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Saudi Journal of Kidney Diseases and Transplantation
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REVIEW ARTICLE Table of Contents   
Year : 2000  |  Volume : 11  |  Issue : 4  |  Page : 567-576
Glomerulonephritis in Saudi Arabia: A Review


Department of Medicine, King Khalid University Hospital, Riyadh, Saudi Arabia

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   Abstract 

Glomerulonephritis (GN) is one of the leading causes of end-stage renal disease. A good understanding of its pattern and prevalence as well as exploration of effective therapeutic strategies for protecting the glomerulus, would have tremendous impact on public health. In the Kingdom of Saudi Arabia (KSA), focal and segmental glomerulo sclerosis (FSGS) is the commonest type of primary glomerular diseases (PGD) encountered in clinical practice. Its prevalence varies from less than 4% in Gizan, in the southern part of KSA, to approximately 35% in Riyadh, central Saudi Arabia. In our experience, the nephrotic syndrome was the commonest mode of presentation of FSGS. Response to corticosteroid therapy is generally poor and the mortality rate is high. Mesangioproliferative GN is the second most common GN constituting up to 25% of PGD in our experience. Other researchers from different parts of the Kingdom, however, have given prevalence rates ranging from 8 to 57.1%. The reported prevalence of Immunoglobulin-A nephropathy (IgAN) in KSA ranges from 5.8% to 13.6%. It is more common in the elderly, and men are affected more often than women. In contrast to KSA, IgAN is the commonest PGD in Japan, China, Hong Kong, Singapore and Taiwan. Membranous GN (MGN) is less common in KSA than encountered elsewhere, the prevalence ranging from 3.9 to 21.8%. Nephropathy secondary to systemic diseases are also common in KSA. Lupus nephritis (LN) accounted for 48.5% of secondary glomerular diseases (SGD) with the combination of WHO classes III and IV (aggressive types of LN) accounting for 56% of all patients. LN is another disease where differences in racial susceptibility may account for the uneven distribution. Post-streptococcal GN seems to be declining in frequency in KSA, the reported prevalence ranging from 2.7% to 2.9%.

Keywords: Glomerular disease, Lupus nephritis, Proteinuria, Prevalence, Saudi Arabia.

How to cite this article:
Mitwalli AH. Glomerulonephritis in Saudi Arabia: A Review. Saudi J Kidney Dis Transpl 2000;11:567-76

How to cite this URL:
Mitwalli AH. Glomerulonephritis in Saudi Arabia: A Review. Saudi J Kidney Dis Transpl [serial online] 2000 [cited 2017 Dec 11];11:567-76. Available from: http://www.sjkdt.org/text.asp?2000/11/4/567/36645

   Introduction Top


Glomerular diseases constitute one of the commonest causes of end-stage renal disease (ESRD) in many countries including Saudi Arabia. The glomeruli are injured by a variety of external factors and also during the course of a number of systemic diseases e.g., autoimmune disorders such as systemic lupus erythematosus (SLE), vascular diseases like hypertension (HTN), metabolic diseases like diabetes mellitus (DM) and hereditary diseases such as Alport's syndrome. While these constitute secondary glomerular diseases (SGD), the primary glomerular diseases (PGD) are those wherein, kidneys are the predominant organs that are involved. Primary glomerular diseases include; focal and segmental glomerulosclerosis (FSGS), memb-ranous glomerulonephritis (MGN) membrano­proliferative glomerulonephritis (MPGN), lipoid nephrosis or minimal change disease (MCD), IgA nephropathy (IgAN), and rapidly progressive glomerulonephritis (RPGN). [1]

