption of copper from dialysis fluids (Go to Adverse Effects and Treatment).

Haemodialysis-induced cramp.

Muscle cramps commonly occur during haemodialysis procedures, and are often associated with hypotension as a result of inappropriate volume removal. In addition, they may be exacerbated by cellulose-derived membranes or the use of acetate as a bicarbonate precursor. Sodium chloride tablets (Go to Uses and Administration), intravenous sodium chloride 0.9%, intravenous hypertonic glucose (Go to Haemodialysis-induced cramp.), and quinine (Go to Muscle spasm.) have been used in the prevention or treatment of haemodialysis-induced cramp.

Hypersensitivity.

For anaphylactic reactions associated with the use of ethylene oxide for the disinfection of dialysis equipment, see Go to Hypersensitivity..

Infections.

Patients undergoing haemodialysis are at risk of infections from microbial contamination of dialysis fluid, and from inadequate care of vascular access sites. Maximum microbial counts and limits for endotoxins have been specified for water used in dialysis fluids. Bicarbonate-based dialysis solutions are more susceptible to microbial growth than acetate-based solutions.

Peritonitis is common in patients receiving peritoneal dialysis. The risk of infection may be minimised by using disconnect systems, good aseptic technique, and by good care of catheters. Treatment of bacterial peritonitis requires intraperitoneal antibacterials, which are usually added to the dialysis fluid (see Go to Peritonitis).

Dialysis equipment should be regularly disinfected with agents such as formaldehyde (Go to Uses and Administration) or ethylene oxide (Go to Uses), but for mention of ethylene oxide anaphylactoid reactions, see Go to Hypersensitivity..

Metabolic complications.

The high concentrations of glucose in peritoneal dialysis solutions required to form an osmotic gradient can lead to weight gain, hyperglycaemia, hyperlipidaemia, and increased protein loss. Alternative osmotic agents such as icodextrin (Go to Icodextrin) can be used, and amino acid-based solutions are also available.

References.

  1. 1. Burkart J. Metabolic consequences of peritoneal dialysis. Semin Dial 2004; 17: 498–504. PubMed

Precautions

Peritoneal dialysis is not appropriate for patients with abdominal sepsis, previous abdominal surgery, or severe inflammatory bowel disease.

Haemodialysis should be used with caution in patients with unstable cardiovascular disease or active bleeding. During haemodialysis and haemofiltration, heparin (see Extracorporeal Circulation, Go to Extracorporeal circulation.) or epoprostenol (Uses, Go to Uses and Administration) are required to prevent clotting of the blood in the extracorporeal circuit.

Dialysis solutions should be warmed to body temperature with dry heat because wet heat carries a risk of microbial contamination.

Interactions

The effects of dialysis and filtration procedures on drug concentrations in the body can be complex. More drug may be removed by one dialysis technique than another. In general, drugs of low molecular weight, high water solubility, low volume of distribution, low protein binding, and high renal clearance are most extensively removed by dialysis. For example, aminoglycosides are extensively removed by dialysis procedures, and extra doses may be needed to replace losses. Specific drug dosage adjustments for dialysis procedures may be used where these are known. For drugs where the effect of dialysis is unknown, it is usual to give maintenance doses after dialysis. Dialysis has been used to remove some drugs in the treatment of overdosage and poisoning (see Go to Overdosage and poisoning.).

Dialysis-induced changes in fluids and electrolytes have the potential to alter the effects of some drugs. For example, hypokalaemia predisposes to digoxin toxicity.

In patients undergoing peritoneal dialysis, drugs such as insulin and antibacterials may be added to the dialysis fluid. Consideration should be given to the possibility of adsorption of drugs onto the PVC bags.

References.

  1. 1. Aronson JK. The principles of prescribing in renal failure. Prescribers' J 1992; 32: 220–31.
  2. 2. Cotterill S. Antimicrobial prescribing in patients on haemofiltration. J Antimicrob Chemother 1995; 36: 773–80. PubMed
  3. 3. et al. Drug prescribing in renal failure: dosing guidelines for adults. 4th ed. Philadelphia: American College of Physicians, 1999.

Uses and Administration

Dialysis and filtration procedures are used in renal failure to correct electrolyte imbalance, correct fluid overload, and remove metabolites. They also have a limited role in the treatment of overdosage and poisoning. The two main techniques are haemodialysis and peritoneal dialysis; haemofiltration is used less frequently. The choice of technique will depend on the condition to be treated, the clinical state of the patient, patient preference, and availability.

