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Saudi Journal of Kidney Diseases and Transplantation
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RENAL DATA FROM THE ARAB WORLD Table of Contents   
Year : 2002  |  Volume : 13  |  Issue : 4  |  Page : 515-519
Spectrum of Glomerular Disease in Iraqi Patients from a Single Center


1 Department of Nephrology, Rasheed Hospital, Baghdad, Iraq
2 Department of Pathology, Rasheed Hospital, Baghdad, Iraq
3 Department of Pathology, College of Medicine, University of Baghdad, Baghdad, Iraq
4 Consultant Nephrologist, Rasheed Hospital, Baghdad, Iraq

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   Abstract 

To evaluate the patterns of glomerular disease in our center, we reviewed and categorized a series of 520 kidney biopsies performed for proteinuric patients between June 1994 and June 2001. There were 445 (85.5%) biopsies labeled as primary glomerular disease, 55 (10.5%) as secondary glomerular disease and 20 (4%) as miscellaneous. The primary glomerular disease included 117 (26.3%) cases of focal segmental glomerulo­sclerosis, 100 (22.5%) of mesangial proliferative glomerulonephritis (GN), 76 (17.1%) of minimal change disease, 72 (16.2%) of membranoproliferative GN, 65 (14.5%) of membranous GN, and 15 (3.4%) of rapidly progressive GN. The secondary glomerular diseases included 25 (45.5%) cases of lupus nephritis, 15 (27.3%) of amyloidosis, eight (14.5%) of diabetic nephropathy, six (10.9%) of hereditary nephritis, and one (1.8%) hypertensive nephropathy. Because immunofluorescence was not used, we could not label any biopsy as IgA nephropathy. In conclusion, our study suggests that the patterns of histopathology found in the biopsies of the patients with proteinuria may reflect the patterns in Iraq and may not be different from those in the other Arab countries, especially those in the Middle East.

Keywords: Glomerular disease, Proteinuria, Prevalence, Rasheed Hospital, Iraq.

How to cite this article:
Shaker IK, Al-Saedi AJ, Al-Salam S, Saleem MS, Al-Shamma IA. Spectrum of Glomerular Disease in Iraqi Patients from a Single Center. Saudi J Kidney Dis Transpl 2002;13:515-9

How to cite this URL:
Shaker IK, Al-Saedi AJ, Al-Salam S, Saleem MS, Al-Shamma IA. Spectrum of Glomerular Disease in Iraqi Patients from a Single Center. Saudi J Kidney Dis Transpl [serial online] 2002 [cited 2014 Nov 23];13:515-9. Available from: http://www.sjkdt.org/text.asp?2002/13/4/515/33110

   Introduction Top


Glomerular disease constitutes a common cause of end-stage renal disease in many countries. [1] The glomeruli are usually injured by a variety of external factors, systemic diseases, [2],[3] and hereditary diseases. [4] Primary glomerular diseases include, focal and seg­mental glomerulosclerosis (FSGS), mesangial proliferative GN, membranous GN (MGN) membranoproliferative GN (MPGN), lipoid nephrosis or minimal change disease (MCD), IgA nephropathy (IgAN) and rapidly progressive GN (RPGN). [5],[6],[7],[8],[9]

All glomerular diseases were generally present with a variable range proteinuria, hematuria hypertension, and impaired renal function. [10],[11],[12],[13],[14] Moreover, glomerular disease may manifest as insidious development of uremia secondary to chronic glomerular disease. [15] The structural changes due to the deposition of immune complexes cause changes in the electrical charge of the glomerular basement membrane and modify the permeability to proteins. [16] There is usually associated inflammatory proliferative response within the injured glomerulus involving the endothelial, mesangial or epithelial cells that lead eventually to the damage of the kidneys. [17],[18]

Renal biopsy has a fundamental role in the evaluation of proteinuric patients. In some patients, the renal biopsy appears essential to determine an accurate diagnosis and prognosis and the choice of an appropriate treatment. [19],[20]

We report in this study the patterns of pathology we found in the renal biopsies performed at our center for proteinuric patients referred from other centers in the country, which may reflect the patterns elsewhere in Iraq.


