Pediatric Nephrology
5th Edition

75E
Africa
Bahia Hassan Moustafa
Felicia Eke
RajendRa Bhimma
Many children with kidney disease in Africa do not receive proper medical care. Pediatric nephrologists are lacking in many African countries, and even when they are available, their numbers are far below that required for the child population in their areas. In Egypt there is one pediatric nephrologist per 500,000 child population, in Nigeria there is one per 10 million, and in South Africa there is one per 1.5 million. Therefore, pediatricians and general practitioners commonly treat these children (1). In the last two decades pediatric nephrology units have developed throughout the continent. They are concentrated mainly (a) in the northern region in Egypt, Tunisia, Algeria, Libya, and Morocco; (b) in the eastern region in Kenya, Sudan, and Ethiopia; (c) in the western region in Nigeria; and (d) in the southern region in South Africa. Most of these units provide primary and secondary renal care. Some provide tertiary care (i.e., limited dialysis), and very few provide quaternary care (i.e., comprehensive dialysis and transplantation). In the northern region of Africa dialysis and transplantation programs are well developed; however, they are run by internist nephrologists in many areas because of the high ratio of internist to pediatric nephrologists. In Egypt, efficient pediatric nephrology units are university-related units. There are approximately 12 university pediatric nephrology units. They act as regional centers for upper and lower Egypt and provide training and treatment. Over the last 2 years the Ministry of Health has established a number of pediatric hemodialysis units in national hospitals. Medical insurance covers the costs for patients treated in university or national hospital units. Transplantation for children is provided mainly by adult nephrologists. This situation is slowly changing as more pediatric nephrologists are being trained.
In the east, only Kenya has organized renal services including peritoneal dialysis, hemodialysis, and renal transplantation. In the western and central zones, Nigeria is the largest and richest country. There are seven pediatric nephrologists serving a child population of approximately 80 million, among whom 7.5 children per million per year are expected to develop end-stage renal failure. There are 12 adult hemodialysis units of variable quality and reliability. There are no transplantation centers and no pediatric hemodialysis units, but peritoneal dialysis is available for children with acute renal failure (ARF). Continous ambulatory peritoneal dialysis (CAPD) is not undertaken because of poor socioeconomic and hygienic conditions. Children with chronic renal failure (CRF) whose parents can afford the costs travel to Western countries for dialysis and transplantation. In South Africa, in spite of the deficiency of trained pediatric nephrologists in relation to child population, there are several centers that provide secondary levels of renal care, and most have facilities and expertise for peritoneal dialysis. Care for children with end-stage renal disease who need dialysis and transplantation is centralized in three major centers: Cape Town, Johannesburg, and Durban. In Durban, renal replacement therapy is limited to older children, but with the commissioning of the Inkosi Albert Luthuli Central Hospital, tertiary and quaternary renal care will be offered to all age groups. The policy of the country is to centralize quaternary care to limited designated sites for the entire country, whereas provision of various levels of renal replacement therapy will remain regionalized within a handful of cities.
The profile of renal diseases prevalent in Africa is unique with respect to etiology and clinical presentation. Endemic infections are a major cause of many renal diseases. The low socioeconomic status in many areas, lack of clean water supply, poor sanitation and irrigation systems, and overcrowded housing promote endemic infections such as schistosomiasis, malaria, tuberculosis, hepatitis, and infection with Streptococcus, Salmonella, Shigella, Filaria, and human immunodeficiency virus (HIV). The second major category contributing to the unique pattern of renal diseases in Africa includes the overuse of drugs, use of herbal and traditional medicines, toxins from bites, and local environmental pollutants. Obviously the dry environment and tropical climate with inadequate water supply leads to a high incidence of nephrolithiasis in the population.
African children demonstrate unique clinical presentations for various renal diseases. Infection and malnutrition
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commonly complicate the picture of the renal disorder. Infection either may be the primary cause of the kidney disease or may be acquired during treatment. The higher mortality and morbidity observed in these children can be attributed in large extent to late diagnosis and late referral to specialized units. Moreover, the poor intradialytic care children receive in some units because of limited resources or insufficient staff explains poor quality of life compared to that of similarly treated children in developed countries. The most prevalent renal disorders in Africa include nephrotic syndrome (NS), urinary tract infections (UTIs), and ARF and CRF (Fig. 75E.1).
FIGURE 75E.1 Renal disorders in northern, eastern, western, and southern Africa. Anom., anomalies; ARF, acute renal failure; CRF, chronic renal failure; GN, glomerulonephritis; Henoch-S. Purpura, Henoch-Schönlein purpura; Hepatorenal S., hepatorenal syndrome; HUS, hemolytic uremic syndrome; LE, lupus erythematosus; Misc., miscellaneous; NS, nephrotic syndrome; R., renal; RTA, renal tubular acidosis; U., uropathy; UTI, urinary tract infection.
