Some people who are receiving dialysis treatment have virus infection such as hepatitis B, hepatitis C and/or HIV that is present in their blood. These infections can be transmitted to other patients if blood is contaminated by the blood of another with a viral infection. Haemodialysis is performed by passing blood from a patient through a dialysis machine, and multiple patients receive dialysis within a dialysis unit. Therefore, there is a risk that these viruses may be transmitted around the dialysis session. This documents sets out recommendations for minimising this risk.There are sections describing how machines and equipment should be cleaned between patients. There are also recommendations for dialysing patients with hepatitis B away from patients who do not have hepatitis B. Patients should be immunised against hepatitis B, ideally before starting dialysis if this is possible. There are guidelines on how and when to do this, for checking whether immunisation is effective, and for administering booster doses of vaccine. Finally there is a section on the measures that should be taken if a patient receiving dialysis is identified as having a new infection of hepatitis B, hepatitis C or HIV.

No abstract

Hyperkalemia is exacerbated by angiotensin converting enzyme inhibitors (ACE-I). Distal potassium (K(+)) secretion is negligible in anuric patients. ACE-I therapy may reduce renal, peritoneal, and colonic K(+) losses. We examined the effect of ACE-I therapy on serum, urinary, and dialysate K(+) in a cross-section of peritoneal and hemodialysis patients. Serum, 24-h urine K(+), and peritoneal dialysate excretion K(+) levels were measured and the results were compared in the various dialysis and treatment groups. Eighty-one hemodialysis (HD) and 32 peritoneal dialysis (PD) patients were included. Serum K(+) in HD patients with no residual renal function (RRF) was higher in those receiving ACE-I therapy (P = 0.02). Serum K(+) levels in HD patients receiving ACE-I treatments with RRF was similar to that in oligoanuric HD patients not receiving an ACE-I. Urinary K(+) excretion was significantly reduced in those on ACE-I therapy versus those not on an ACE-I (P < 0.05). Mean serum K(+) was lower in PD versus HD patients (P < 0.05). PD patients with no RRF on ACE-I therapy had higher serum K(+) concentrations (P = 0.002) and dialysate K(+) excretion was lower (P = 0.05), in comparison with PD patients not on an ACE-I. PD patients with RRF on ACE-I therapy had higher serum K(+) concentrations compared with those not on ACE-I therapy (P = 0.03). Both urinary and dialysate K(+) excretion were reduced (P = 0.001 and P = 0.002, respectively). ACE-I therapy increases serum K(+) concentration in dialysis patients. PD patients have relatively lower serum K(+) levels compared with HD patients. In PD patients, ACE-I therapy reduces dialysate K(+). These changes may result from reduced peritoneal movement of K(+).

No abstract