1Department of Renal Medicine, Westmead Hospital, Westmead, NSW, Australia, 2Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand and 3Australia and New Zealand Dialysis and Transplant Registry, Queen Elizabeth Hospital, Woodville, SA, Australia
Correspondence and offprint requests to: Dr Margaret McCredie, Department of Preventive and Social Medicine, University of Otago, PO Box 913, Dunedin, New Zealand. Email: margaret.mccredie{at}stonebow.otago.ac.nz
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Abstract |
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Methods. From data provided to the Australia and New Zealand Dialysis and Transplant Registry (ANZDATA), truncated age- and sex-standardized incidence rates were calculated for treated ESRD due to all causes and by primary renal disease, in four broad age groups of Maori, Pacific Island people and all other New Zealanders and Indigenous and non-indigenous Australians, for the period 19922001.
Results. The incidence of ESRD did not differ in persons aged 014 years. In adults, Maori and Pacific Island people had similar rates of ESRD, a little more than half those of Indigenous Australians except in persons aged 65 years and over in whom the rates were nearly equal, but two to ten times the rates in other New Zealanders and non-indigenous Australians. The excess of ESRD in Indigenous Australians was due principally to type II diabetic nephropathy and glomerulonephritis (all common types except lupus nephritis), but was seen also in respect of type I diabetic nephropathy, hypertensive renal disease and analgesic nephropathy, while the excess in Maori and Pacific Island people was confined to type II diabetic nephropathy, hypertensive renal disease and glomerulonephritis (especially lupus nephritis and type I mesangiocapillary glomerulonephritis, but not mesangial IgA disease).
Conclusions. The incidence and pattern of treated ESRD differs quantitatively and qualitatively between Maori, Pacific Island people and other New Zealanders, and Indigenous and non-indigenous Australians.
Keywords: end-stage renal disease; glomerulonephritis; incidence; Indigenous Australians; New Zealand Maori; Pacific Island people
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Introduction |
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In this paper, we present truncated age- and sex-standardized incidence rates for treated ESRD, from all causes and according to primary renal disease, in New Zealanders (Maori, Pacific Island people, all other) and Australians (Indigenous, non-indigenous) in four broad age groups (representing children, young adults, the middle-aged and the elderly) calculated from data reported to the Australia and New Zealand Dialysis and Transplant Registry (ANZDATA) for 19922001.
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Subjects and methods |
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Statistics New Zealand and the Australian Bureau of Statistics provided estimated resident populations by sex and 5-year age group (04, 59, ... , 85+ years) for individual years (19922001 inclusive) for New Zealanders as a whole, Maori and Australians as a whole. Populations for Pacific Island people in New Zealand and Indigenous Australians were available from each census1991, 1996 and 2001by sex and 5-year age group up to the age of 85+ years for Pacific Island people and 65+ years for Indigenous Australians. Populations for intercensal years were calculated by linear interpolation and populations for non-indigenous Australians and for other New Zealanders were calculated by subtraction (with 5-year age groups only to 65+ years for non-indigenous Australians).
Average annual incidence rates, directly age- and sex-standardized to the world population [7], with 95% confidence intervals were calculated for broad age groups in order to improve statistical power. Differences between the truncated age-standardized incidence rates were considered statistically significant if their 95% confidence intervals did not touch or overlap.
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Results |
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Primary renal diseases leading to ESRD in young and middle-aged adults
The incidence of treated ESRD attributable to the most common primary renal diseases was calculated for each population group in young and middle-aged adults except when numbers were too small for statistical stability (Table 3). In every case, the highest recorded incidence was in Indigenous Australians, the rates being significantly higher than in non-indigenous Australians or other New Zealanders in all categories except reflux nephropathy. They also had significantly higher rates than Maori or Pacific Island people of treated ESRD due to type II diabetic nephropathy, glomerulonephritis, analgesic nephropathy (there were no cases in Maori or Pacific Island people) and hypertensive renal disease (only in comparison with Maori aged 1544 years).
