Home About us Current issue Back issues Submission Instructions Advertise Contact Login   

Search Article 
  
Advanced search 
 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 2533 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 
 


 
Table of Contents   
REVIEW ARTICLE  
Year : 2011  |  Volume : 22  |  Issue : 4  |  Page : 651-661
Can we improve the diagnosis of renal failure? A revised coding system for the Middle East and North Africa


1 UCL Centre for Nephrology, Royal Free Campus, London, United Kingdom
2 Nicosia State Hospital, Burhan Nalbantoglu General Hospital, North Cyprus
3 Department of Nephrology, H Chaker Hospital, 3029 Sfax, Tunisia

Click here for correspondence address and email

Date of Web Publication9-Jul-2011
 

   Abstract 

We reviewed the regional data on primary renal disease (PRD) causing end-stage renal failure (ESRF) during the decade 2000-2009. Reporting was generally inconsistent and diagnostic groups were poorly defined. We propose a system in which all diagnoses fall into one of eight broad groups: ESRF of uncertain etiology, congenital abnormalities of the kidney and urinary tract (CAKUT) and acquired uropathy, glomerular diseases, tubulo-interstitial disease (TID), other congenital and familial diseases, diabetes, renovascular disease and other specified diagnoses. Each group has sub-headings; for instance, primary glomerulonephritis, secondary glomerulonephritis, and hereditary glomerular disease. For each sub-heading, there is a list of specific diagnoses similar to that used by the European Dialysis and Transplant Association (EDTA) and United States Renal Data System (USRDS) coding systems. We also recommend that "etiology unknown" group should be reported in more detail as either "glomerular phenotype" or "tubular phenotype" and careful attention be paid to evidence for a family history of renal disease. To improve reporting, all patients who are diabetic, and all who have evidence of familial inheritance, should be recorded and a diagnostic category should be chosen. Thus, a diabetic patient is designated as "diabetic nephropathy" only if he/she fulfils the case definition for that diagnosis. We believe that the collection can be done much better as exemplified by the pediatric community, where data collection is very consistent, and there is a low rate of "unknown disease".

How to cite this article:
Neild GH, Oygar D D, Hmida MB. Can we improve the diagnosis of renal failure? A revised coding system for the Middle East and North Africa. Saudi J Kidney Dis Transpl 2011;22:651-61

How to cite this URL:
Neild GH, Oygar D D, Hmida MB. Can we improve the diagnosis of renal failure? A revised coding system for the Middle East and North Africa. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2019 Sep 17];22:651-61. Available from: http://www.sjkdt.org/text.asp?2011/22/4/651/82640

(This review has been simultaneously published in the Arab Journal of Nephrology and Transplantation)


   Introduction Top


Before we treat patients, we should know what is wrong with them. Yet, in adult registry data, "etiology unknown" is often the most common diagnosis mentioned. [1] There may be many reasons for this, and poor quality reporting and late presentation account for some. But results are so consistent that it would seem that many patients defy diagnosis.

The objective of this study is: a) to review the published literature from this part of the world, b) report the similarities and differences, and c) recommend a system for reporting primary renal disease (PRD) that can be used by all. This will allow direct comparisons of national data sets.

Apart from patients who are actually designated as "etiology unknown", there are many others in whom the diagnosis assigned is no more than an informed guess. This is not necessarily a problem as long as terms are used precisely, consistently and above all are clearly defined. For instance, we must know what percentage of those categorized as "glomerulonephritis" have had a renal biopsy. Currently, common diagnostic categories such as hypertension and renovascular disease are undefined.

We report the regional data published during the decade 2000-2009, and highlight the current problems and issues to be addressed. We propose a system in which all specific diagnoses can be summarized into one of eight broad groups. We recommend that the unknown group should be reported in more detail as either "glomerular phenotype" or "tubular phenotype" and careful attention be paid to evidence for a family history of renal disease.


   Methodology Top


We identified all papers published from the regions that include Eastern Mediterranean, Middle East, Arabia and North Africa and that are reflected in the membership of the Arab Society of Nephrology and Transplantation. We used PubMed, Google, and the following cited references to find papers that report data on PRD in patients reaching end-stage renal failure (ESRF) in this region.