All glomerular diseases generally present with proteinuria, hypertension, hematuria, impaired renal function, singly or in combination. They can present as: the nephrotic syndrome (NS) with marked proteinuria, hypo-albuminemia and edema or; the nephritic syndrome characterized by hematuria, red blood cell (RBC) casts, decreased glomerular filtration rate, hyper­tension, and azotemia or; as RPGN with profound oliguria and rapid progression to renal failure. Also, glomerular diseases may manifest as insidious development of uremia secondary to chronic glomerular diseases (CGD). The NS is associated with structural changes as well as changes in electrical charge of the glomerular basement membrane (GBM) due to deposition of immune­complexes, thus modifying its permeability to proteins. The nephritic syndrome presents as an entity which evokes an inflammatory proliferative response within the glomeruli involving endothelial, mesangial or epithelial cells and infiltration of macrophages within the capillary lumens, Bowman's capsule or peri-glomerular interstitial tissue. In chronic renal disease, hyalinization is present and structural detail of glomeruli is lost.

PGDs constitute the commonest GN [2],[3] occurring mostly in young adults between 21-40 years of age. At the King Khalid University Hospital (KKUH), Riyadh, Saudi Arabia, biopsy proven PGDs constituted 79% of total renal biopsies. [2] In this review article, the patterns of glomerular diseases and their clinicopathological presentations are reviewed. Also, their prevalence in Saudi Arabia is compared with the prevalence reported from other parts of the world.

[Table - 1],[Table - 2] summarize the prevalence of various glomerular diseases in Saudi Arabia and other parts of the world while [Table - 3],[Table - 4] summarize the clinico­pathologic features.

Focal and Segmental Glomerulosclerosis

FSGS is the commonest type of PGD encountered in Saudi Arabia. [2],[3] In FSGS, a few glomeruli are affected initially, and then, as the disease progresses to a more advanced form, there is widespread involvement of all cortical glomeruli. In the affected glomeruli, mesangial deposits of IgM and complement are noted. Histolo­gically, FSGS is characterized by sclerosis and hyalinization within the glomerulus. FSGS generally presents with hematuria, proteinuria and/or hypertension. In our experience, 61.7% of the patients with FSGS presented as the NS, 86.7% had hypertension and 33.3% had renal insuf­ficiency. [2] of FSGS Response to cortico­steroid therapy is poor. [4] The mortality rate is quite high and 50% of the affected patients die within 10 years of onset of the disease. Those who survive have persistent urinary abnormalities. FSGS is the most common cause of the NS in children. [5] It is the most common PGD in Ghana; [6] also its prevalence is high in Italy, being 11%. [7] The prevalence of FSGS was 40.8% in our earlier study [2] and is 34.6% in our recent study [3] at KKUH. The prevalence within Saudi Arabia varies from less than 4% in Gizan in the southern part of Saudi Arabia to approxi­mately 35% in Riyadh, central province [8],[9],[10] [Table - 1]. Comparable results (36%) are reported from Ghana and other African countries such as Senegal. [11] Also, it is reported to be the most common cause of the NS in black adults in the USA. [12],[13] It occurs more commonly in the age-group 40-60 years.

FSGS is said to carry a high risk for the development of ESRD, [14] especially if associated with poor prognostic factors like hypertension, [15] the NS and renal insuf­ficiency. [16] The incidence of FSGS is increasing with the passage of time. Piero et al found a 10-fold increase in the incidence of FSGS over a period of 20 years in Europe. [7] The prevalence of FSGS is 7.8% in European countries. [17],[18] Some researchers have found that FSGS has a marked racial predominance, [19],[20] as also a genetic pre­disposition. [21],[22],[23],[24] Familial forms of FSGS have recently been reported. [25] Recently, FSGS was found running in eight families in an autosomal dominant form. [26] It is also reported to be associated with hepatitis C virus infection. [27] In separate studies, it was found that mice transgenic for recombinant retrovirus MPSV neo and the early portion of simian virus 40 have both been demonstrated to develop FSGS. [28],[29] Also, it has been found that infection with human immune deficiency virus (HIV) predisposes a person to develop FSGS. [30],[31],[32],[33] Agati et al have found association of HIV infection with a rapidly progressive FSGS. [34] Further studies are required to know if there are any other predisposing factors for the development of FSGS.