NEPHROTIC SYNDROME
NS is the most common childhood renal disorder in Africa. It accounts for 14.6% of renal disorders in eastern Nigeria (2), 40% in Sudan (3), and 40% in Egypt (4). It has a very diverse profile in the black continent. In northern regions it resembles that in Western countries to a great extent; minimal change NS (MCNS) constitutes the major cause with a prevalence of 88% in Egypt (4), 85% in Libya (5), and 37% in Sudan (3). In Tunisia (6), however, it is not considered the most common pattern. In Egypt, children with nil disease show an excellent response to steroids and a satisfactory outcome. Children experiencing frequent relapse and steroid-dependent children constitute 42% and 36% of children with MCNS in the Cairo unit (4) and 21% and 15% in the Mansoura unit (7), respectively. In most patients, relapse rate correlates with compliance with the steroid therapy regimen. Infection is the main complication commonly reported. Pneumonia, subcutaneous abscesses, UTIs, peritonitis, and septicemia show prevalences of 35%, 22%, 28%, 5%, and 2%, respectively. Hypovolemic shock after infectious diarrhea was reported in 5% of nephrotic
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children. Intravascular thrombosis was reported in 2%. The death rate in this study was 2% (4). Among other pathologic types of NS in Egypt, a high prevalence of focal segmental glomerulosclerosis (FSGS) was seen during the 1980s in the Cairo unit (4). Later data from the same unit in the 1990s showed an almost equal prevalence of mesangial proliferative glomerulonephritis (MPGN) (22.7%) and FSGS (21.3%) (8). Subsequently MPGN (34.3%) was prevalent through the next 10 years when data for 394 nephrotic children undergoing renal biopsy were analyzed. Secondary forms of NS are less common in northern Africa than in other parts of the continent. An incidence of 6.6% was reported in Egypt (7). A postinfection pattern is the most common, with schistosomal nephropathy endemic in the north in the Nile delta in Egypt, Ethiopia, and Sudan. The causative parasite is Schistosoma haematobium in East, West, and Central Africa as well as the Nile delta. Schistosoma mansoni is endemic in the Nile valley, and the western and southern regions of Africa. Such patterns correlate with prevalence of the snail host and poor hygiene. Infected children present with hematuria, glomerulonephritis, NS, or renal failure. Hepatosplenomegaly with the presence of bilharzial ova in urine or stools commonly point to the diagnosis. Patients demonstrate unselective proteinuria, marked reduction in total serum levels of proteins with a characteristic high gamma globulin fraction, normal serum cholesterol level, normal to low serum complement profile, low urine osmolality, and normal to low glomerular filtration rate (GFR). Many such patients are chronic Salmonella carriers with intermittent bacteruria, especially those with refractory anemia and persistent fever. Urinary tract imaging may reveal bladder calcification and/or obstructive uropathies and vesicoureteral reflux (VUR); renal biopsy results revealed diffuse MPGN (38%), FSGS (20%), membranous nephropathy (12%), focal MPGN (7%), or mesangiocapillary glomerulonephritis (18%) (9). Different immune mechanisms have been implicated in the pathogenesis of these lesions (10). Current statistics have shown a marked decline in the prevalence of schistosomal nephropathy in many African countries, mainly the Nile delta of Egypt. This has been attributed to aggressive use of chemotherapy among schoolchildren and extensive snail eradication. Trials for manufacture of a new protective vaccine are promising (11).
Hepatitis B is increasingly more prevalent as a cause of NS in northern Africa, with a 44% incidence among secondary forms of NS reported in Egypt (12). Hepatitis C was less commonly reported in the same region (13). Tuberculosis and filariasis are now less prevalent in the northern region. Lupus erythematosus nephropathy is found in 8% of nephrotic children undergoing biopsy (4) in Egypt. Sickle cell nephropathy is rare in North Africa, although the disease is not rare. Ochratoxins and aflatoxins, which are common constituents in foodstuffs in Africa, were detected in urine, serum, and kidney biopsy specimens of children with NS or renal failure in Tunisia and Egypt (14). Cadmium and aluminum, which are common environmental pollutants in Africa, were recorded as toxic causes for NS in Africa.