   Lessons from Pediatric Nephrology Top


Since 1976, pediatric registries have reduced the number of children with "no specific diagnosis" from 39% [2] to less than 5%. Registry data from around the world, recording the PRD resulting in ESRF in children, show that around 50% of cases are caused by "congenital abnormalities of the kidney and urinary tract" (CAKUT) and a further 20% by "other congenital and inherited diseases". [3] Data from the Middle East are consistent with this worldwide view [Table 1].
Table 1: Review of pediatric literature from the Middle East and North Africa.

Click here to view


Since 2008, the British Association for Pediatric Nephrology (BAPN) has taken the view, "renal dysplasia, with or without vesicoureteric reflux (VUR), is the most common cause of ESRF in the pediatric population. On the basis that the clinical overlap between reflux nephropathy and renal dysplasia is so great and that clinical distinction between these two groups is quite arbitrary, these two categories have been united". [12]

In our review, we use the term CAKUT for all forms of congenital malformations and they can be broadly divided into obstructive and non-obstructive causes. The latter group includes the synonyms: reflux nephropathy, renal dysplasia, renal hypo-dysplasia and chronic pyelonephritis.


   Review of Adult Literature from the Middle East and North Africa Top


In 2003, Professor Barsoum published a review of this topic, from the literature and his personal experience, and concluded that the principal causes of ESRF in North Africa were interstitial nephritis (14-32%), glomerulonephritis (11-24%), diabetes (5-20%), nephrosclerosis (5-21%), polycystic and other hereditary diseases (<5%). [13] His paper also makes helpful comments about geographical and historical differences in schistosomiasis, amyloid, sickle cell disease, tuberculosis, renal stones, and Takayasu's disease.

The literature published from this region in the past 10 years that we reviewed is summarized in [Table 2]. Several problems emerge when the data are analyzed. None of the papers uses a methodology similar to another. All papers are characterized by lack of case definitions, by lack of details of whether diagnoses are supported by biopsies and whether biopsies are supported by immuno-peroxidase (IP)/immuno-fluorescence (IF), or electron microscopy (EM). Three papers specifically recognize tubulointerstitial disease (TID) as a significant diagnostic group, while others mention it as a minor sub-group and the remainder make no mention of TID. We noticed that the sum of "unknown" plus "hypertension" is usually 45-50%.
Table 2: Review of published renal data in adults from the Middle East and North Africa.

Click here to view



   Specific Comments from Individual Papers Top


Iran (2009)

The PRD data are presented as the whole group and subdivided in ages <40, 40-60 and >60 years. They found that in the <40 years age-group, the commonest cause of PRD was unknown (25%) followed by hypertension (21%) [Table 2]. [16]

Tunisia (2008)

Data on PRD were expressed as incident rates. They highlighted the fact that idiopathic chronic TID was common and varied from region to region. Geographical variation of data is shown in both tables and map. [18]

Yemen (2003)

Patients had "CRF" that was not defined, but two thirds required dialysis. About 58% were described as "unknown", none had a diagnosis of glomerulonephritis (so presumably none had renal biopsies) and 25% were classified as post-renal, which included bilateral renal stones (7%), ureteral stones (4%), bladder stone (4%), bilateral hydronephrosis (4%), schistosomiasis (4%), enlarged prostate 2% and bladder carcinoma (1%). [25]


   Definitions Top


In our proposal for a regional classification, we define some of the terms that are commonly used.

Diabetic nephropathy

Not all renal failure in diabetic patients is caused by diabetic nephropathy (DN). The term should be used for patients with significant proteinuria and evidence of other complications of diabetes (e.g. retinopathy) consistent with the likely duration of the diabetes. The other criteria used are as follows:

  • long duration of diabetes before the onset of CRF (usually more than 10 years).
  • normal sized kidneys on ultrasound.
  • presence of diabetic retinopathy on fundus examination.
  • absence of hematuria or red blood cell casts in urine.
  • presence of proteinuria even after the patient has begun dialysis. [24]


Familial (inherited, family history)

Any patient with a known member of the family, however remote, who has had renal disease, should be considered as having a positive family history.