   Materials and Methods Top


We studied the biopsies of 520 patients with proteinuria; their age ranged from 12 to 66 years and 342 (65.7%) were males. The patients were referred for diagnosis, evaluation, treatment and follow-up to the renal unit in Rasheed Hospital, Baghdad, Iraq, from June 1994 to June 2001,

All patients were subjected to clinical and histopathological studies. After stabilizing the patients' general condition, they had percutaneous kidney biopsies with modified Mengini (sure cut) 1.8 mm needle gauge 15. Most of the biopsies were performed as an outpatient procedure. [21]

Two pieces from the kidney tissue were obtained and sent to two histopathologists. The slides obtained from the specimens were stained with hematoxyn and eosin, Periodic Acid Schiff and silver impregnate; Congo red stain was used when amyloidosis was suspected. All tissue slides were examined by only light microscope.


   Results Top


There were 445 (85.5%) biopsies labeled as primary glomerular disease, 55 (10.5%) as secondary glomerular disease and 20 (4%) as miscellaneous. [Table - 1] shows the number, age range and gender of the different categories of the primary glomerular diseases that included 117 (26.3%) cases of FSGS, 100 (22.5%) of mesangial proliferative GN, 76 (17.1%) of MCD, 72 (16.2%) of MPGN, 65 (14.5%) of MGN, and 15 (3.4%) of RPGN.

[Table - 2], shows the number, age range and gender of the different categories of the secondary glomerular diseases that included 25 (45.5%) cases of lupus nephritis, 15 (27.3%) of amyloidosis, eight (14.5%) of diabetic nephropathy, six (10.9%) of here­ditary nephritis, and one (1.8%) hyperten­sive nephropathy.

The miscellaneous group included 16 cases of glomerulosclerosis; three of interstitial nephritis and one of shunt nephritis.


   Discussion Top


Our present study is more extensive than previously reported patterns of glomerular diseases from Iraq [Table - 3]. [21],[22] The most frequently diagnosed lesion in our patients with primary glomerular disease was FSGS.

This is less than the incidence in Saudi Arabia where FSGS represented 34.9% of cases. [23] However, in some countries, the frequency of FSGS was reported to be less than 15% [Table - 4]. [24] On the other hand, a higher incidence of FSGS had been reported from Hong Kong (23.6% adults) and Ghana (36% adults). The explanation for this variable frequency of FSGS in these surveys is not well understood. Since many of our study patients were labeled as steroid resistant nephrotic syndrome before referral for biopsy, referral bias may explain the high frequency of FSGS. Further studies may help to understand the various factors responsible for the high frequency of FSGS in the country.

The second most common primary glome­rulopathy in our study was mesangial proliferative GN. This lesion is characterized histologically by the presence of mild to moderate mesangial hypercellularity with varying degrees of expansion of the mesangial matrix. [25] Clinically, this disease is closely related to the other causes of the nephrotic syndrome, such as MCD and FSGS. [26] Diagnosis of IgA nephropathy was not made because of the lack of immuno­fluorescence microscopy. The incidence of RPGN was comparable to that in Saudi

Arabia [27].

The incidence of renal amyloidosis was relatively high in our study. This, however, is not out of the range of the 11.1 to 32.4% incidence reported from the countries in the Middle East; which is most probably related to the increased prevalence of familial  Mediterranean fever More Details [27] In other countries such as India, Germany, Sweden and USA, the incidence of amyloidosis is much lower varying from 1.3 to 3.3%. [27]

In conclusion, our study suggests that the patterns of histopathology found in the biopsies of the patients with proteinuria may reflect the pattern of glomerular diseases in Iraq and may not be different from those in the other Arab countries, especially those in the Middle East.

