Saudi Journal of Kidney Diseases and Transplantation

LETTER TO THE EDITOR
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


Guy H Neild1, D Deren Oygar2, Mohamed Ben Hmida3,  
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

Correspondence Address:
Guy H Neild
UCL Centre for Nephrology, Royal Free Campus, London NW3 2QG
United Kingdom




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;22:573-575


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 2021 Sep 20 ];22:573-575
Available from: https://www.sjkdt.org/text.asp?2011/22/3/573/80506


Full Text

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, andother 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

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