Haemodialysis is more efficient than peritoneal dialysis at clearing small molecules such as urea, whereas peritoneal dialysis may be better at clearing larger molecules. Haemodialysis is considered to be less physiological as it alternates periods of high clearance with periods of no clearance.

Haemodialysis is usually performed intermittently (often 3 times a week); a typical session takes 3 to 5 hours. More recently high-flux dialysers have been developed which have reduced the time required for dialysis sessions.

Peritoneal dialysis may be performed continuously or intermittently. Continuous ambulatory peritoneal dialysis (CAPD) is the most commonly used technique. Patients remain mobile, except during exchanges, and can carry out the procedure themselves. There is always dialysis solution in the peritoneal cavity, and this is drained and replaced 3 to 5 times daily. Continuous cycle peritoneal dialysis (CCPD) is similar, except that exchanges are carried out automatically overnight, and patients do not have to carry out any exchanges during the day. Intermittent peritoneal dialysis (IPD) requires the patient to be connected to a dialysis machine for 12 to 24 hours 2 to 4 times a week. During this time, dialysis solution is pumped into and out of the peritoneal cavity, with a dwell time of about 10 to 20 minutes.

Haemofiltration is usually performed as a continuous technique and, as it is not portable, its principal use is in intensive care units. It may also be used intermittently as an adjunct to haemodialysis in patients with excess fluid weight gain. Continuous arteriovenous or venovenous haemodiafiltration (CAVHD or CVVHD) combines dialysis and filtration.

Assessing serum concentrations of urea or creatinine before the next dialysis session is not a good measure of the adequacy of the dialysis, so various other measures have been developed including the urea reduction ratio and urea kinetic modelling. The use of such measures is more established for haemodialysis than for peritoneal dialysis.

References.

  1. 1. Zucchelli P, Santoro A. How to achieve optimal correction of acidosis in end-stage renal failure patients. Blood Purif 1995; 13: 375–84. PubMed
  2. 2. Carlsen DB, Wild ST. Grams to milliequivalents: a concise guide to adjusting hemodialysate composition. Adv Ren Replace Ther 1996; 3: 261–5. PubMed
  3. 3. Passlick-Deetjen J, Kirchgessner J. Bicarbonate: the alternative buffer for peritoneal dialysis. Perit Dial Int 1996; 16 (suppl 1): S109–S113. PubMed
  4. 4. Pastan S, Bailey J. Dialysis therapy. N Engl J Med 1998; 338: 1428–37. PubMed
  5. 5. Ifudu O. Care of patients undergoing hemodialysis. N Engl J Med 1998; 339: 1054–62. PubMed
  6. 6. Mallick NP, Gokal R. Haemodialysis. Lancet 1999; 353: 737–42. PubMed
  7. 7. Gokal R, Mallick NP. Peritoneal dialysis. Lancet 1999; 353: 823–8. PubMed
  8. 8. Fischbach M, et al. Hemodialysis in children: principles and practice. Semin Nephrol 2001; 21: 470–9. PubMed
  9. 9. Schröder CH. The choice of dialysis solutions in pediatric chronic peritoneal dialysis: guidelines by an ad hoc European committee. Perit Dial Int 2001; 21: 568–74. PubMed
  10. 10. Teehan GS, et al. Update on dialytic management of acute renal failure. J Intensive Care Med 2003; 18: 130–8. PubMed
  11. 11. Locatelli F, et al. Optimal composition of the dialysate, with emphasis on its influence on blood pressure. Nephrol Dial Transplant 2004; 19: 785–96. PubMed
  12. 12. Lameire N. Volume control in peritoneal dialysis patients: role of new dialysis solutions. Blood Purif 2004; 22: 44–54. PubMed
  13. 13. Maduell F. Hemodiafiltration. Hemodial Int 2005; 9: 47–55. PubMed
  14. 14. Nanovic L. Electrolytes and fluid management in hemodialysis and peritoneal dialysis. Nutr Clin Pract 2005; 20: 192–201. PubMed
  15. 15. Saxena R. Peritoneal dialysis: a viable renal replacement therapy option. Am J Med Sci 2005; 330: 36–47. PubMed Correction. ibid.; 110.
  16. 16. Ikizler TA, Schulman G. Hemodialysis: techniques and prescription. Am J Kidney Dis 2005; 46: 976–81. PubMed

Acute renal failure.

