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

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1 Nephrol Dial Transplant (2004) 19: DOI: /nt/gfg592 Original Article The incience of treate en-stage renal isease in New Zealan Maori an Pacific Islan people an in Inigenous Australians John H. Stewart 1, Margaret R. E. McCreie 2 an Stephen P. McDonal 3 1 Department of Renal Meicine, Westmea Hospital, Westmea, NSW, Australia, 2 Department of Preventive an Social Meicine, University of Otago, Dunein, New Zealan an 3 Australia an New Zealan Dialysis an Transplant Registry, Queen Elizabeth Hospital, Wooville, SA, Australia Abstract Backgroun. Although Inigenous Australians, New Zealan Maori an Pacific Islan people comprise an unuly high proportion of patients treate for enstage renal isease (ESRD) in the two countries, no population-base age- an isease-specific rates have been publishe. Methos. From ata provie to the Australia an New Zealan Dialysis an Transplant Registry (ANZDATA), truncate age- an sex-stanarize incience rates were calculate for treate ESRD ue to all causes an by primary renal isease, in four broa age groups of Maori, Pacific Islan people an all other New Zealaners an Inigenous an noninigenous Australians, for the perio Results. The incience of ESRD i not iffer in persons age 0 14 years. In aults, Maori an Pacific Islan people ha similar rates of ESRD, a little more than half those of Inigenous Australians except in persons age 65 years an over in whom the rates were nearly equal, but two to ten times the rates in other New Zealaners an non-inigenous Australians. The excess of ESRD in Inigenous Australians was ue principally to type II iabetic nephropathy an glomerulonephritis (all common types except lupus nephritis), but was seen also in respect of type I iabetic nephropathy, hypertensive renal isease an analgesic nephropathy, while the excess in Maori an Pacific Islan people was confine to type II iabetic nephropathy, hypertensive renal isease an glomerulonephritis (especially lupus nephritis an type I mesangiocapillary glomerulonephritis, but not mesangial IgA isease). Conclusions. The incience an pattern of treate ESRD iffers quantitatively an qualitatively between Maori, Pacific Islan people an other New Zealaners, an Inigenous an non-inigenous Australians. Keywors: en-stage renal isease; glomerulonephritis; incience; Inigenous Australians; New Zealan Maori; Pacific Islan people Introuction The buren of en-stage renal isease (ESRD) falls heavily upon Maori an Pacific Islan people in New Zealan [1,2] as it oes upon Inigenous peoples (Aboriginal Australians an Torres Strait Islaners) in Australia [2,3]. While there have been excellent publications escribing the nature an pathogenesis of kiney isease, especially glomerulopathy, in Aboriginal Australians [4,5], no age-specific population-base rates have been publishe that can be use to ascertain the extent to which iniviual primary renal iseases 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 receive little attention outsie the region. In this paper, we present truncate age- an sexstanarize incience rates for treate ESRD, from all causes an accoring to primary renal isease, in New Zealaners (Maori, Pacific Islan people, all other) an Australians (Inigenous, non-inigenous) in four broa age groups (representing chilren, young aults, the mile-age an the elerly) calculate from ata reporte to the Australia an New Zealan Dialysis an Transplant Registry (ANZDATA) for Downloae from at Pennsylvania State University on February 27, 2014 Corresponence an offprint requests to: Dr Margaret McCreie, Department of Preventive an Social Meicine, University of Otago, PO Box 913, Dunein, New Zealan. margaret. mccreie@stonebow.otago.ac.nz Subjects an methos From the entire ANZDATA ataset [2,6] we restricte the analysis to all persons normally resient in Australia or Nephrol Dial Transplant Vol. 19 No. 3 ß ERA EDTA 2004; all rights reserve

