The incidence of treated end-stage renal disease in New Zealand Maori and Pacific Island people and in Indigenous Australians

John H. Stewart1, Margaret R. E. McCredie2 and Stephen P. McDonald3

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



   Abstract
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Background. Although Indigenous Australians, New Zealand Maori and Pacific Island people comprise an unduly high proportion of patients treated for end-stage renal disease (ESRD) in the two countries, no population-based age- and disease-specific rates have been published.

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 1992–2001.

Results. The incidence of ESRD did not differ in persons aged 0–14 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



   Introduction
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 
The burden of end-stage renal disease (ESRD) falls heavily upon Maori and Pacific Island people in New Zealand [1,2] as it does upon Indigenous peoples (Aboriginal Australians and Torres Strait Islanders) in Australia [2,3]. While there have been excellent publications describing the nature and pathogenesis of kidney disease, especially glomerulopathy, in Aboriginal Australians [4,5], no age-specific population-based rates have been published that can be used to ascertain the extent to which individual primary renal diseases contribute to the excess of ESRD in these three peoples, or to compare them with other populations. The lesser, but nevertheless serious, problem in Polynesian peoples has received little attention outside the region.

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 1992–2001.



   Subjects and methods
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 
From the entire ANZDATA dataset [2,6] we restricted the analysis to all persons normally resident in Australia or New Zealand, and first treated for ESRD (including those who died within 90 days of starting treatment) between January 1, 1992 and December 31, 2001. Information about these patients, recorded for ANZDATA by the treating renal units, comprised: date of first treatment, age at first treatment (0–4, 5–9, ... , 85+ years); sex; primary renal disease (glomerulonephritis by type, diabetic nephropathy—type I or type II, hypertensive renal disease—which included non-inflammatory arteriopathy, reflux nephropathy, analgesic nephropathy, other known diagnoses and unknown); and ethnicity (Maori, Pacific Islander according to island nation of origin, or ‘other’ New Zealander, Indigenous Australian—Australian Aboriginal or Torres Strait Islander—or non-indigenous Australian), country of birth, and for ‘other’ New Zealanders and non-indigenous Australians, racial origin (European, Asian, Pacific Islander, other).

Statistics New Zealand and the Australian Bureau of Statistics provided estimated resident populations by sex and 5-year age group (0–4, 5–9, ... , 85+ years) for individual years (1992–2001 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 census—1991, 1996 and 2001—by 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.



   Results
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Demographic data describing the five populations and patient groups are given in Table 1. The Pacific Island patients were chiefly (88%) first generation New Zealanders; they comprised Samoans 48%, Cook Islanders 26%, Tongans 15%, Niueans 6%, Tokelau Islanders 3% (all Polynesian) and Fijians (Melanesian) 2%. The majority of Indigenous Australian patients were Aboriginal (94%), the remainder being Torres Strait Islanders (of Melanesian origin). Of ‘other’ New Zealanders, 89% were European and 10% Asian, while of the non-indigenous Australian patients, 88% were European, 10% Asian and 2% Pacific Islanders.


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Table 1. Demographic characteristics of populations and patients

 
ESRD due to all causes
The incidence of treated ESRD due to all causes is shown in Table 2 according to age and population group. Incidence rates were not significantly different in persons aged 0–14 years, but there were significant differences, many quite pronounced, in every older age category. Generally speaking, rates were highest in Indigenous Australians, intermediate in Maori and Pacific Island people, and lowest in ‘other’ New Zealanders and non-indigenous Australians. The proportion of patients who were women followed a similar pattern.


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Table 2. Mean annual age- and sex-standardized incidence rates of treated ESRD from all causes in 1992–2001 in New Zealand and Australia

 
In persons aged 15–44 and 45–64 years, rates were about twice as high in Indigenous Australians as in Maori and Pacific Island people, who in turn had rates two to ten times those of ‘other’ New Zealanders and non-indigenous Australians. The differences between Indigenous Australians on the one hand, and Maori and Pacific Island people on the other, were no longer significant in persons aged 65 years and over. Only in persons aged 15–44 years was there a significant difference between Maori and Pacific Island people, the incidence being lower in Maori. Non-indigenous Australians had a higher incidence of treated ESRD than recorded in ‘other’ New Zealanders in the 45–64 years and 65 years and over age groups.