Glomerular phenotype

Glomerulonephritis can present in various ways but not as asymptomatic ESRF. All forms of primary glomerulonephritis will present either with macroscopic hematuria, nephritic syndrome, nephrotic syndrome, fluid retention, malignant hypertension, or some will be diagnosed based on routine investigations. Glomerular phenotype is defined by the presence of clinical history consistent with glomerulonephritis, without performing a renal biopsy.

Hypertensive nephropathy (HN)

This is (probably) a rare condition, except in patients who have sub-Saharan African ethnicity. Patients can be classified as HN if a renal biopsy shows that the primary pathology is nephro-angiosclerosis. [27],[28] Without a biopsy, they should be classified as unknown etiology (glomerular or tubular phenotype).

The nephrotic syndrome

This is defined as patients with the triad of nephrotic range proteinuria (>3 g/day, >300 mg/mmol), hypoalbuminemia (albumin below the laboratory normal, <35 g/L), and peripheral (dependent) edema. This must be differentiated from the patient who has only nephroticrange proteinuria (see below).

Nephrotic-range proteinuria (alone)

This is defined as proteinuria (>3 g/day or >300 mg/mmol) occurring in a patient with normal plasma albumin and no peripheral edema.

Primary glomerulonephritis

Primary focal and segmental glomerulosclerosis (FSGS) with the nephrotic syndrome

Renal biopsy showing features of FSGS in a patient with the nephrotic syndrome.

IgA nephropathy (proven by IP or IF)

Renal biopsy showing mesangioproliferative glomerulonephritis with mesangial deposits of IgA.

Membranous nephropathy

Renal histology showing thickening of the peripheral glomerular basement membrane, presence of "spikes" on silver stain, with IF showing C3 and IgG deposits around the glomerular basement membrane (GBM).

Membranoproliferative (mesangiocapillary) GN

Renal histology characterized by thickening of the peripheral basement membrane of the glomeruli, with demonstration of double contours on silver stain (reduplication of the GBM). Also, IF should demonstrate variable degrees of C3 and IgG deposits.

Crescentic (extracapillary) glomerulonephritis (idiopathic)

Renal histology showing the presence of crescentic and necrotizing glomerulonephritis, without evidence of systemic disease.

Secondary FSGS (without the nephrotic syndrome)

Patients with biopsy proven FSGS without history of the nephrotic syndrome (may have nephrotic-range proteinuria).

Mesangioproliferative (other, unspecified)

Mesangioproliferative glomerulonephritis without mesangial deposits of IgA.

Idiopathic endocapillary GN (including post-infectious)

Characterized by enlarged and hypercellular glomeruli due to swelling and proliferation of glomerular cells (endocapillary proliferation), with neutrophil exudation and IF showing granular deposits of IgG and complement in the GBM and mesangium and EM showing large sub-epithelial deposits (humps).

Renal stones

Renal stones, with or without nephrocalcinosis, rarely cause renal failure in the absence of obstruction and infection. Co-existence of renal stones and renal failure suggests hyperoxaluria (code 48), magnesium-losing nephropathy (code 40) or Dent's disease (code 36). In patients with recurrent stones causing obstruction, one must exclude cystinuria (code 50) and hyperoxaluria (code 48). Staghorn calculi are caused by triple phosphate (struvite) stones growing in the presence of infection (code 64) [Table 3].
Table 3: Classification of primary renal disease (PRD).

Click here to view


Renovascular disease

Diagnosis is suspected in patients with evidence of atheroma and asymmetric kidneys. The EDTA reports the broad group of renovascular disease from two non-specific codes: "Renal vascular disease - type unspecified (code 70)", and "Renal vascular disease - due to other cause (not given above) (code 79)".

Tubular phenotype

This entity is defined by patients who reach ESRF with minimal symptoms, minimal proteinuria (urine dipstick 1+ or less), in the absence of peripheral edema and malignant hypertension.