In West and Central Africa the profile of NS is unlike that in the Western world. Idiopathic NS is not common. When it affects black children it is often associated with a high rate of steroid nonresponse. This is true in Togo, West Africa (15), western Nigeria (16), northern Nigeria (17), Uganda (18), and Zaire (19). In Port Harcourt (20) and Yaoude, Cameroon (21), however, steroid responsiveness is not uncommon. Infections play a major role in the pathogenesis of NS in West and Central Africa. Quartan malarial nephropathy, first described in Ibadan, western Nigeria, is detected in up to 81% of renal biopsy specimens in children (16). Quartan malarial nephropathy is predominantly associated with Plasmodium malariae and also with Plasmodium falciparum infection (17). Typically there is focal and segmental glomerulonephritis with thickening of capillary walls but without endothelial cell proliferation. Finding of P. malariae or P. falciparum antigen in the glomeruli by immunofluorescence is diagnostic. In eastern Nigeria, MCNS is the most common pathologic diagnosis in cases undergoing biopsy (21). Other infections reported in West and Central Africa include hepatitis B with membranous nephropathy (22). NS often complicates poststreptococcal glomerulonephritis in this region. Schistosomiasis, filariasis, and leprosy are also recorded.
In eastern Nigeria, sickle cell nephropathy is common and sickle cell anemia is common with a heterozygous carrier rate of 25%. FSGS and renal papillary necrosis are explained by endothelial damage caused by occlusion by sickled cells and microinfarcts. There are numerous cases of unexplained renal pathology, with NS possibly caused by toxins found in herbal remedies or environmental contamination.
In South Africa, the etiology of NS has undergone considerable change after 1995 as compared to earlier records (Table 75E.1). During the 1970s and 1980s, the pattern in Indian and white children was similar to that seen in the
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Western world (23). Those of mixed race had a similar histologic pattern of disease but a less gratifying response to steroid therapy. In all of these racial groups, minimal change disease, the presence of which strongly correlated with steroid responsiveness, was the most common lesion. NS among black children in South Africa is characterized by a paucity of minimal change disease, steroid resistance, and a less satisfactory outcome and unidentifiable causative agents in many (24,25). During these two decades the most common histopathologic form of NS seen among black children in the coastal regions was membranous nephropathy, whereas that seen in regions such as Johannesburg was FSGS (26). Membranous nephropathy accounted for 40% of all cases of NS in black children; it was associated with chronic hepatitis B virus carriage in over 86% of cases and showed a strong male predominance (27,28). Minimal change disease accounted for 14 to 25% of all cases of NS; it was less common in coastal regions such as Durban (24,27). Over the last decade there has been a substantial change in the pattern of NS in coastal regions of South Africa. FSGS has increased among Indian and black children, accounting for 50% of all cases of NS in children. More than 95% of these patients are steroid unresponsive. Black patients tend to have more aggressive disease with progression to end-stage disease over a short of period of time (29). The introduction of hepatitis B vaccine in April 1995 had a major impact on the incidence of hepatitis B virus–associated NS. In Durban, the number of new cases remained steady up to 1999 with a marked decline thereafter (30). Other secondary causes of NS in South Africa include congenital syphilis, cytomegalovirus infection, and poststreptococcal glomerulonephritis. Schistosomal nephropathy and malarial nephropathy are rare in South Africa. The HIV infection and acquired immunodeficiency syndrome that have overwhelmed Sub-Saharan Africa over the last decade have had little reported impact on the pattern of NS seen in children. There have been no reports on HIV-associated nephropathies in children in South Africa to date.
TABLE 75E.1. HISTOLOGIC PATTERN OF NEPHROTIC SYNDROME BEFORE AND AFTER 1995 IN DURBAN, SOUTH AFRICA
Histologic findings 1976–1994 1995–2000
Minimal change disease 95 11
Focal segmental glomerulosclerosis 41 43
Membranous nephropathy 44 6
Membranous nephropathy (hepatitis B associated) 63 24
Diffuse mesangial proliferative glomerulonephritis 26 1
Focal mesangial proliferative glomerulonephritis 13 2
Mesangiocapillary glomerulonephritis 4 1
Total 286 88
URINARY TRACT INFECTIONS
UTIs are common in Africa, in both rural and urban areas and among neonates, preschool children, and school-aged children. UTIs show a prevalence of 22% in symptomatic children in Cairo, Egypt. Asymptomatic bacteruria has a recorded incidence of 4.2% in girls and 2.8% in boys among schoolchildren in urban Egypt (31) and 11% in girls and 3.6% in boys in rural Egypt (32). In Central and West Africa, UTIs have an incidence from 8.2 to 72% in symptomatic children (33) and of 48% in an asymptomatic rural community (34). In Cape Town, approximately 1000 cases of UTI are seen yearly. In fact, because of the nonspecific complaints in neonates and young children, many cases are missed, especially in rural areas. The microbiology of UTIs in Africa is consistent over the continent (35). In the northern region of Egypt, the recorded causative organism is Escherichia coli in 70% of cases, Proteus in 10%, Klebsiella in 5%, and Pseudomonas in 5% (36). Schistosomiasis is considered a common predisposing factor for UTI in Egypt (36), Senegal (37), and Cameroon (38). Stones, developmental anomalies of the urinary tract, and VUR are also common structural changes that favor infection in Egypt, with prevalences of 2.5%, 12%, and 17%, respectively (36). VUR is rare in West and Central Africa whereas posterior urethral valves and meatal and urethral strictures are reported to have an incidence of 29.3% among children with UTIs (35). In South Africa, local predisposing factors include malnutrition, congenital anomalies, immunodeficiency states, and VUR. The latter is rare in black children but common in whites (39,40). Adhikari (40) reported 2 Indian children with VUR out of 26 children with anomalies, and 7 cases of PUV out of 14 with obstructive uropathies. Renal growth and GFR are commonly affected in African children with UTI because of late diagnosis and referral, as well as patient noncompliance with treatment. Impaired renal growth was reported in 36% of cases referred to the Cairo University unit, whereas low GFR was reported in 5% of the same patients (36). E. coli strains resistant to amoxicillin and co-trimoxazole were reported in Africa with 88% and 86% resistance to these drugs, respectively, in Cape Town.