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 15–44 years).


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Table 3. Mean annual age- and sex-standardized incidence of treated ESRD in young and middle-aged adult New Zealanders and Australians in 1992–2001, by primary renal disease

 
The higher incidence of treated ESRD in Maori and Pacific Island people, compared with ‘other’ New Zealanders and non-indigenous Australians, was accounted for entirely by diabetic nephropathy (type II only), glomerulonephritis and hypertensive renal disease. The only significant difference between these two peoples was that persons from the Pacific Islands aged 15–44 years had twice the rate of ESRD due to glomerulonephritis than did Maori.

The difference between ‘other’ New Zealanders and non-indigenous Australians in the 45–64 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 15–64 years in each population, a single summary incidence rate (directly standardized to the ‘world’ population) was calculated for each type of glomerulonephritis commonly causing ESRD—there 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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Table 4. Mean annual age- and sex-standardized incidence of treated ESRD due to glomerulonephritis in New Zealanders and Australians aged 15–64 years in 1992–2001

 
The recorded incidence of glomerulonephritic ESRD in Indigenous Australians was significantly higher than in non-indigenous Australians or ‘other’ New Zealanders for all sub-types except lupus nephritis. Hereditary and membranous glomerulopathies, and anti-GBM disease were too infrequent in Indigenous Australians for statistically valid comparisons. Pacific Island people and Maori had higher rates of ESRD due to lupus nephritis and mesangiocapillary glomerulonephritis (type I) than did ‘other’ New Zealanders or non-indigenous Australians; in addition, the incidence of focal glomerulosclerosis was raised in Pacific Island people, and of focal necrotizing/crescentic nephritis in Maori. Neither of these Polynesian peoples had an excess of mesangial IgA disease. Mesangial proliferative disease (not recorded as IgA positive), anti-GBM disease, hereditary glomerulopathy and, in Pacific Island people, membranous glomerulopathy were too infrequent for valid comparisons. The only significant difference between ‘other’ New Zealanders and non-indigenous Australians was the higher rate of mesangial IgA disease in Australians.



   Discussion
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Maori are Polynesians who inhabited New Zealand prior to European colonization, while Pacific Island people, who for the most part also are Polynesian, have settled there in large numbers only since the 1950s. Like Indigenous Australians, both peoples have a substantial excess of ESRD due largely to type II diabetic nephropathy, but with significantly increased rates also of glomerulonephritis and hypertensive renal disease. There was no excess ESRD due to type I diabetic nephropathy, reflux nephropathy or analgesic nephropathy in these two peoples, and the numbers with polycystic kidney disease were too small for statistical evaluation. The differences between Maori and Pacific Island people on the one hand, and Indigenous Australians on the other, were that: women were clearly more at increased risk than men in Indigenous Australians but not in Maori—the numbers were equal in Pacific Island people; Indigenous Australians had numerically small, but significant, increases in ESRD due to type I diabetic nephropathy and analgesic nephropathy not seen in the New Zealanders; different types of glomerulonephritis were implicated; and, overall, Indigenous Australians had about twice as much ESRD as Maori or Pacific Island people. The only common primary renal diseases not seen to excess in at least one of the non-European populations were the hereditary conditions—polycystic kidney disease, reflux nephropathy and hereditary glomerulopathy.

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 Australians—this 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 other—the 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 1972–1983, 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 Zealanders—lupus 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 glomerulonephritis—type 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 15–44 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.



   Acknowledgments
 
We thank Marylon Coates for statistical advice. The authors gratefully acknowledge the dedication and care with which the professional and clerical staffs of dialysis and transplantation units throughout Australia and New Zealand have regularly submitted to the ANZDATA Registry the information on which this analysis has been performed, and ANZDATA personnel who have created and maintained the database so accurately. Dr Margaret McCredie is supported by the Ingster Ross Memorial Fund, University of Otago, and Dr Stephen McDonald by an unconditional grant to ANZDATA by AMGEN Australia.

Conflict of interest statement. None declared.



