Australia and New Zealand is a key epidemiological setting in the book’s account of hepatitis C virus infection in renal replacement therapy. Registry and population-based studies from the region repeatedly connect anti-HCV positivity with increased mortality in dialysis patients, while also supplying comparative evidence on transplantation, graft failure, liver-related death, and cardiovascular risk. The region therefore appears not as a backdrop but as a testing ground where long-term follow-up turns an infectious status into measurable consequences across dialysis and transplantation.

Registry Evidence in Dialysis

Australia and New Zealand contribute large longitudinal cohorts to the analysis of survival among patients receiving dialysis. In one study of 23,046 patients followed for ten years, anti-HCV-positive serologic status was independently associated with higher all-cause mortality, with a hazard ratio of 1.25. Hepatic failure was also more frequent as a cause of death in the anti-HCV-positive group, with an adjusted hazard ratio of 5.79, although the absolute rate remained low at 0.34 deaths per 100 patients per year.

The same study complicates any simple assumption that HCV-infected dialysis patients usually die from advanced liver disease. Among malignancy-related deaths in the anti-HCV-positive group, one of nine was attributed to primary liver cancer, whereas twelve of 583 malignancy-related deaths in the anti-HCV-negative group were attributed to that cause. The authors consequently suggested that many infected dialysis patients may not survive long enough to reach the distant complications of chronic HCV-related liver disease, such as hepatocellular carcinoma and cirrhosis.

A separate Asia-Pacific registry analysis reinforced the regional pattern. In the Australia and New Zealand cohort of 21,487 patients, all-cause mortality was associated both with anti-HCV positivity at baseline and with acquisition of anti-HCV antibody during dialysis. The adjusted hazard ratio was 1.29 for baseline positivity and 1.27 for antibody acquisition during follow-up. The analysis did not provide separate information on liver-related or cardiovascular mortality, but it showed that risk was associated not only with an established antibody-positive state but also with infection identified during the dialysis course.

Cardiovascular and Nutritional Context

The regional evidence also places HCV within the broader causes of death affecting dialysis patients. In another population-based study from Australia and New Zealand, cardiovascular disease was the predominant cause of death. Even after adjustment for age, pre-existing cardiovascular disease, and other patient characteristics, anti-HCV-positive patients retained a significantly higher risk of cardiovascular death, with a hazard ratio of 1.34. When follow-up continued through transplantation rather than being censored at the time of transplant, the association remained, with an adjusted hazard ratio of 1.27.

This finding matters because it shifts the interpretation of HCV beyond direct hepatic injury. Across dialysis cohorts, HCV-positive patients have also shown lower serum albumin levels than their uninfected counterparts, a pattern interpreted as evidence of effects on nutritional status and inflammation. Chronic infection may contribute to cardiovascular mortality through inflammatory pathways, while HCV has additionally been associated with hepatic steatosis, insulin resistance, and reduced adiponectin. In this framework, the excess mortality observed in Australia and New Zealand is part of a larger metabolic and inflammatory burden that conventional dialysis risk factors do not fully explain.

Transplantation and Survival

Australian and New Zealand data help establish the distinction between two propositions that can otherwise appear contradictory: HCV infection worsens outcomes among kidney transplant recipients, yet kidney transplantation still offers a survival advantage over remaining on dialysis or on the waiting list. Studies of HCV-infected end-stage renal disease patients consistently found lower mortality after transplantation than among comparable patients who remained listed or continued dialysis. One analysis reported an especially marked reduction in death during the period seven to forty-eight months after transplantation, while another found that the early post-transplant hazard was higher during the first six months but fell substantially thereafter.

The regional evidence therefore supports transplantation as the preferred renal replacement strategy for an HCV-infected patient who does not have advanced liver injury. The qualification is decisive: pretransplant assessment must identify cirrhosis or decompensated liver disease, because established or decompensated cirrhosis may instead require referral for simultaneous liver–kidney transplantation. For candidates with active HCV infection, liver biopsy remains the most reliable method for staging fibrosis despite the procedural concerns associated with chronic uremia.

Graft Outcomes and Donor Serology

Australia and New Zealand also supply important evidence on graft survival. In the Australia and New Zealand Dialysis and Transplant Registry, five-year graft survival was worse among anti-HCV-positive recipients, with an adjusted hazard ratio of 1.71 for graft failure. Graft loss in the HCV-positive group was more likely to result from glomerulonephritis, with an adjusted hazard ratio of 2.71, or chronic allograft nephropathy, with an adjusted hazard ratio of 1.87. These findings place HCV-related renal injury within the transplant allograft itself rather than treating infection as an exclusively hepatic problem.

The broader transplant literature reports some conflicting findings, including studies showing nonsignificant reductions in graft loss among HCV-positive recipients. Nevertheless, the dominant evidence links HCV with inferior long-term graft and patient survival, especially in studies with more than ten years of post-transplant follow-up. The apparent delay is significant: shorter studies often found little difference between anti-HCV-positive and anti-HCV-negative recipients, whereas the disadvantage became clearer over longer observation.

Evidence for Expanded Donor Use

Australia and New Zealand are also part of the policy debate over kidneys from HCV-positive deceased donors. Comparative studies have examined HCV-positive recipients receiving kidneys from HCV-positive donors against those receiving kidneys from HCV-negative donors. In the Spanish experience, which included 162 recipients of kidneys from HCV-positive donors and 306 recipients of kidneys from HCV-negative donors, long-term patient survival was not different, and liver-related deaths were rare in both groups. The lower graft survival observed with HCV-positive donor kidneys was attributed to older donor and recipient age and to a higher frequency of pretransplant HCV RNA positivity, rather than to donor HCV-positive serology as an independent risk factor.

These data support a restricted rather than universal use of HCV-positive kidneys. Such organs should be offered to candidates who are HCV RNA-positive, have consented in advance, and understand that transmission is not completely prevented by transplanting within an already infected population. Decision models described in the book found that restricting HCV-positive kidneys to HCV RNA-positive recipients could avoid new infections and graft losses while preserving organs that would otherwise be discarded. The policy reflects the central tension visible throughout the Australia and New Zealand evidence: HCV increases long-term risk, but refusing transplantation or usable organs can impose a greater immediate danger through prolonged dialysis and waiting-list mortality.