Acute renal failure is characterised by a rapid decline in kidney function, and has a variety of causes.1-7 It is often classified by origin as prerenal (e.g. due to hypovolaemia such as that associated with shock, burns, or dehydration; congestive heart failure; or renal artery obstruction), renal (such as acute tubular necrosis or interstitial nephritis of various causes, including nephrotoxic drugs and infections), or postrenal (acute urinary tract obstruction). The prognosis depends on the underlying disease, which should be identified and treated if possible, but the mortality may still be as high as 60%, particularly after surgery or trauma and in patients who become oliguric. Management is essentially supportive in the hope that renal function will recover. Complications of acute renal failure include extracellular volume overload and hyponatraemia, hyperkalaemia, metabolic acidosis, hyperphosphataemia and hypocalcaemia. Those complications requiring urgent treatment, often including the use of dialysis, are severe hyperkalaemia (Go to Hyperkalaemia.), pulmonary oedema, pericarditis, and severe metabolic acidosis (Go to Metabolic acidosis.). The use of dialysis before clinical signs of uraemia is a matter of debate since it does not appear to hasten recovery per se,1 but all save the shortest episodes of acute renal failure will require some form of renal replacement therapy with dialysis or filtration. Intermittent haemodialysis and peritoneal dialysis are both used, but the newer haemofiltration techniques have theoretical advantages in terms of volume control and cardiovascular stability, and are increasingly preferred.2,8,9

Numerous drugs have been tried in attempts to attenuate renal injury or hasten recovery in patients with acute tubular necrosis due to ischaemia or nephrotoxins.1,5,10,11 These include drugs to increase renal blood flow (e.g. low-dose dopamine, atrial natriuretic peptide, or prostaglandins), drugs to increase urine flow and protect the epithelial cells (mannitol and loop diuretics, calcium-channel blockers), or the use of chelating agents or antidotes against specific nephrotoxins. Consistent clinical benefit has not, however, been demonstrated.

Acute renal failure is reversible in about 95% of patients who survive the complications. A few patients who survive acute renal failure will require long-term dialysis or kidney transplantation (Go to Kidney transplantation.).

For further information on the substances mentioned above, see:

  • Atrial Natriuretic Peptide, Go to Natriuretic Peptides
  • Calcium-channel Blockers, Go to Calcium-channel blockers
  • Dialysis Solutions, Go to Dialysis Solutions
  • Dopamine, Go to Dopamine Hydrochloride
  • Loop Diuretics (see Furosemide, Go to Furosemide)
  • Mannitol, Go to Mannitol
  1. 1. Brady HR, Singer GG. Acute renal failure. Lancet 1995; 346: 1533–40. PubMed
  2. 2. Morgan AG. The management of acute renal failure. Br J Hosp Med 1996; 55: 167–70. PubMed
  3. 3. Evans JHC. Acute renal failure in children. Br J Hosp Med 1994; 52: 159–61. PubMed
  4. 4. Klahr S, Miller SB. Acute oliguria. N Engl J Med 1998; 338: 671–5. PubMed
  5. 5. Dishart MK, Kellum JA. An evaluation of pharmacological strategies for the prevention and treatment of acute renal failure. Drugs 2000; 59: 79–91. PubMed
  6. 6. Ashley C, Holt S. Acute renal failure. Pharm J 2001; 266: 625–8.
  7. 7. Lameire N, et al. Acute renal failure. Lancet 2005; 365: 417–30. PubMed
  8. 8. McCarthy JT. Renal replacement therapy in acute renal failure. Curr Opin Nephrol Hypertens 1996; 5: 480–4. PubMed
  9. 9. Joy MS, et al. A primer on continuous renal replacement therapy for critically ill patients. Ann Pharmacother 1998; 32: 362–75. PubMed
  10. 10. Albright RC. Acute renal failure: a practical update. Mayo Clin Proc 2001; 76: 67–74. PubMed
  11. 11. Pruchnicki MC, Dasta JF. Acute renal failure in hospitalized patients: part II. Ann Pharmacother 2002; 36: 1430–42. PubMed

Chronic renal failure.

Chronic renal failure is the irreversible, usually progressive, loss of renal function that eventually results in end-stage renal disease (ESRD) and the need for renal replacement therapy (dialysis or renal transplantation). The rate of decline in renal function is generally constant for each patient and is usually monitored by measuring serum-creatinine concentrations as an indirect index of the glomerular filtration rate (GFR). In its early stages when the patient is asymptomatic, progressive loss of renal function is described as diminished renal reserve or chronic renal insufficiency. When the limits of renal reserve have been exceeded and symptoms become apparent, it is termed chronic renal failure or overt renal failure. When renal function is diminished to such an extent that life is no longer sustainable (GFR less than 5 mL/minute), the condition is termed ESRD or uraemia. Many diseases can lead to ESRD, the most common being diabetes (Go to Diabetic complications), glomerulonephritis (Go to Glomerular kidney disease), and hypertension (Go to Hypertension).