   Proposal Top


The proposed classification is shown in [Table 3]. We propose a system in which all diagnoses fall into one of eight groups:

  • ESRF of uncertain etiology,
  • CAKUT and acquired uropathy,
  • glomerular diseases,
  • tubulo-interstitial disease,
  • other congenital and familial diseases,
  • diabetes,
  • renovascular disease, and
  • other specified diagnoses.
Each group has sub-headings, for instance, primary glomerulonephritis, secondary glomerulonephritis, and hereditary glomerular disease (see column 2 of [Table 3]). For each sub-heading, there is a list of specific diagnoses similar to that used by EDTA and USRDS coding systems.

We also recommend that "etiology unknown" group should be reported in more detail as either "glomerular phenotype" (code 1) or "tubular phenotype" (code 2) and careful attention should be paid to evidence for a family history of renal disease.

To improve reporting, all patients who are diabetic as well as those with evidence of familial inheritance should be recorded separately, following which a diagnostic category should be chosen. Consequently, a diabetic patient is designated as "diabetic nephropathy" only if he fulfils the case definition as the most likely diagnosis.


   Discussion Top


The motivation behind these proposals is to improve the knowledge of how much we know, or more specifically how much we currently do not know. This information will direct future research. There are a number of key clinical issues that need to be resolved which relate to clinical terminology.

The nephrotic syndrome is something very specific. It should not be confused with nephrotic-range proteinuria (>3 g/day or >300 mg/ mmol) occurring in a patient with normal plasma albumin and no peripheral edema.

FSGS : Primary FSGS is a cause of the nephrotic syndrome commonly leading to renal failure in children and sometimes adults (EDTA codes 11, 17). Many patients with slowly progressive renal disease, such as reflux nephropathy/renal dysplasia, develop secondary FSGS. This is commonly associated with heavy proteinuria (nephrotic-range) but normal plasma albumin. This has important clinical implications because patients with true nephrotic syndrome will respond poorly to ACE inhibitors (ACEI) while patients with secondary FSGS should have a prompt reduction in proteinuria when blood pressure is reduced with ACEI. The EDTA has no code for secondary FSGS. The USRDS has only a catch all "focal glomerulosclerosis, focal sclerosing -code 5" (with no clinical conditions attached).

Essential hypertension in young white patients does not cause renal failure. [29] The underlying renal disease can lead to malignant or accelerated hypertension, which can result in rapid loss of the remaining renal function. This is not true in those of West African ethnicity, who do develop renal failure with hypertension and renal biopsy shows a conspicuous nephroangiosclerosis. [28] In 2008, the association of renal failure was reported in this ethnic group with polymorphisms of MYH9 gene encoding the non-muscle myosin (NMM) heavy chain IIA (NMMHC-IIA), which is present on chromosome 22q11-13. [30],[31] In fact, the region responsible also includes the gene APOL1 which codes for apolipoprotein L1. [32] It remains to be investigated whether "hypertensive nephropathy" is a common cause of renal failure in the Middle East and North Africa, as is currently believed.

Hereditary glomerular disease . Although Alport's disease is a type of glomerulonephritis, it is more appropriate to have it listed with other congenital forms of glomerulonephritis because it is not an acquired, immunological disease that might be treated with immunosuppressive drugs.

Diabetes . Over the age of 50 years, approximately one in five patients with non-diabetic renal disease will also be diabetic. [33] More effort is therefore required to classify patients who are diabetic and have renal failure as having either "diabetic nephropathy" (see definitions) or some other non-diabetic form of disease.

The next major issue is the problem of patients with "no known diagnosis". We have found that even in the West, when renal registries are examined carefully and all uncertain diagnoses are added together ("etiology unknown", "glomerulonephritis; histologically examined but unspecified", "hypertension: unspecified with renal failure") in young adults, rates of unknown diagnosis range from 26 to 36%. [1] Two main issues will probably account for most genuine cases of "etiology unknown". Firstly, in patients who present late when biopsy may be difficult, and secondly, in diseases that are still uncharacterized and therefore unknown in this part of the world. It is beyond doubt that novel renal diseases, hitherto unrecognized in the West, occur commonly in some countries. [34],[35],[36]

We have previously argued that late presentation with ESRF is not a feature of glomerulonephritis (at least in the West). [1] Late presentation without earlier symptoms is suggestive of "a tubular phenotype". In the West, there has been traditionally reluctance to biopsy such people, probably with the opinion that it would not change management. We believe that uncharacterized tubular disease is much more common than is recognized.