2 ESRD in New Zealan Maori, Pacific Islan people an Inigenous Australians 679 New Zealan, an first treate for ESRD (incluing those who ie within 90 ays of starting treatment) between January 1, 1992 an December 31, Information about these patients, recore for ANZDATA by the treating renal units, comprise: ate of first treatment, age at first treatment (0 4, 5 9,..., 85þ years); sex; primary renal isease (glomerulonephritis by type, iabetic nephropathy type I or type II, hypertensive renal isease which inclue non-inflammatory arteriopathy, reflux nephropathy, analgesic nephropathy, other known iagnoses an unknown); an ethnicity (Maori, Pacific Islaner accoring to islan nation of origin, or other New Zealaner, Inigenous Australian Australian Aboriginal or Torres Strait Islaner or non-inigenous Australian), country of birth, an for other New Zealaners an non-inigenous Australians, racial origin (European, Asian, Pacific Islaner, other). Statistics New Zealan an the Australian Bureau of Statistics provie estimate resient populations by sex an 5-year age group (0 4, 5 9,...,85þ years) for iniviual years ( inclusive) for New Zealaners as a whole, Maori an Australians as a whole. Populations for Pacific Islan people in New Zealan an Inigenous Australians were available from each census 1991, 1996 an 2001 by sex an 5-year age group up to the age of 85þ years for Pacific Islan people an 65þ years for Inigenous Australians. Populations for intercensal years were calculate by linear interpolation an populations for noninigenous Australians an for other New Zealaners were calculate by subtraction (with 5-year age groups only to 65þ years for non-inigenous Australians). Average annual incience rates, irectly age- an sexstanarize to the worl population [7], with 95% confience intervals were calculate for broa age groups in orer to improve statistical power. Differences between the truncate age-stanarize incience rates were consiere statistically significant if their 95% confience intervals i not touch or overlap. Results Demographic ata escribing the five populations an patient groups are given in Table 1. The Pacific Islan patients were chiefly (88%) first generation New Zealaners; they comprise Samoans 48%, Cook Islaners 26%, Tongans 15%, Niueans 6%, Tokelau Islaners 3% (all Polynesian) an Fijians (Melanesian) 2%. The majority of Inigenous Australian patients were Aboriginal (94%), the remainer being Torres Strait Islaners (of Melanesian origin). Of other New Zealaners, 89% were European an 10% Asian, while of the non-inigenous Australian patients, 88% were European, 10% Asian an 2% Pacific Islaners. ESRD ue to all causes The incience of treate ESRD ue to all causes is shown in Table 2 accoring to age an population group. Incience rates were not significantly ifferent in persons age 0 14 years, but there were significant ifferences, many quite pronounce, in every oler age category. Generally speaking, rates were highest in Inigenous Australians, intermeiate in Maori an Pacific Islan people, an lowest in other New Zealaners an non-inigenous Australians. The proportion of patients who were women followe a similar pattern. In persons age an years, rates were about twice as high in Inigenous Australians as in Maori an Pacific Islan people, who in turn ha rates two to ten times those of other New Zealaners an non-inigenous Australians. The ifferences between Inigenous Australians on the one han, an Maori an Pacific Islan people on the other, were no longer significant in persons age 65 years an over. Only in persons age years was there a significant ifference between Maori an Pacific Islan people, the incience being lower in Maori. Non-inigenous Australians ha a higher incience of treate ESRD than recore in other New Zealaners in the years an 65 years an over age groups. Primary renal iseases leaing to ESRD in young an mile-age aults The incience of treate ESRD attributable to the most common primary renal iseases was calculate for each population group in young an mile-age aults except when numbers were too small for statistical stability (Table 3). In every case, the highest recore incience was in Inigenous Australians, the rates being significantly higher than in non-inigenous Downloae from at Pennsylvania State University on February 27, 2014 Table 1. Demographic characteristics of populations an patients Populations Patients Mean annual population % of national population Meian age % male n % of national cases Meian age % male New Zealan Maori Pacific Islan people Other Australia Inigenous Non-inigenous