Mesangioproliferative Glomerulonephritis

Mesangioproliferative GN is the second most common GN constituting 21% of PGD [3] in our present study, while it was 25.1% [2] in our previous study. The prevalence varies in different parts of KSA ranging from 8 - 57.1% [Table - 1], as also in other parts of the world being 37.5% in Jamaica and 68.7% in Singapore [Table - 2].

Membranous Glomerulonephritis

MGN is a slowly progressive disease of young and middle aged adults. It is characterized by a well defined alteration in GBM, [35] namely thickening of GBM due to immune deposits. It is an immune-complex disease, 85% of cases are idiopathic while 15% of cases have known etiological factors. They include tumour antigens in patients with cancer, [36] a known association with hepatitis B surface antigen (HBsAg), DNA antigen-antibody complexes in patients with SLE, drugs like penicillamine, and metals like gold and mercury which can all evoke lesions of MGN. [1] MGN is characterized by an insidious development of the NS; 25% of the patients progress to renal failure. [1] Of the remaining patients, about 50% remit while the remaining will have persistent proteinuria. The prevalence of MGN was 3.9% [3] and 13.6 [2] in our two studies. The prevalence ranges from 3.9 to 21.8% in different reports from KSA [Table - 1] while in other parts of the world, MGN constitutes 6.8% of PGD in India and 11.5% of total PGD in Italy. [7] The report prevalence of MGN in Africa and Southeast Asia is quite high being 21.4%. [10],[37],[38],[39],[40]

IgA Nephropathy

IgAN or Berger's disease usually affects children and young adults. It manifests as gross hematuria lasting for several days that subsides spontaneously, only to recur after a few months. Histologically, there is IgA deposition in the mesangium. [41] It is a variant of Henoch Schonlein Purpura and has similar renal histology wherein, the glomeruli may show mesangial widening and segmental proliferation. Characteristic immunofluorescent picture is deposition of IgA in the mesangium often with C3. There is a genetic determinant of the synthesis of IgA which is entrapped in the mesangium. About 50% of patients with IgAN develop ESRD over a 20-year period. [1]

The prevalence of IgAN in our previous studies were 10.2% [3] and 13.6% [2] while in other parts of KSA, the reported prevalence of IgAN ranges from 5.8% to 13.6% [Table - 1]. It is more common in the elderly, and men are affected more often than women, 12.5% vs 8.5%. [2] In contrast to KSA, IgAN is the commonest PGD in Japan, China, Hong Kong, Singapore and Taiwan and accounts for about 50% of all patients [42],[43],[44],[45],[46] while in India the prevalence is low at 4.7%. Similarly in the USA, blacks have a low prevalence of IgAN disease (2%). [45] IgAN is common in Europe and accounts for 34.5% of PGD. [7]

Minimal Change Disease

Although this disease can develop at any age, it is most common in children between two to three years of age. Histologically, there is diffuse fusion and loss of foot processes of epithelial cells. The disease manifests by insidious development of the NS while renal function is preserved. The prognosis is relatively good and 90% of the cases respond to steroids although proteinuria may recur (relapses are more common in adults) and a few patients may go to renal failure. In one large study of biopsy proven cases followed-up for up to 10 years, 71% had complete remission, 22% had persistent disease and 7% died of renal failure. [47] In our earlier studies, the prevalence of MCD in adults was 8.6% [3] and 1.4%. [2] In other reports from the KSA, the reported prevalence of the disease in adults ranges from 1.1% to 11.2% [Table - 1]. The incidence of MCD in Ghana is 10%, Tunisia 16%, and South Africa 10.7% while it is more common in India at 29%. 10 In Italy, the reported incidence of MCD is 7.4%, and is more frequent in the age-group 15-44 years (0.49%), while it is low in ages 65-75 years being 0.13 - 0.31%. [7]

Post-streptococcal Glomerulonephritis

It is less common in developed countries and commoner in tropics. [46] In our recent study, the prevalence of post-streptococcal GN was 2.7%, [3] while in other reports from the KSA, the prevalence has ranged from 2.7%-2.9% [Table - 1]. The prevalence of the disease is reported to be 28% in Zimbabwe and it is generally associated with the NS. [46]