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The difference between other New Zealanders and non-indigenous Australians in the 4564 year age group was accounted for by the rarity of analgesic nephropathy in New Zealand, and the significantly higher Australian rate of glomerulonephritic ESRD, attributable to mesangial IgA disease (see below).
Glomerulonephritic ESRD
For persons aged 1564 years in each population, a single summary incidence rate (directly standardized to the world population) was calculated for each type of glomerulonephritis commonly causing ESRDthere were too few cases aged <15 or >65 years among Maori and Pacific Island people or Indigenous Australians to warrant their inclusion (Table 4). Throughout this table, the calculated rate is less than the actual rate (except for all glomerulonephritis), as cases for which the type of glomerulonephritis had not been ascertained (no biopsy, or histological findings not diagnostic) could not be included.
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Discussion |
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Each of the non-European peoples considered here has retained considerable cultural identity, and each suffers, but to different degrees and in different ways, socio-economic disadvantage [2,3,5,8], a known risk factor for ESRD [3]. Evidence for their reluctance to undergo, or lack of access to, medical investigation is provided in this study by the higher proportion of patients whose diagnosis was never ascertained or whose glomerulonephritis was not confirmed by biopsy, and elsewhere by the proportion who were not prepared to join the waiting list for renal transplantation [2]. These observations are in accord with known under utilization of medical services by Maori [8] and, at least in respect of procedures, by Indigenous Australians [9].
Type II diabetes is some two to five times more common, and appears at an earlier age, in Maori, Pacific Island people and Aboriginal Australians than in the predominantly European majority population [1013], while the prevalence of hypertension is about doubled [1315]. Thus, the excess incidences of diabetic and hypertensive ESRD shown in this study are substantially more than can be explained simply by underlying disease prevalence.
The vulnerability to ESRD exhibited by these disadvantaged peoples certainly resides in a broader spectrum of causes than under utilization of medical services or a higher prevalence of diabetes and hypertension. Increased exposure to risk factors for a range of primary conditions that lead to renal disease, increased susceptibility to the nephropathic effects of kidney disease, harmful life-styles, maladaptation to westernization and the detrimental consequences of an adverse intrauterine environment upon nephrogenesis, all contribute [1,3,4,5,8,16].
Three explanations suggest themselves for the excess of type I diabetic ESRD in Indigenous Australians. First, type I diabetes may be more prevalent in Indigenous than non-indigenous Australiansthis is unknown, but unlikely [17]. Secondly, Indigenous Australians may be more susceptible than persons of European lineage to the nephropathic effects of type I diabetes, a real possibility but as yet without supporting evidence. Finally, there probably has been numerically significant misclassification of type II diabetics as having type I disease on account of an early age of onset and requirement for insulin, a source of error that would have had a disproportionate effect upon Indigenous rates because of the frequency of type II diabetes in young adult Aboriginal Australians [12].
Only a conservative interpretation of the findings is permissible in relation to the types of glomerulonephritis contributing to the excess of ESRD because of the high proportion of cases for which there was no precise histopathological diagnosis. Moreover, in many categories the number of cases was small. Nevertheless, it is clear there are real differences between Indigenous Australians on the one hand, and Maori and Pacific Island people on the otherthe most common form of glomerulonephritis in one group (mesangial proliferative disease in Indigenous Australians, lupus nephritis in Pacific Island people and Maori) being relatively uncommon in the other.
The only population-based study of the pattern of non-end-stage, biopsy-proven glomerulonephritis in adult New Zealanders showed that, in the period 19721983, mesangiocapillary glomerulonephritis, post-infectious glomerulonephritis and focal glomerulosclerosis were significantly more common, and IgA nephropathy less common, in Maori and Pacific Island people (considered together) than in other New Zealanderslupus nephritis was not included [1]. This study also reported that the prognosis for renal survival was significantly less good in Maori and Pacific Island people than in other New Zealanders.
Other New Zealanders appear to have less mesangial IgA disease than non-indigenous Australians. A possible explanation would be differences in diagnostic practice, but this is unlikely in view of the close professional association between nephrologists and histopathologists in the two countries, and the similarity of rates of ESRD due to each of the other principal types of glomerulonephritis, including those without type defined. A more likely explanation is the relatively high proportion in the Australian population of persons born in East or South East Asia or Southern Europe, in whom mesangial IgA disease is unduly common (ANZDATA, unpublished).