3 680 J. H. Stewart et al. Table 2. Mean annual age- an sex-stanarize incience rates of treate ESRD from all causes in in New Zealan an Australia New Zealan Australia Age, year Maori Pacific Islan people Other Inigenous Non-inigenous n Rate a n Rate n Rate n Rate n Rate ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) 65þ ( ) ( ) ( ) ( ) ( ) a Truncate age- an sex-stanarize (to the worl population [7]) incience rate per million (95% confience interval). Australians or other New Zealaners in all categories except reflux nephropathy. They also ha significantly higher rates than Maori or Pacific Islan people of treate ESRD ue to type II iabetic nephropathy, glomerulonephritis, analgesic nephropathy (there were no cases in Maori or Pacific Islan people) an hypertensive renal isease (only in comparison with Maori age years). The higher incience of treate ESRD in Maori an Pacific Islan people, compare with other New Zealaners an non-inigenous Australians, was accounte for entirely by iabetic nephropathy (type II only), glomerulonephritis an hypertensive renal isease. The only significant ifference between these two peoples was that persons from the Pacific Islans age years ha twice the rate of ESRD ue to glomerulonephritis than i Maori. The ifference between other New Zealaners an non-inigenous Australians in the year age group was accounte for by the rarity of analgesic nephropathy in New Zealan, an the significantly higher Australian rate of glomerulonephritic ESRD, attributable to mesangial IgA isease (see below). Glomerulonephritic ESRD For persons age years in each population, a single summary incience rate (irectly stanarize to the worl population) was calculate for each type of glomerulonephritis commonly causing ESRD there were too few cases age <15 or >65 years among Maori an Pacific Islan people or Inigenous Australians to warrant their inclusion (Table 4). Throughout this table, the calculate rate is less than the actual rate (except for all glomerulonephritis ), as cases for which the type of glomerulonephritis ha not been ascertaine (no biopsy, or histological finings not iagnostic) coul not be inclue. The recore incience of glomerulonephritic ESRD in Inigenous Australians was significantly higher than in non-inigenous Australians or other New Zealaners for all sub-types except lupus nephritis. Hereitary an membranous glomerulopathies, an anti-gbm isease were too infrequent in Inigenous Australians for statistically vali comparisons. Pacific Islan people an Maori ha higher rates of ESRD ue to lupus nephritis an mesangiocapillary glomerulonephritis (type I) than i other New Zealaners or noninigenous Australians; in aition, the incience of focal glomerulosclerosis was raise in Pacific Islan people, an of focal necrotizing/crescentic nephritis in Maori. Neither of these Polynesian peoples ha an excess of mesangial IgA isease. Mesangial proliferative isease (not recore as IgA positive), anti-gbm isease, hereitary glomerulopathy an, in Pacific Islan people, membranous glomerulopathy were too infrequent for vali comparisons. The only significant ifference between other New Zealaners an non-inigenous Australians was the higher rate of mesangial IgA isease in Australians. Downloae from at Pennsylvania State University on February 27, 2014

4 ESRD in New Zealan Maori, Pacific Islan people an Inigenous Australians 681 Table 3. Mean annual age- an sex-stanarize incience of treate ESRD in young an mile-age ault New Zealaners an Australians in , by primary renal isease Cause of ESRD Age, year New Zealan Australia Maori Pacific Islan people Other Inigenous Non-inigenous n Rate a n Rate n Rate n Rate n Rate Glomerulonephritis Diabetes, type I Diabetes, type II ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) ( ) Reflux nephropathy ( ) ( ) ( ) ( ) ( ) Analgesic nephropathy ( ) ( ) ( ) % with other known iagnoses % 5.5% 19.0% 5.5% 16.9% % 3.4% 26.8% 4.1% 21.7% % with unknown iagnosis % 11.7% 3.2% 8.1% 2.3% % 3.0% 3.0% 7.8% 3.9% a Truncate age- an sex-stanarize (to the worl population [7]) incience rate per million (95% confience interval); ata presente for age group only if there were 10 or more cases in at least one of the Maori, Pacific Islan or Inigenous Australian populations. b Inclues non-inflammatory arteriopathy. Downloae from at Pennsylvania State University on February 27, 2014