Rapidly Progressive Glomerulonephritis

This disease is associated with rapid and progressive loss of renal function with oliguria and the vast majority of patients develop ESRD within weeks to months [1] . It is characterized by the presence of crescents in most of the glomeruli, formed by marked proliferation of parietal epithelial cells of Bowman's capsule and infiltration of macrophages and monocytes. It may be idiopathic, post-infectious (e.g. post-strep-tococcal) or due to SLE, where it is mediated by immune-complexes. Anti­GBM antibodies are found in 95% of cases of RPGN. [48] These antibodies also react with the alveolar basement membrane in the lung and produce pulmonary hemorrhage. In our recent study, the prevalence of RPGN was 1.5% [3] while in some other studies in KSA the reported prevalence of RPGN was 2.2% [63] and 4.4%. [10]

Lupus Nephritis

Renal manifestations of SLE are variable, ranging from mild proteinuria to RPGN, causing renal insufficiency within weeks. [49],[50] Lupus nephritis (LN) can be classified into six groups and sub-groups according to the recently modified WHO classification. [51] There is a close association between histological findings and clinical findings. [52] The main feature of LN is deposition of immunoglobulins and comp­lement either in the mesangium (WHO Class II) or in the mesangium and capillary loops (WHO Class III, IV or V). [53] Nucleosomes bind these deposits to the cell surface, [54] or to heparan sulfate in GBM, [55] as well as to endothelial and mesangial cells. [56] These nucleosomes are major auto­antigens which activate B-cells [57] and can also produce tissue lesions. [58]

The prevalence of LN is quite high in KSA. In our previous study, LN accounted for 48.5% of SGD, and of this 37% were Class III, 25% Class II, 18.8% Class IV, 12.2% Class I and 6.25% Class V. [2] LN is more common in females than males (15.9% vs 2.9%). [2] Similar high prevalence of LN was found by Akhtar et al who reported a 46.7% prevalence rate amongst all SGDs. [10] The prevalence of LN in different areas of KSA is given in [Table - 1].

Difference in racial susceptibility may account for the uneven distribution of LN. In Jamaica, it is the most prevalent cause of the NS and accounts for 38% of all NS patients. A 3-fold greater prevalence of the disease was found in blacks than whites in the USA. [59]

Hypertensive Nephrosclerosis

Post-hypertensive GN occurs due to a rise in the systemic blood pressure. Increase in blood pressure increases the filtration of fibrinogen and other plasma proteins from small blood vessels; the fibrinogen gets deposited in the wall of these vessels where it stimulates the clotting process. On microscopy, there is formation of micro­thrombi and fibrinoid necrosis of the arteriole. Often, there may be infiltration of inflammatory cells giving rise to necrotizing arteriolitis which may eventually progress to involve all glomeruli. The most characteristic response is proliferation of intimal cells of the blood vessels giving rise to an onion peel appearance which is called hyperplastic arteriosclerosis. Due to the narrowing of the lumen of the blood vessels, blood flow to the kidney is reduced, the kidney becomes markedly ischemic and later on, atrophic. A viscious cycle develops in a way that ischemia stimulates the renin-angiotensin system, which produces intra-renal vasoconstriction, which further produces renin causing further vasoconstriction and so on. Aldosterone secretion is increased which results in salt and water retention which further increases blood pressure and the cycle goes on. The disease presents as constant proteinuria and microscopic hema-turia with occasional intermittent gross hematuria. Untreated patients could die of uremia or cerebrovascular accidents but with treatment, the 5-year survival rate is 50% and the overall prognosis depends on early treatment before kidney damage occurs. [1]

In the benign form of hypertension, renal failure is rare. There is only mild impairment of renal functions e.g. glomerular filtration rate is reduced, concentrating ability of the kidney is decreased and there may be mild but constant proteinuria. In our previous studies, the prevalence of hypertensive nephrosclerosis were found to be 3.3% [3] and 17.6% [63] while in other studies in the Kingdom, the prevalence of hypertensive nephrosclerosis ranges from 3.3 to 40% [Table - 1].