The management of patients with chronic renal failure prior to ESRD involves measures to conserve renal function and compensate for renal insufficiency. Methods to slow the progression of renal failure include the treatment of hypertension (Go to Hypertension), reduction of proteinuria, and the reduction of hyperlipidaemia (Go to Hyperlipidaemias). ACE inhibitors (Go to Kidney disorders.) or angiotensin II receptor antagonists (Go to Kidney disorders.) are used for the reduction of proteinuria and the control of hypertension. Dietary protein restriction (see Renal Failure, Go to Renal failure.) has also been used for control of proteinuria, but conclusive evidence for a renal protective effect is lacking. Anaemia (Go to Anaemias.), hyperphosphataemia (Go to Hyperphosphataemia.), secondary hyperparathyroidism (Go to Hyperparathyroidism), and renal osteodystrophy (Go to Renal osteodystrophy) often require active treatment. Nephrotoxic drugs, including NSAIDs, should be avoided.

The choice between haemodialysis, peritoneal dialysis, and organ transplantation is considered, and the patient prepared, before it is actually required. In patients for whom transplantation is the preferred option, dialysis may still be required while waiting for a kidney. Kidney transplantation is discussed on Go to Kidney transplantation.. There are differences between countries in the choice of dialysis technique for patients with ESRD. For example, in-centre haemodialysis is used in about 80% of patients in the USA, whereas CAPD is used in over 50% of patients in the UK. Overall survival appears to be similar between the 2 techniques, but more patients on CAPD will eventually require a change to another dialysis method because of treatment failure.

Unlike renal transplant patients, dialysis patients still require replacement therapy with hormones that are usually produced by the kidney. Thus, recombinant erythropoietin and hydroxylated vitamin D analogues are commonly given.

References.

For further information on the substances mentioned above, see:

  • ACE Inhibitors, Go to ACE Inhibitors
  • Angiotensin II Receptor Antagonists, Go to Angiotensin II receptor antagonists
  • Dialysis Solutions, Go to Dialysis Solutions
  • Erythropoietin (see Epoetins, Go to Epoetins)
  • Vitamin D Substances, Go to Vitamin D Substances
  1. 1. NIH. Morbidity and mortality of dialysis. NIH Consens Statement 1993; 11: 1–33. PubMed
  2. 2. Friedman AL. Etiology, pathophysiology, diagnosis, and management of chronic renal failure in children. Curr Opin Pediatr 1996; 8: 148–51. PubMed
  3. 3. Steinman TI. Kidney protection: how to prevent or delay chronic renal failure. Geriatrics 1996; 51: 28–35.
  4. 4. Walker R. General management of end stage renal disease. BMJ 1997; 315: 1429–32. PubMed
  5. 5. McCarthy JT. A practical approach to the management of patients with chronic renal failure. Mayo Clin Proc 1999; 74: 269–73. PubMed Correction. ibid.; 538.
  6. 6. Morlidge C, Richards T. Managing chronic renal disease. Pharm J 2001; 266: 655–7.
  7. 7. Currie A, O'Brien P. Renal replacement therapies. Pharm J 2001; 266: 679–83.
  8. 8. Ruggenenti P, et al. Progression, remission, regression of chronic renal diseases. Lancet 2001; 357: 1601–8. PubMed
  9. 9. Renal Association. Treatment of adults and children with renal failure: standards and audit measures. 3rd ed. London: Royal College of Physicians of London and the Renal Association, 2002. Also available at: online (accessed 26/04/05)
  10. 10. Taal MW. Slowing the progression of adult chronic kidney disease: therapeutic advances. Drugs 2004; 64: 2273–89. PubMed
  11. 11. Meguid El Nahas A, Bello AK. Chronic kidney disease: the global challenge. Lancet 2005; 365: 331–40. PubMed

Electrolyte disturbances.

Haemodialysis with magnesium-free dialysis solution has been used to remove magnesium from the body in severe hypermagnesaemia (Go to Hypermagnesaemia.). Similarly, haemodialysis, and sometimes peritoneal dialysis, has been used in treating hypercalcaemia (Go to Hypercalcaemia.), hyperkalaemia (Go to Hyperkalaemia.), hypernatraemia (Go to Hypernatraemia.), and hyperphosphataemia (Go to Hyperphosphataemia.).

Overdosage and poisoning.