The nature of glomerular disease in Aboriginal Australians has been investigated in recent years [4,5,16]. A relevant observation in relation to susceptibility to glomerulonephritic ESRD is the association of worsening albuminuria with low birth weight [5], which may amplify the harmful effects on the kidney microvasculature of several other cardiovascular and nephritic risk factors [4]. Intrauterine conditions that are responsible for low birth weight are believed also to result in a reduced number of nephrons in the newborn kidney, leading in time to compensatory glomerulomegaly, an abnormality that is not easily identified by routine histopathology but which, as a consequence of associated hyperfiltration, progresses to focal glomerulosclerosis [5]providing an explanation for the excess of this histological diagnosis in Indigenous Australians. In interpreting these comments, it must be remembered that focal glomerulosclerosis is the outcome of several different glomerular insults, and therefore is a heterogeneous entity rather than a specific disease.
There were, in this data set, fewer than 10 cases of ESRD with post-streptococcal or post-infectious glomerulonephritis identified as the causative renal disease in any of the five populations studied, or of lupus nephritis in Indigenous Australians, despite observations that these primary renal diseases not only are unduly common in Australian Aboriginal people, but also are associated with persisting proteinuria [16,18], and that post-streptococcal or post-infectious glomerulonephritis is frequent in Maori and Pacific Island people [1]. However, this study lacked statistical power to detect differences in incidence of ESRD due to uncommon primary renal diseases and, moreover, these diagnoses may have been under-enumerated in the non-European populations due to their high proportion of glomerulonephritis, type uncertain.
The excess incidence of ESRD in Indigenous Australians, Maori and Pacific Island people, is greater relative to the white population than that described in Mexican-Americans or Blacks in the US [19], or Asians (chiefly of Indian race) or Blacks in Britain [20], but encompassed a similar spectrum of primary renal disease.
Sources of error
In any study based upon disease registration, completeness and accuracy of recording are potential sources of error. In the data set provided for this study there was virtually no missing information. With regard to primary renal disease, ANZDATA has a lower rate of unknown diagnosis, or of presumed glomerulonephritistype unspecified, or of chronic pyelonephritis without a more precise diagnosis, than do USRDS or EDTA [6], indicating that reporting clinicians generally have taken care to provide precise information. However, the proportion of patients with diagnosis or type of glomerulonephritis unknown was unduly high in Indigenous Australians, less so in Maori and Pacific Island people. The likelihood of diagnostic error in recording type of diabetes has been noted above.
Caution should be employed when interpreting data from the 65 years and older age group because of the significant, but unknown, rate of non-registration due to failure to enter ESRD treatment [2], a source of error that is likely to differ between the five study populations.
Classification bias will be introduced if disadvantaged persons fail to correctly identify, or alter, their ethnic status due to fear of discrimination, or if there is inconsistency in the way ethnicity is determined. Neither can be ruled out [2,3,8,9], but their effect is unlikely to be great enough to jeopardize the essential message conveyed by the data.
Because small Pacific island nations have few resources to treat ESRD, yet travel to New Zealand from several of them is relatively unrestricted, it is possible that the incidence of treated ESRD in Pacific Island people has been inflated by those who emigrated in order to get treatment. This may explain the higher incidence of ESRD in Pacific Island people aged 1544 years than in Maori of the same age. On the other hand, some Pacific Island people, especially if elderly, may have returned home for family or quality of life reasons on learning they had diabetes, cardiovascular disease or chronic renal failure.
Allowing for these sources of error, the incidence and pattern of treated ESRD differs strikingly between Maori, Pacific island people and other New Zealanders, and between Indigenous and non-indigenous Australians. It is not only Indigenous Australians, but also New Zealand Maori and Pacific Island people, who have alarmingly high rates of ESRD.
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Acknowledgments |
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Conflict of interest statement. None declared.
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References |
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