Concluding Remarks

It seems likely that development of new therapeutic regimens to protect the glomerular function will continue to be a major area of research. The prevalence, presentation and predisposing factors of the most common diseases like FSGS and LN will be feasible paradigms for the develop­ment of new insight into pharmacological approaches. However, glomerular diseases are clinically heterogenous. The co-existence of other diseases and risk factors could modify the outcome and prognosis of renal disease. Wider investigations could shed some light on underlying pathology of the intriguing glomerulopathies and will contribute greatly in creating a healthy society[64].


   Acknowledgement Top


The author wishes to express his thanks and special appreciation to Dr. Durdana Hammad for her help and Miss Miriam Culanding Tampos for her secretarial assistance.

 
   References Top

1.Kumar V, Cotran R, Robbins S. The kidney and its collecting system. In: Basic Pathology, 6th edition (ed), W.B. Saunders Company, 1997;439-70.  Back to cited text no. 1    
2.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. 2    
3.Mitwalli AH, Al-Wakeel J, Abu-Aisha H, et al. Prevalence of glomerular diseases: King Khalid University Hospital, Saudi Arabia. Saudi J Kidney Dis Transplant 2000;11(3):442-8.  Back to cited text no. 3    
4.Goldszer RC, Sweet J, Cotran RS. Focal segmental glomerulosclerosis. Ann Rev Med 1984;35:429-49.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Habib R, Kleinknecht C. The primary nephrotic syndrome of childhood. Classifi­cation and clinicopathologic study of 406 cases. Pathol Annu 1971;6:417-74.  Back to cited text no. 5    
6.Adu D, Anim Addo Y, Foli AK, et al. The nephrotic syndrome in Ghana. Clinical and pathological aspects. Q J Med 1981; 50:297-306.  Back to cited text no. 6    
7.Stratta P, Segoloni-GP, Canavese-C, et al. Incidence of biopsy-proven primary glomerulonephritis in an Italian province. Am J Kidney Dis 1996;27(5):631-9.  Back to cited text no. 7    
8.Jorgensen HE, Malik SH, Paul TT, Whorra PC. Renal disease in Saudi Arabia. Pediatr Nephrol 1985;5:195.  Back to cited text no. 8    
9.Qunibi WY, Al-Sibai MB, Taher S, Akhtar M. Renal disease in Saudi Arabia: A study of 147 renal biopsies. King Faisal Specialist Hospital Journal 1984;4:317-23.  Back to cited text no. 9    
10.Akhtar M, Qunibi W, Taher S, et al. Spectrum of renal disease in Saudi Arabia. Ann Saudi Med 1990;10:37-44.  Back to cited text no. 10    
11.Morel-Maroger L, Saimot AG, Sloper JC, et al. Tropical nephropathy and tropical extramembranous glomerulonephritis of unknown aetiology in Senegal. Br Med J 1975;1:541-6.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Bakir AA, Bazilinski NG, Rhee HL, Ainis H, Dunea G. Focal segmental glomerulo­sclerosis. A common entity in nephrotic black adults. Arch Intern Med 1989;149:1802-4.  Back to cited text no. 12    
13.Pontier PJ, Patel TG. Racial differences in the prevalence and presentation of glomerular disease in adults. Clin Nephrol 1994;42:79-84.  Back to cited text no. 13  [PUBMED]  
14.Korbet SM, Schwartz MM, Lewis EJ. The prognosis of focal segmental glomerular sclerosis of adulthood. Medicine 1986;65: 304-11.  Back to cited text no. 14  [PUBMED]  