Haemodialysis, or less often peritoneal dialysis, can be used to remove some substances from the body after overdosage or poisoning. Substances most readily removed have a low molecular weight, low volume of distribution, low protein binding, high water solubility, and high renal clearance. Examples of agents for which haemodialysis may have a role in the treatment of severe overdosage include alcohol (Go to Treatment of Adverse Effects), ethylene glycol (Go to Treatment of Adverse Effects), methyl alcohol (Go to Treatment of Adverse Effects), lithium (Go to Treatment of Adverse Effects), and salicylates such as aspirin (Go to Adverse Effects and Treatment). Dialysis may be particularly important when poisoning with these agents is complicated by renal failure.

Preparations

Single-ingredient Preparations

The symbol ¤ denotes a preparation which is discontinued or no longer actively marketed.

Denmark: Bicbag¤; Finland: Gambrosol; Netherlands: Icodial; Sweden: Altracart II¤; BiCart¤; Bicbag¤; Biosol B¤;

Multi-ingredient Preparations

The symbol ¤ denotes a preparation which is discontinued or no longer actively marketed.

Australia: Dianeal; Extraneal; Austria: Acetat-Haemodialyse¤; Bicaflac; Dianeal; Extraneal; HAMFL; Hamofiltrasol¤; Monosol; Nutrineal PD4; Peritofundin¤; Physioneal; Brazil: Extraneal¤; HD¤; HF¤; Nutrineal¤; Peritofundin¤; Solurin; Canada: Nutrineal PD4¤; Chile: Concentrado Acido; Czech Republic: CAPD; Dianeal; Extraneal; Gambrosol; Medisol K; Nutrineal PD4; Denmark: balance glucose calcium; Bicaflac; Bicavera Glucose; CAPD/DPCA; Dianeal; Extraneal; Gambrosol; Hemosol Bicar; Lactasol; Lockolys¤; Nutrineal PD4; Physioneal; Prismasol; Finland: Balance; Bicavera; CAPD/DPCA; Dianeal; Extraneal; Lockolys¤; Physioneal; France: Dialysol Acide¤; Dialysol Bicarbonate¤; Dialytan H¤; DPCA 2¤; Germany: Extraneal; Nutrineal PD4; Physioneal; Greece: Peritoneal; Hungary: CAPD; Dianeal; Gambrosol; Peridisol; Israel: CAPD; D-204; D-248; D-300; D-326; Dialine; Dianeal; G-204; G-248; Hemosol BO; Nutrineal PD4; Italy: Extraneal; Icodial; Nutrineal PD4; Physioneal; Mexico: Bipodial¤; Solucion DP; Netherlands: Balance; Bicavera; Duosol; Multibic; Nutrineal; Physioneal; New Zealand: Extraneal; Portugal: Balance; Bicavera; CAPD/DPCA; Dianeal¤; Multibic; Nutrineal¤; Peritofundinas¤; Renofundina¤; South Africa: Sabax Dianeal; Sterisol Peridiasol; Spain: Balance Glucosa Calcio; Bicaflac; Bicavera Glucosa; CAPD/DPCA; CAPD; Dialisis Perit; Dialisol¤; Dianeal; DPCA¤; Extraneal; Gambrosol; Hemofiltracion E2 and E3; Hemofiltracion E4 and E5; Hemofiltracion HF 01¤; Hemofiltracion HF 02¤; Hemofiltracion HF 11 and HF 23¤; Hemosol BO; Icodial¤; Nutrineal PD4; Peritoflex¤; Physioneal Glucosa; Prismasol; Sol Dial Perit¤; Sweden: Balance; BiCart¤; Bicavera; Biorenal¤; Biosol A¤; CAPD/DPCA; Dianeal; Diasol¤; Dicalys 11; Dicalys 17; Duolys A¤; Duolys B¤; Extraneal; Gambrolys¤; Gambrosol; Haemovex 4; Haemovex 8; Hemofiltrasol; Hemofiltrationslosning 401; Hemoset A glucos¤; Hemoset A¤; Hemosol B0; HF-BIC35+HF-EL010¤; HF-BIC35+HF-EL210¤; Nutrineal PD4; Peritolys med glukos¤; Physioneal; Schiwalys Hemofiltration; Spectralys Hemofiltration 19, 20¤; Sterilys B 84¤; Switzerland: Clear-Flex Formula 13, 15, 55, 62, 91, AA, AB, AC¤; Dianeal; DPCA; Extraneal; Gambrosol¤; HF; Multibic; Nutrineal PD4; Physioneal; SK-F, BIC-F¤; Thailand: Dialyte¤; United Kingdom: Dialaflex Solutions¤; Diambulate Solutions¤; Dianeal¤; Difusor¤; Nutrineal PD4; Physioneal; United States: Dialyte; Dianeal¤; Extraneal; Inpersol¤; Venezuela: Dianeal;



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