Data from a large biopsy series in Egypt, described by Barsoum and Francis, [27] reported that 21% of all renal biopsies (n = 1234) were performed because of unexplained CRF, of which 33% had chronic interstitial nephritis (IN), 8% had FSGS, 5% had nephroangiosclerosis and 11% had ESRF. These diagnoses would all be compatible with primary tubular disease (such as medullary cystic kidney disease) and together represent 57% of all their CRF biopsies.

With late presentation of renal failure, renal imaging is often unrewarding. Imaging patients with advanced renal failure was virtually impossible until the advent of routine ultrasound (circa 1980). It is difficult to obtain accurate information on the shape of small contracted kidneys. Computerized tomography (CT) scan and magnetic resonance imaging (MRI) scanning should give useful information, but there is very little published data on renal imaging in uremia with the exception of analgesic nephropathy. [37],[38]

Similarly, renal biopsy is often not an option. One good reason not to biopsy patients with ESRF is that the sample is unlikely to show enough viable tissue to make a specific diagnosis. The majority of glomeruli will show global sclerosis. The only EDTA code for this would be "glomerulonephritis; histologically examined, not given above" (EDTA code 19). We propose that this small group be reported as "etiology unknown, glomerular phenotype".

In conclusion, we hope that a simple and unified system of reporting ESRF will allow our colleagues around the Middle East and North Africa to pool and share data and that this will lead to regional registries that will help direct our future clinical activities and research.

 
   References Top

1.Neild GH. Primary renal disease in young adults with renal failure. Nephrol Dial Transplant 2010;25:1025-32.  Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.Schaerer K, Chantler C, Brunner FP, et al. Combined report on regular dialysis and transplantation of children in Europe, 1976. Proc Eur Dial Transplant Assoc 1975;59-105.  Back to cited text no. 2
    
3.Neild GH. What do we know about chronic renal failure in young adults? I. Primary renal disease. Pediatr Nephrol 2009;24:1913-9.  Back to cited text no. 3
    
4.NAPRTCS. North American Pediatric Renal Trials and Collaborative Studies. http://web.emmes.com/study/ped/annlrept/ann lrept2007.pdf.2007   Back to cited text no. 4
    
5.British Association for Paediatric Nephrology. Report from the Paediatric Renal Registry. In: Ansell D, Feest TG, Byrne C, eds. The UK Renal Registry 8th Annual Report. 2005;269-91.  Back to cited text no. 5
    
6.Ardissino G, Dacco V, Testa S, et al. Epidemiology of chronic renal failure in children: data from the ItalKid project. Pediatrics 2003; 111:e382-7.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.Al Eisa A, Naseef M, Al Hamad N, Pinto R, Al Shimeri N, Tahmaz M. Chronic renal failure in Kuwaiti children: An eight-year experience. Pediatr Nephrol 2005;20:1781-5.  Back to cited text no. 7
    
8.Hamed RM. The spectrum of chronic renal failure among Jordanian children. J Nephrol 2002;15:130-5.  Back to cited text no. 8
[PUBMED]    
9.Madani K, Otoukesh H, Rastegar A, Van Why S. Chronic renal failure in Iranian children. Pediatr Nephrol 2001;16:140-4.  Back to cited text no. 9
[PUBMED]  [FULLTEXT]  
10.Sirin A, Emre S, Alpay H, Nayir A, Bilge I, Tanman F. Etiology of chronic renal failure in Turkish children. Pediatr Nephrol 1995;9:549-52.  Back to cited text no. 10
[PUBMED]    
11.Mattoo TK, Al-Mohalhal S, Al-Sowailem A, Mahmood MA. Chronic renal failure in children in Saudi Arabia. Ann Saudi Med 1990; 10:496-499.  Back to cited text no. 11
    
