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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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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 2018 Oct 22];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.

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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]  

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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