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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2011  |  Volume : 22  |  Issue : 3  |  Page : 573-575
Can we improve diagnosis of renal failure? A revised coding system for Middle East and North Africa

1 UCL Centre for Nephrology, Royal Free Campus, London NW3 2QG, United Kingdom
2 Nicosia State Hospital, Burhan Nalbantoglu General Hospital, North Cyprus, Tunisia
3 Department of Nephrology, H Chaker Hospital, 3029 Sfax, Tunisia

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Date of Web Publication7-May-2011

How to cite this article:
Neild GH, Oygar D D, Hmida MB. Can we improve diagnosis of renal failure? A revised coding system for Middle East and North Africa. Saudi J Kidney Dis Transpl 2011;22:573-5

How to cite this URL:
Neild GH, Oygar D D, Hmida MB. Can we improve diagnosis of renal failure? A revised coding system for Middle East and North Africa. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2022 Dec 9];22:573-5. Available from: https://www.sjkdt.org/text.asp?2011/22/3/573/80506
To the Editor,

In registry data, "etiology unknown" is often the most common designation. [1] There may be many reasons for this, such as poor quality reporting and late presentation. Diagnosis terms should be used precisely and consistently; for instance, we must know what percentage of those categorized as "glomerulonephritis" had a renal biopsy. Currently, common diagnostic categories such as hypertension and renovascular disease are undefined.

We reviewed the regional data published during the decade 2000-2009, and propose a system in which all specific diagnoses can be summarized. We recommend that 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 kidney disease.

We reviewed the published studies on primary renal disease (PRD) in patients reaching end-stage renal failure (ESRF) from Eastern Mediterranean, Middle East, Arabia and North Africa, and we used PubMed, Google, and the following cited references to find these studies.

Since 1976, pediatric registries have reduced the number of children with "no specific diagnosis" from 39% to less than 5%. [2],[3] However, our review of studies in the adult population showed that none used a methodology similar to another. All papers were characterized by lack of case definitions and details of biopsies including immuno-peroxidase (IP)/immunoflourescence (IF) and/or electron microscopy. We noticed that the percentage of "unknown" plus "hypertension" diagnosis of primary kidney disease was around 45-50%. [4],[5],[6],[7],[8],[9],[10],[11],[12],[13]

For studies in our region, we propose a system in which all diagnoses should fall into one of the following eight 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 should have sub-headings, for instance, primary glomerulonephritis, secondary glomerulonephritis, and hereditary glomerular disease. Under each sub-heading, there is a list of specific diagnoses similar to those 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 be paid to evidence for a family history of renal disease.

There are a number of key clinical issues that need to be resolved, which relate to clinical terminology; many patients with slowly progressive renal disease such as reflux nephropathy/ renal dysplasia develop secondary focal segmental glomerulosclerosis (FSGS). EDTA has no code for secondary FSGS. 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. [14] Underlying renal disease can result in malignant or accelerated hypertension, which can certainly result in rapid loss of the remaining kidney function. There is a new change in the designation of hypertensive nephropathy since the discovery of a gene related to the development of ESRF. 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. [15]

Furthermore, late presentation without earlier symptoms, no edema, and minimal proteinuria may be 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, [16] 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.

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 which 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
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;14:70-112.  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.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. 4
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5.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. 5
[PUBMED]  Medknow Journal  
6.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. 6
7.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. 7
8.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. 8
9.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. 9
10.Afshar R, Sanavi S, Salimi J. Epidemiology of chronic renal failure in Iran: A four year singlecenter experience. Saudi J Kidney Dis Transpl 2007;18:191-4.  Back to cited text no. 10
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11.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. 11
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12.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;10:620-6.  Back to cited text no. 12
13.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. 13
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14.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. 14
15.Freedman BI, Sedor JR. Hypertension-associated kidney disease: Perhaps no more. J Am Soc Nephrol 2008;19:2047-51.  Back to cited text no. 15
16.Barsoum RS, Francis MR. Spectrum of glomerulonephritis in Egypt. Saudi J Kidney Dis Transpl 2000;11:421-9.  Back to cited text no. 16
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Correspondence Address:
Guy H Neild
UCL Centre for Nephrology, Royal Free Campus, London NW3 2QG
United Kingdom
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Source of Support: None, Conflict of Interest: None

PMID: 21566326

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