15.Ritz E, Rambausek M, Hasslacher C, Mann J. Pathogenesis of hypertension glomerular disease. Am J Nephrol 1989;9:85-90.  Back to cited text no. 15    
16.Rydel JJ, Korbet SM, Borok RZ, Schwartz MM. Focal segmental glomerular sclerosis in adults: presentation course and response to treatment. Am J Kidney Dis 1995;25: 534-42.  Back to cited text no. 16  [PUBMED]  
17.Jungers P, Nochy D, Geffriaud C, Droz N, Noel LH, Berger J. Epidemiology of primary glomerulonephritis GN in French Urban Area XII th International Congress of Nephrology 1993;pp 77.  Back to cited text no. 17    
18.Simon P, Ramee MP, Autuly V, et al. Epidemiology of primary glomerular disease in a French region. Variations according to period and age. Kidney Int 1994;46:1192-8.  Back to cited text no. 18    
19.Haas M, Spargo BH, Coventry S. Increasing incidence of focal segmental glomerulo­sclerosis among adult nephropathies: a 20­year renal biopsy study. Am J Kidney Dis 1995;26:740-50.  Back to cited text no. 19  [PUBMED]  
20.Barisoni L, D'AGati V. The changing epidemiology of focal segmental glome­rulosclerosis in New York City. Mod Pathol 1994;7:156A.  Back to cited text no. 20    
21.D'Agati V. The many masks of focal segmental glomerulosclerosis. Kidney Int 1994;46:1223-41.  Back to cited text no. 21  [PUBMED]  
22.D'Agati V, Suh JI, Carbone L, Cheng JT, Appel G. Pathology of HIV associated nephropathy: a detailed morphologic and comparative study. Kidney Int 1989;35: 1358-70.  Back to cited text no. 22  [PUBMED]  
23.Detwiler RK, Falk RJ, Hogan SL, Jennette JC. Collapsing glomerulopathy: a clinically and pathologically distinct variant of focal and segmental glomerulosclerosis. Kidney Int 1994;45:1416-24.  Back to cited text no. 23  [PUBMED]  
24.Haskell LP, Glicklich D, Senitzer D. HLA associations in heroin-associated nephro­pathy. Am J Kidney Dis 1988;12:45-50.  Back to cited text no. 24  [PUBMED]  
25.Conlon-PJ, Butterly-D, Albers F, Rodby R, Gunnells JC, Howell DN. Clinical and pathologic features of familial focal segmental glomerulosclerosis. Am J Kidney Dis 1995;26(1):34-40.  Back to cited text no. 25    
26.Winn-MP, Conlon-PJ, Lynn-KL, et al. Linkage of a gene causing familial focal segmental glomerulosclerosis to chromo­some II and further evidence of genetic heterogeneity. Genomics 1999;58(25): 113-­20.  Back to cited text no. 26    
27.Stehman-Breen-C, Alpers CE, Fleet WP, Johnson RJ. Focal segmental glomerular sclerosis among patients infected with hepatitis C virus. Nephron 1999;81:37-40.  Back to cited text no. 27    
28.Weiher H, Noda T, Gray DA, Sharpe AH, Jaenisch R. Transgenic mouse model of kidney disease: Insertional inactivation of ubiquitously expressed gene leads to nephrotic syndrome. Cell 1990;62:425-34.  Back to cited text no. 28  [PUBMED]  [FULLTEXT]
29.MacKay K, Striker LJ, Pinkert CA, Brinster RL, Striker GE. Glomerulo-sclerosis and renal cysts in mice trans-genic for the early region of SV 40. Kidney Int 1987;32:827-­37.  Back to cited text no. 29  [PUBMED]  
30.Kimmel PL, Phillips TM, Ferreira-Centeno A, Farkas-Szallasi T, Abraham AA, Garrett CT. HIV associated immune mediated renal disease. Kidney Int 1993;44:1327-40.  Back to cited text no. 30  [PUBMED]  
31.Casanova S, Mazzuco G, Barbiano-di­Belgiojoso G, et al. Pattern of glomerular involvement in human immunodeficiency virus infected patients: an Italian study. Am J Kidney Dis 1995;26:446-53.  Back to cited text no. 31    