5 682 J. H. Stewart et al. Table 4. Mean annual age- an sex-stanarize incience of treate ESRD ue to glomerulonephritis in New Zealaners an Australians age years in Type of glomerulonephritis New Zealan Australia Maori Pacific Islan people Other Inigenous Non-inigenous n Rate (95%CI) a n Rate (95%CI) n Rate (95%CI) n Rate (95%CI) n Rate (95%CI) Mesangial proliferative, IgAþve ( ) ( ) ( ) ( ) ( ) Mesangial proliferative, other b ( ) ( ) ( ) Mesangiocapillary (type I) ( ) ( ) ( ) ( ) ( ) Lupus nephritis ( ) ( ) ( ) ( ) ( ) Focal proliferative an necrotizing/crescentic c ( ) ( ) ( ) ( ) ( ) Anti-glomerular basement membrane isease ( ) ( ) Focal sclerosing ( ) ( ) ( ) ( ) ( ) Membranous ( ) ( ) ( ) Hereitary/familial ( ) ( ) Type not ientifie e (39%) (40%) (22%) (54%) (20%) All ( ) ( ) ( ) ( ) ( ) a Truncate age- an sex-stanarize (to the worl population [7]) incience per million (95% confience interval); rates in italics inicate categories with fewer than 10 cases. b Either negative for IgA or immunopathology not known. c Incluing cases: specifie as Wegeners or microscopic polyarteritis; with pauci-immune appearance on immunopathology or if ANCA positive, in the absence of another more specific iagnosis. Excluing cases: specifie as anti-glomerular basement membrane isease; with glomerular immune eposits; or seconary to other ientifiable glomerular or systemic iseases. Rate not calculate because of small numbers. e Percentage of all glomerulonephritis in patient group. In each patient group, 79 84% of cases in this category ha no biopsy; in the remaining 16 21% the histological appearances were insufficiently characteristic to etermine type. Downloae from at Pennsylvania State University on February 27, 2014

6 ESRD in New Zealan Maori, Pacific Islan people an Inigenous Australians 683 Discussion Maori are Polynesians who inhabite New Zealan prior to European colonization, while Pacific Islan people, who for the most part also are Polynesian, have settle there in large numbers only since the 1950s. Like Inigenous Australians, both peoples have a substantial excess of ESRD ue largely to type II iabetic nephropathy, but with significantly increase rates also of glomerulonephritis an hypertensive renal isease. There was no excess ESRD ue to type I iabetic nephropathy, reflux nephropathy or analgesic nephropathy in these two peoples, an the numbers with polycystic kiney isease were too small for statistical evaluation. The ifferences between Maori an Pacific Islan people on the one han, an Inigenous Australians on the other, were that: women were clearly more at increase risk than men in Inigenous Australians but not in Maori the numbers were equal in Pacific Islan people; Inigenous Australians ha numerically small, but significant, increases in ESRD ue to type I iabetic nephropathy an analgesic nephropathy not seen in the New Zealaners; ifferent types of glomerulonephritis were implicate; an, overall, Inigenous Australians ha about twice as much ESRD as Maori or Pacific Islan people. The only common primary renal iseases not seen to excess in at least one of the non-european populations were the hereitary conitions polycystic kiney isease, reflux nephropathy an hereitary glomerulopathy. Each of the non-european peoples consiere here has retaine consierable cultural ientity, an each suffers, but to ifferent egrees an in ifferent ways, socio-economic isavantage [2,3,5,8], a known risk factor for ESRD [3]. Evience for their reluctance to unergo, or lack of access to, meical investigation is provie in this stuy by the higher proportion of patients whose iagnosis was never ascertaine or whose glomerulonephritis was not confirme by biopsy, an elsewhere by the proportion who were not prepare to join the waiting list for renal transplantation [2]. These observations are in accor with known uner utilization of meical services by Maori [8] an, at least in respect of proceures, by Inigenous Australians [9]. Type II iabetes is some two to five times more common, an appears at an earlier age, in Maori, Pacific Islan people an Aboriginal Australians than in the preominantly European majority population [10 13], while the prevalence of hypertension is about ouble [13 15]. Thus, the excess inciences of iabetic an hypertensive ESRD shown in this stuy are substantially