 
   References Top

1.Richard J. Johnson, John Fechally. Comp­rehensive clinical nephrology. Hacourt Publishers Limited 2000.  Back to cited text no. 1    
2.Myers BD, Guasch A. Mechanisms of proteinuria in nephrotic humans. Pediatr Nephrol 1994;8:107-12.  Back to cited text no. 2    
3.Cameron IS. Systemic lupus erythematosus. In: Nielson EG, Couser WG, eds, Immuno­logic Renal Disease, Philadelphia, Lippincot­Raven 1997:1055-94.  Back to cited text no. 3    
4.Hamburger Crosmer. Nephrology hereditary chronic nephritis and variants 1979;977-82.  Back to cited text no. 4    
5.Couser WG. Glomerular disorder. In: Wyngarden Smith LH, Jr (eds), Cecil Text­book of Medicine JB. 19 th ed. Philadelphia. WB Saunders 1992; p. 551-68.  Back to cited text no. 5    
6.Couser WG. Glomerular and vascular disease, In: Jacobson HR, Striker GE, Klahr S, (eds): The Principles and Practice of Nephrology, 2nd ed. St Louis, Mosby- Yearbook Inc. 1995;102-2000.  Back to cited text no. 6    
7.Glassock RJ, Cohen AH, Adler SG. Primary glomerular diseases. In: Brenner BM (ed), The Kidney, 5 th ed. Philadelphia, WB Saunders 1996;1392-479.  Back to cited text no. 7    
8.Glassock RJ, Cohen AH, Adler SG. Secon­dary glomerular diseases. In: Porenner BM (ed) The Kidney. 5 th ed. Philadelphia, WB Saunder 1996;1498-596.  Back to cited text no. 8    
9.Shah SV. Mechanisms of glomerular injury. Semin Nephrol 1991;11:253-372.  Back to cited text no. 9    
10.Mitwalli AH, Al-Wakeel JS, Al-Mohaya SS, et al. Pattern of glomerular disease in Saudi Arabia. Am J Kidney Dis 1996; 27(6):797-802.  Back to cited text no. 10    
11.Madaio MP. Renal biopsy. Kidney Int 1990;38:529-43.  Back to cited text no. 11    
12.Azerus JM, Brenner BM. Acute renal failure, 3rd ed, New York, Churchill Livingstone 1993.  Back to cited text no. 12    
13.The Principles and Practice of Nephrology, 2nd ed. Jacobson HR, Striker GE, Klahr S (eds) St. Louis, Mosby-Yearbook 1995;544-94.  Back to cited text no. 13    
14.Vane JR, Anggard EE, Botting RM. Regu­latory functions of the vascular endo­thelium. N Engl J Med 1990;323:27-36.  Back to cited text no. 14    
15.Albers FJ. Clinical characteristics of athero­sclerotic renovascular disease. Am J Kidney Dis 1994;24(4):636-41.  Back to cited text no. 15    
16.Hudson BG, Kalluri R, Gunwar S, et al. Molecular characteristics of the good pasture autoantigen. Kidney Int 1993;43:135-9.  Back to cited text no. 16    
17.Cecil Essentials of Medicine 4 th ed. WB Saunders Company 1997;215.  Back to cited text no. 17    
18.Churg J, Habib R, White RH. Pathology of the nephrotic syndrome in children: a report for the International Study of Kidney diseases in Children. Lancet 1970;760:1299-302.  Back to cited text no. 18    
19.Pirani CL. Evaluation of kidney biopsy specimens. In: Tisher CG, Biopsy Speci­mens, in Tisher CG, AJKDs 2000.  Back to cited text no. 19    
20.Brenner BM (eds): Renal pathology with clinical and functional correlations (ed 2). Philadelphia, PA, Lippincott 1994;85-115.  Back to cited text no. 20    
21.Mahassin SS, Waleed R. Ezzat. Renal histopathological lesion in Iraq with particular reference to glomerulonephritis. J Fac Medic 39(4):352-8.  Back to cited text no. 21    
22.Al Habbal MJ. Clinicopathological study of adult patients with proteinuria during the period of 1996-1998 from Mousl-Iraq. The Sixth Congress of the Arab Society of Nephrology and Renal Transplantation February 21-24-2000, Marrakech Morocco.  Back to cited text no. 22    
23.Nass K, O'Neill WC. Bedside renal biopsy. Ultrasound guidelines by the nephrologist. Am J Kidney Dis 1999;34:955-9.  Back to cited text no. 23    
24.Akhtar M, Quinbi W, Taher S. Spectrum of renal disease in Saudi Arabia, a study of 380 kidney biopsies. Ann Saudi Med 1990; 10(1).  Back to cited text no. 24    
25.Abrass CK. Renal Biopsy in the elderly. Am J Kidney Dis 2000;35(3):544-6.  Back to cited text no. 25    
26.Special issue on Glomerular Diseases. Saudi J Kidney Dis Transplant 2000;11(3).  Back to cited text no. 26    
27.Qunibi WY, Al-Sibat B, Taher S, Akhtar M. Renal disease in Saudi Arabia; a study of 147 renal biopsies King Faisal Specialist Hospital J 1984;4:317-23.  Back to cited text no. 27    

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Correspondence Address:
Ihsan A Al-Shamma
Consultant Nephrologist, Rasheed Hospital, P.O. Box 26003, Baghdad
Iraq
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PMID: 17660678

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