   References
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 

  1. New Zealand Glomerulonephritis Study Group. The New Zealand Glomerulonephritis Study: introductory report. Clin Nephrol 1989; 31: 239–246[ISI][Medline]
  2. McDonald SP, Russ GR. Current incidence, treatment patterns and outcome of end stage renal disease among indigenous peoples in Australia and New Zealand. Nephrology 2003; 8: 42–48[CrossRef][ISI]
  3. Cass A, Cunningham J, Snelling P, Wang Z, Hoy W. Exploring the pathways leading from disadvantage to end-stage renal disease for Indigenous Australians. Soc Sci Med 2004; 58: 767–785[CrossRef][ISI][Medline]
  4. Hoy WE, Mathews JD, McCredie D et al. The multidimensional nature of renal disease: rates and associations of albuminuria in an Australian Aboriginal Community. Kidney Int 1998; 54: 1296–1304[CrossRef][ISI][Medline]
  5. Hoy WE, Rees M, Kyle E et al. A new dimension to the Barker hypothesis: low birthweight and susceptibility to renal disease. Kidney Int 1999; 56: 1072–1075[CrossRef][ISI][Medline]
  6. Maisonneuve P, Agodoa L, Gellert R et al. Distribution of primary renal diseases leading to end-stage renal failure in the United States, Europe, and Australia/New Zealand: results from an international comparative study. Am J Kidney Dis 2000; 35: 157–165[ISI][Medline]
  7. dos Santos Silva I. Cancer Epidemiology: Principles and Methods. International Agency for Research on Cancer, Lyon, 1999; 57–82
  8. Pomare E, Keefe-Ormsby V, Ormsby C et al. Hauora: Maori Standards of Health III. A Study of the Years 1970–1991. Eru Pomare Maori Health Research Centre, Wellington, 1995
  9. Cunningham J. Diagnostic and therapeutic procedures among Australian hospital patients identified as Indigenous. Med J Aust 2002; 176: 58–62[ISI][Medline]
  10. Scragg R, Baker J, Metcalfe P, Dryson E. Prevalence of diabetes mellitus and impaired glucose tolerance in a New Zealand multiracial workforce. NZ Med J 1991; 104: 395–397
  11. Simmins D, Harry T, Gatland B. Prevalence of known diabetes in different ethnic groups in urban South Auckland. NZ Med J 1999; 112: 316–319
  12. Daniel M, Rowley KG, McDermott R, Mylvaganam A, O’Dea K. Diabetes incidence in an Australian aboriginal population. A 8-year follow-up study. Diabetes Care 1999; 22: 1993–1998[Abstract]
  13. Abbott P, Close G. Vascular health risks in the Aboriginal community—a cultural approach. Aust Family Physician 2002; 31: 605–610[Medline]
  14. Bullen C, Tipene-Leach D, Vander Hoorn S, Jackson R, Norton R, MacMahon S. Ethnic differences in blood pressure: findings from the Fletcher Challenge-Auckland University Heart and Health Study. NZ Med J 1996; 109: 395–397
  15. Scragg R, Baker J, Metcalfe P, Dryson E. Hypertension and its treatment in a New Zealand multicultural workforce. NZ Med J 1991; 106: 147–150
  16. White AV, Hoy WE, McCredie D. Childhood post-streptococcal glomerulonephritis as a risk factor for chronic renal disease in later life. Med J Aust 2001; 174: 492–496[ISI][Medline]
  17. Karvonen M, Pitkaniemi M, Pitkaniemi J et al. for the World Health Organization DIAMOND Project Group. Sex difference in the incidence of insulin-dependent diabetes mellitus: an analysis of the recent epidemiological data. Diabetes Metab Rev 1997; 13: 275–291[CrossRef][ISI][Medline]
  18. Anstey NM, Bastian I, Dunckley H, Currie BJ. Systemic lupus erythematosus in Australian aborigines: high prevalence, morbidity and mortality. Aust NZ J Med 1993; 23: 646–651[ISI][Medline]
  19. Pugh JA, Stern MP, Haffner SM, Eifler CW, Zapata M. Excess incidence of treatment of end-stage renal disease in Mexican Americans. Am J Epidemiol 1988; 127: 135–144[Abstract]
  20. Roderick PJ, Raleigh VS, Hallam L, Mallick NP. The need and demand for renal replacement therapy in ethnic minorities in England. J Epidemiol Comm Health 1996; 50: 334–339[Abstract]
Received for publication: 29. 6.03
Accepted in revised form: 10.10.03





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