more than can be explaine simply by unerlying isease prevalence. The vulnerability to ESRD exhibite by these isavantage peoples certainly resies in a broaer spectrum of causes than uner utilization of meical services or a higher prevalence of iabetes an hypertension. Increase exposure to risk factors for a range of primary conitions that lea to renal isease, increase susceptibility to the nephropathic effects of kiney isease, harmful life-styles, malaaptation to westernization an the etrimental consequences of an averse intrauterine environment upon nephrogenesis, all contribute [1,3,4,5,8,16]. Three explanations suggest themselves for the excess of type I iabetic ESRD in Inigenous Australians. First, type I iabetes may be more prevalent in Inigenous than non-inigenous Australians this is unknown, but unlikely [17]. Seconly, Inigenous Australians may be more susceptible than persons of European lineage to the nephropathic effects of type I iabetes, a real possibility but as yet without supporting evience. Finally, there probably has been numerically significant misclassification of type II iabetics as having type I isease on account of an early age of onset an requirement for insulin, a source of error that woul have ha a isproportionate effect upon Inigenous rates because of the frequency of type II iabetes in young ault Aboriginal Australians [12]. Only a conservative interpretation of the finings 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 iagnosis. Moreover, in many categories the number of cases was small. Nevertheless, it is clear there are real ifferences between Inigenous Australians on the one han, an Maori an Pacific Islan people on the other the most common form of glomerulonephritis in one group (mesangial proliferative isease in Inigenous Australians, lupus nephritis in Pacific Islan people an Maori) being relatively uncommon in the other. The only population-base stuy of the pattern of non-en-stage, biopsy-proven glomerulonephritis in ault New Zealaners showe that, in the perio , mesangiocapillary glomerulonephritis, postinfectious glomerulonephritis an focal glomerulosclerosis were significantly more common, an IgA nephropathy less common, in Maori an Pacific Islan people (consiere together) than in other New Zealaners lupus nephritis was not inclue [1]. This stuy also reporte that the prognosis for renal survival was significantly less goo in Maori an Pacific Islan people than in other New Zealaners. Other New Zealaners appear to have less mesangial IgA isease than non-inigenous Australians. A possible explanation woul be ifferences in iagnostic practice, but this is unlikely in view of the close professional association between nephrologists an histopathologists in the two countries, an the similarity of rates of ESRD ue to each of the other principal types of glomerulonephritis, incluing those without type efine. 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 isease is unuly common (ANZDATA, unpublishe). The nature of glomerular isease in Aboriginal Australians has been investigate in recent years [4,5,16]. A relevant observation in relation to Downloae from at Pennsylvania State University on February 27, 2014

7 684 J. H. Stewart et al. susceptibility to glomerulonephritic ESRD is the association of worsening albuminuria with low birth weight [5], which may amplify the harmful effects on the kiney microvasculature of several other cariovascular an nephritic risk factors [4]. Intrauterine conitions that are responsible for low birth weight are believe also to result in a reuce number of nephrons in the newborn kiney, leaing in time to compensatory glomerulomegaly, an abnormality that is not easily ientifie by routine histopathology but which, as a consequence of associate hyperfiltration, progresses to focal glomerulosclerosis [5] proviing an explanation for the excess of this histological iagnosis in Inigenous Australians. In interpreting these comments, it must be remembere that focal glomerulosclerosis is the outcome of several ifferent glomerular insults, an therefore is a heterogeneous entity rather than a specific isease. There were, in this ata set, fewer than 10 cases of ESRD with post-streptococcal or post-infectious glomerulonephritis ientifie as the causative renal isease in any