32.Cantor ES, Kimmel PL, Bosch JP. Effect of race on expression of acquired immuno­deficiency syndrome associated nephro­pathy. Arch Intern Med 1991;151:125-8.  Back to cited text no. 32  [PUBMED]  
33.Nochy D, Glotz D, Dosquet P, et al. Renal disease associated with HIV infection: a multicentric study of 60 patients from Paris hospitals. Nephrol Dial Transplant 1993;8:11-9.  Back to cited text no. 33  [PUBMED]  [FULLTEXT]
34.D'Agati V, Appel GB. HIV infection and the kidney. J Am Soc Nephrol 1997;8(1):138-52.  Back to cited text no. 34    
35.Arnaut MA. Membranous glomerulo­nephritis. Nephrotic syndrome. Contem­porary issue in Nephrology. Vol 3, New York, Churchill Livingstone 1982;pp199-236.  Back to cited text no. 35    
36.Gandini E, Allaria P, Castiglioni A, d'Amato-I, Schiaffino E, Giangrande SE. Minimal change nephrotic syndrome with cecum adenocarcinoma. Clin Nephrol 1996;45(4):268-70.  Back to cited text no. 36    
37.Li LS. Renal disease in China. An overview. Proceedings 3rd Asian Pacific Congress of Nephrology, Singapore 1986; pp 292-6.  Back to cited text no. 37    
38.Lim GJ. Hepatitis B virus associated membranous glomerulonephritis in children in Taiwan. Proc 7th Asian Colloquium Nephrol Taipei 1987; pp 119-20.  Back to cited text no. 38    
39.Johnson R, Gretch DR, Yamabe H, et al. Membrano proliferative glomeruloneph-ritis associated with hepatitis C virus infection. N Engl J Med 1993;328:465-70.  Back to cited text no. 39    
40.Khan TN, Sinniah R, Naqvi SA, Lal M, Osmani M. IgA nephropathy in Pakistan. J Pakistan Med Assoc 1990;40:31-6.  Back to cited text no. 40    
41.Woodroffe AJ, Clarkson AR, Seymour AE, Lomax-Smith JD. Mesangial IgA nephritis. Springer Semin Immunopathol 1982;5(3): 321-32.  Back to cited text no. 41    
42.Li L, Lei-Shi L, et al. Primary glomerulo­nephritis in China. Chinese Med J 1989;102:159-64.  Back to cited text no. 42    
43.Chiang GS, Woo KT, Edmondson RP, et al. Pattern of glomerulonephritis in Singapore. Proc 3rd Asian Pacific Congr Nephrol, Singapore 1986,pp 249-61.  Back to cited text no. 43    
44.Lim GJ. Hepatitis B virus associated membranous glomerulonephritis in children in Taiwan. Proc 7th Asian Colloquium Nephrol, Taipei 1987,pp 119-20.  Back to cited text no. 44    
45.Levy M, Berger J. Worldwide perspective of IgA nephropathy. Am J Kidney Dis 1988;12:340-7.  Back to cited text no. 45  [PUBMED]  
46.Chugh KS, Sakhuja V. Glomerular diseases in the tropics. Am J Nephrol 1990;10:437-50.  Back to cited text no. 46  [PUBMED]  
47.Habib R, Kleinknecht C. The primary nephrotic syndrome of childhood. Classifi­cation and clinicopathologic study of 406 cases. Pathol Annu 1971;6:417-74.  Back to cited text no. 47    
48.Lewis EJ, Schwartz MM. Idiopathic crescentic glomerulonephritis. Semin Nephrol 1982;2:193.  Back to cited text no. 48    
49.Briggs WA, Johnson JP, Teichman S, Yeager HC, Wilson CB. Antiglomerular basement membrane antibody-mediated glomerulonephritis and Goodpasture's syndrome. Medicine 1979;58:348-61.  Back to cited text no. 49  [PUBMED]  
50.Adler S, Cohen AH, Glassock RJ. Secondary glomerular diseases, in The Kidney. Edited by BRENNER BM. Philadelphia. Saunders 1996,pp 1498.  Back to cited text no. 50    