12.Lewis MA. Demography of renal disease in childhood. Semin Fetal Neonat Med 2008; 13:118-24.  Back to cited text no. 12
    
13.Barsoum RS. End-stage renal disease in North Africa. Kidney Int Suppl 2003;S111-4.  Back to cited text no. 13
    
14.Elamin S, Obeid W, Abu-Aisha H. Renal replacement therapy in Sudan, 2009. Arab J Nephrol Transpl 2010;3:31-6.  Back to cited text no. 14
    
15.Moukeh G, Yacoub R, Fahdi F, Rastam S, Albitar S. Epidemiology of hemodialysis patients in Aleppo city. Saudi J Kidney Dis Transpl 2009;20:140-6.  Back to cited text no. 15
[PUBMED]  Medknow Journal  
16.Malekmakan L, Haghpanah S, Pakfetrat M, Malekmakan A, Khajehdehi P. Causes of chronic renal failure among Iranian hemodialysis patients. Saudi J Kidney Dis Transpl 2009;20: 501-4.  Back to cited text no. 16
[PUBMED]  Medknow Journal  
17.Shigidi MM, Ramachandiran G, Rashed AH, Fituri OM. Demographic data and hemodialysis population dynamics in Qatar: A five year survey. Saudi J Kidney Dis Transpl 2009;20: 493-500.  Back to cited text no. 17
[PUBMED]  Medknow Journal  
18.Counil E, Cherni N, Kharrat M, Achour A, Trimech H. Trends of incident dialysis patients in Tunisia between 1992 and 2001. Am J Kidney Dis 2008;51:463-70.  Back to cited text no. 18
[PUBMED]  [FULLTEXT]  
19.Mahdavi-Mazdeh M, Zamyadi M, Nafar M. Assessment of management and treatment responses in haemodialysis patients from Tehran province, Iran. Nephrol Dial Transplant 2008; 23:288-93.  Back to cited text no. 19
[PUBMED]  [FULLTEXT]  
20.Abdallah S, Ahmad AT, Batieha A, Ajlouni K. Diabetes mellitus: the leading cause of haemodialysis in Jordan. East Mediterr Health J 2007;13:803-9.  Back to cited text no. 20
[PUBMED]    
21.Batieha A, Abdallah S, Maghaireh M, et al. Epidemiology and cost of haemodialysis in Jordan. East Mediterr Health J 2007;13:654-63.  Back to cited text no. 21
[PUBMED]    
22.Afshar R, Sanavi S, Salimi J. Epidemiology of chronic renal failure in Iran: A four year single-center experience. Saudi J Kidney Dis Transpl 2007;18:191-4.  Back to cited text no. 22
[PUBMED]  Medknow Journal  
23.Shaheen FA, Al-Khader AA. Epidemiology and causes of end stage renal disease (ESRD). Saudi J Kidney Dis Transpl 2005;16:277-81.  Back to cited text no. 23
[PUBMED]  Medknow Journal  
24.Afifi A, El Setouhy M, El Sharkawy M, et al. Diabetic nephropathy as a cause of end-stage renal disease in Egypt: A six-year study. East Mediterr Health J 2004;10(4-5):620-6.  Back to cited text no. 24
    