of the five populations stuie, or of lupus nephritis in Inigenous Australians, espite observations that these primary renal iseases not only are unuly common in Australian Aboriginal people, but also are associate with persisting proteinuria [16,18], an that post-streptococcal or postinfectious glomerulonephritis is frequent in Maori an Pacific Islan people [1]. However, this stuy lacke statistical power to etect ifferences in incience of ESRD ue to uncommon primary renal iseases an, moreover, these iagnoses may have been uner-enumerate in the non-european populations ue to their high proportion of glomerulonephritis, type uncertain. The excess incience of ESRD in Inigenous Australians, Maori an Pacific Islan people, is greater relative to the white population than that escribe in Mexican-Americans or Blacks in the US [19], or Asians (chiefly of Inian race) or Blacks in Britain [20], but encompasse a similar spectrum of primary renal isease. Sources of error In any stuy base upon isease registration, completeness an accuracy of recoring are potential sources of error. In the ata set provie for this stuy there was virtually no missing information. With regar to primary renal isease, ANZDATA has a lower rate of unknown iagnosis, or of presume glomerulonephritis type unspecifie, or of chronic pyelonephritis without a more precise iagnosis, than o USRDS or EDTA [6], inicating that reporting clinicians generally have taken care to provie precise information. However, the proportion of patients with iagnosis or type of glomerulonephritis unknown was unuly high in Inigenous Australians, less so in Maori an Pacific Islan people. The likelihoo of iagnostic error in recoring type of iabetes has been note above. Caution shoul be employe when interpreting ata from the 65 years an oler age group because of the significant, but unknown, rate of non-registration ue to failure to enter ESRD treatment [2], a source of error that is likely to iffer between the five stuy populations. Classification bias will be introuce if isavantage persons fail to correctly ientify, or alter, their ethnic status ue to fear of iscrimination, or if there is inconsistency in the way ethnicity is etermine. Neither can be rule out [2,3,8,9], but their effect is unlikely to be great enough to jeoparize the essential message conveye by the ata. Because small Pacific islan nations have few resources to treat ESRD, yet travel to New Zealan from several of them is relatively unrestricte, it is possible that the incience of treate ESRD in Pacific Islan people has been inflate by those who emigrate in orer to get treatment. This may explain the higher incience of ESRD in Pacific Islan people age years than in Maori of the same age. On the other han, some Pacific Islan people, especially if elerly, may have returne home for family or quality of life reasons on learning they ha iabetes, cariovascular isease or chronic renal failure. Allowing for these sources of error, the incience an pattern of treate ESRD iffers strikingly between Maori, Pacific islan people an other New Zealaners, an between Inigenous an non-inigenous Australians. It is not only Inigenous Australians, but also New Zealan Maori an Pacific Islan people, who have alarmingly high rates of ESRD. Acknowlegements. We thank Marylon Coates for statistical avice. The authors gratefully acknowlege the eication an care with which the professional an clerical staffs of ialysis an transplantation units throughout Australia an New Zealan have regularly submitte to the ANZDATA Registry the information on which this analysis has been performe, an ANZDATA personnel who have create an maintaine the atabase so accurately. Dr Margaret McCreie is supporte by the Ingster Ross Memorial Fun, University of Otago, an Dr Stephen McDonal by an unconitional grant to ANZDATA by AMGEN Australia. Conflict of interest statement. None eclare. References 1. New Zealan Glomerulonephritis Stuy Group. The New Zealan Glomerulonephritis Stuy: introuctory report. Clin Nephrol 1989; 31: McDonal SP, Russ GR. Current incience, treatment patterns an outcome of en stage renal isease among inigenous peoples in Australia an New Zealan. Nephrology 2003; 8: Cass A, Cunningham J, Snelling P, Wang Z, Hoy W. 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