51.Kashgarian M. Lupus nephritis: lessons from the path lab. Kidney Int 1994;45:928-38.  Back to cited text no. 51  [PUBMED]  
52.Tan EM. Antinuclear antibodies: diagnostic markers for autoimmune diseases and probes for cell biology. Arch Immunol 1989;44:93-151.  Back to cited text no. 52    
53.Churg J, Bernstein J, Glassock RJ. Lupus nephritis. In renal diseases, classification and atlas of glomerular diseases, edited by Churgh J, Bernstein J, Glassock RJ, New York, Igaku-Shoin, 1995,pp 151.  Back to cited text no. 53    
54.Jacob L, Viard JP, Allenet B, et al. A monoclonal anti-double-stranded DNA autoantibody binds to a 94-kDa cell-surface protein on various cell types via nucleosomes or a DNA-histone complex. Proc Natl Acad Sci USA 1989;86:4669-73.  Back to cited text no. 54  [PUBMED]  [FULLTEXT]
55.Termaat RM, Brinkman K, Van Gompel F, et al. Cross-reactivity of monoclonal anti­DNA antibodies with heparan sulfate is mediated via bound DNA/histone complexes. J Autoimmun 1990;3:531-45.  Back to cited text no. 55  [PUBMED]  
56.Termaat RM, Assmann KJ, Van Son JP, Dijkman HB, Koene RA, Berden JH. Antigen-specificity of antibodies bound to glomeruli of mice with systemic lupus erythematosus-like syndromes. Lab Invest 1993;68:164-73.  Back to cited text no. 56  [PUBMED]  
57.Bell DA, Morrison B, Vandenbygaart P. Immunogenic DNA-related factors. Nucleo­somes spontaneously released from normal murine lymphoid cells stimulate proliferation and immunoglobulin synthesis of normal mouse lymphocytes. J Clin Invest 1990;85:1487-96.  Back to cited text no. 57    
58.Berden JH. Lupus nephritis. Kidney Int 1997;52(2):538-58.  Back to cited text no. 58    
59.Fessel WJ. Systemic lupus erythematosus in the community. Incidence prevalence, outcome and first symptoms; the high prevalence in black women. Arch Intern Med 1974;134:1027-35.  Back to cited text no. 59    
60.Sadiq S, Jafarey NA, Naqvi SA. An analysis of percutaneous renal biopsies in fifty cases of nephrotic syndrome. J Pak Med Assoc 1978;28:121-4.  Back to cited text no. 60  [PUBMED]  
61.Musa AR, Veress B, Kordofani AM, et al. Pattern of the nephrotic syndrome in Sudan. Ann Trop Med Parasitol 1980;74:37-44.  Back to cited text no. 61  [PUBMED]  
62.Morgan AG, Shah DJ, Williams W, Forrester TE. Proteinuria and glomerular disease in Jamaica. Clin Nephrol 1984; 21:205-9.  Back to cited text no. 62  [PUBMED]  
63.Huraib SO, Abu-Aisha H, Mitwalli A, et al. The spectrum of renal disease found by kidney biopsies at King Khalid University Hospital. Saudi Kidney Dis Transplant Bull, 1990;1:15-9.  Back to cited text no. 63    
64.Nagy J, Bajtai G, Brasch H, et al. The role of hepatitis B surface antigen in the pathogenesis of glomerulonephritis. Clin Nephrol 1979;12:109-16.  Back to cited text no. 64  [PUBMED]  

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Correspondence Address:
Ahmed Hassan Mitwalli
Department of Medicine, King Khalid University Hospital, P. O. Box 2925, Riyadh 11461
Saudi Arabia
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PMID: 18209347

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  [Table - 1], [Table - 2], [Table - 3], [Table - 4]



 

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    Abstract
    Introduction
    Acknowledgement
    References
    Article Tables
 

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