25.Al-Rohani M. Causes of chronic renal failure at one center in Yemen. Saudi J Kidney Dis Transpl 2003;14:80-3.  Back to cited text no. 25
[PUBMED]  Medknow Journal  
26.Barbari A, Stephan A, Masri M, et al. Consanguinity-associated kidney diseases in Lebanon: an epidemiological study. Mol Immunol 2003; 39:1109-14.  Back to cited text no. 26
[PUBMED]  [FULLTEXT]  
27.Barsoum RS, Francis MR. Spectrum of glomerulonephritis in Egypt. Saudi J Kidney Dis Transpl 2000;11:421-9.  Back to cited text no. 27
[PUBMED]  Medknow Journal  
28.Marcantoni C, Ma LJ, Federspiel C, Fogo AB. Hypertensive nephrosclerosis in African Americans versus Caucasians. Kidney Int 2002;62: 172-80.  Back to cited text no. 28
[PUBMED]  [FULLTEXT]  
29.Freedman BI, Sedor JR. Hypertension-associated kidney disease: Perhaps no more. J Am Soc Nephrol 2008;19:2047-51.  Back to cited text no. 29
[PUBMED]  [FULLTEXT]  
30.Freedman BI, Hicks PJ, Bostrom MA, et al. Polymorphisms in the non-muscle myosin heavy chain 9 gene (MYH9) are strongly associated with end-stage renal disease historically attributed to hypertension in African Americans. Kidney Int 2009;75:736-45.  Back to cited text no. 30
[PUBMED]  [FULLTEXT]  
31.Kopp JB, Smith MW, Nelson GW, et al. MYH9 is a major-effect risk gene for focal segmental glomerulosclerosis. Nat Genet 2008; 40:1175-84.  Back to cited text no. 31
[PUBMED]  [FULLTEXT]  
32.Genovese G, Friedman DJ, Ross MD, et al. Association of trypanolytic ApoL1 variants with kidney disease in African Americans. Science 2010;329:841-5.  Back to cited text no. 32
[PUBMED]  [FULLTEXT]  
33.Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care 2004;27:1047-53.  Back to cited text no. 33
[PUBMED]  [FULLTEXT]  
34.Stavrou C, Koptides M, Tombazos C, et al. Autosomal-dominant medullary cystic kidney disease type 1: clinical and molecular findings in six large Cypriot families. Kidney Int 2002;62:1385-94.  Back to cited text no. 34
[PUBMED]  [FULLTEXT]  
35.Voskarides K, Damianou L, Neocleous V, et al. COL4A3/COL4A4 mutations producing focal segmental glomerulosclerosis and renal failure in thin basement membrane nephropathy. J Am Soc Nephrol 2007;18:3004-16.  Back to cited text no. 35
[PUBMED]  [FULLTEXT]  
36.Gale DP, de Jorge EG, Cook HT, et al. Identification of a mutation in complement factor H-related protein 5 in patients of Cypriot origin with glomerulonephritis. Lancet 2010; 376: 794-801.  Back to cited text no. 36
[PUBMED]  [FULLTEXT]  
37.Henrich WL, Clark RL, Kelly JP, et al. Non-contrast-enhanced computerized tomography and analgesic-related kidney disease: Report of the national analgesic nephropathy study. J Am Soc Nephrol 2006;17:1472-80.   Back to cited text no. 37
[PUBMED]  [FULLTEXT]  
38.Elseviers MM, Waller I, Nenoy D, et al. Evaluation of diagnostic criteria for analgesic nephropathy in patients with end-stage renal failure: Results of the ANNE study. Analgesic Nephropathy Network of Europe. Nephrol Dial Transplant 1995;10:808-14.  Back to cited text no. 38
[PUBMED]  [FULLTEXT]  

Top
Correspondence Address:
Guy H Neild
UCL Centre for Nephrology, Royal Free Campus, London NW3 2QG
United Kingdom
Login to access the Email id


PMID: 21743207

Rights and Permissions



 
 
    Tables

  [Table 1], [Table 2], [Table 3]

This article has been cited by
1 Incidence of End-Stage Renal Disease in the Turkish-Cypriot Population of Northern Cyprus: A Population Based Study
Connor, T.M.F. and Oygar, D.D. and Gale, D.P. and Steenkamp, R. and Nitsch, D. and Neild, G.H. and Maxwell, P.H.
PLoS ONE. 2013; 8(1)
[Pubmed]



 

Top
   
 
 
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  
 


 
    Abstract
   Introduction
   Methodology
    Lessons from Ped...
    Review of Adult ...
    Specific Comment...
   Definitions
   Proposal
   Discussion
    References
    Article Tables
 

 Article Access Statistics
    Viewed2483    
    Printed150    
    Emailed1    
    PDF Downloaded551    
    Comments [Add]    
    Cited by others 1    

Recommend this journal