ACUTE RENAL FAILURE
ARF has unique epidemiology in African children. Infection is the major cause. Bacterial infections commonly reported include streptococcosis, cholera, salmonellosis, shigellosis, leptospirosis, tetanus, and diphtheria. Viral infections include HIV infection, hepatitis B, hepatitis C, hepatitis A, and cytomegalovirus infection. Common parasitic infections are malaria and schistosomiasis. Among all pathogen-related causes, diarrheal diseases, schistosomiasis, and malaria remain the most common. Infection precipitates ARF through immune mechanisms and alteration of kidney hemodynamics (41). Toxins present after snakebites, scorpion stings, or other insect stings, or after ingestion of herbal medicines or overuse of drugs are also unique causes of ARF in Africa. Table 75E.2 summarizes causes of ARF in Egypt (42), Nigeria (43), and South Africa. Septicemia, gastroenteritis, and hemolytic uremic syndrome (HUS) are common causes in the three regions. Epidemic forms of ARF after use of native herbal medicines and holy water were reported in Nigeria (44). In South Africa, an epidemic of Shigella dysentery type 1 occurred in 1994 to 1996 in Sub-Saharan Africa, starting in Burudi and progressing to the Cape (45). One hundred fifty-nine cases of HUS occurred in black children after this bloody diarrhea. Among 81 cases of post-Shigella-induced HUS in Durban, complications included ARF in 90.1%,
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encephalopathy in 37%, convulsions in 14.8%, hemiplegia in 2.3%, intestinal perforation in 9.9%, protein-losing enteropathy in 32.1%, toxic megacolon in 4.9%, rectal prolapse in 6.2%, hepatitis in 13.6%, myocarditis in 6.2%, disseminated intravascular coagulation in 21%, CRF in 32.1%, impaired renal function in 9.9%, ESRD in 1.2%, and death in 17.3% (46). During the last 2 years E. coli–induced HUS, especially coexistent with HIV infection, has been reported in Cape Town.
TABLE 75E.2. CAUSES OF ACUTE AND CHRONIC RENAL FAILURE IN SELECTED LOCATIONS IN AFRICA
  Egypt (%) Nigeria (%) Cape Town (%) Durban blacks (%)
Acute renal failure        
Septicemia and urinary obstruction 21 16 24.1
Gastroenteritis 27 34 7.4
Poststreptococcal glomerulonephritis 29  
Lupus erythematosus 12  
Hemolytic uremic syndrome 6 11 9.3
Nephrotoxins 3  
Unknown 2 5
Acute glomerulonephritis 12  
Malaria 10
Birth asphyxiation 12
Postcardiac surgery 16.7
Myocarditis 11.1
Rapidly progressive glomerulonephritis 9.3
Necrotizing enterocolitis 7.4
Kwashiorkor 7.4
Leukemia 7.4
Chronic renal failure        
Reflux nephropathy 15
Glomerulonephritis 26 72 45
Unknown 28 14
Urinary obstruction 31 7
Pyelonephritis 7
Focal segmental glomerulonephritis 25
Anomalies 26
Other causes 4
CHRONIC RENAL FAILURE
The pattern of CRF in African children is unique with respect to its etiology, clinical presentation, and management. Causes of CRF in Egypt (47), Nigeria (2), and South Africa are summarized in Table 75E.2. It is evident that obstructive uropathies and reflux nephropathy are prevalent causes in Egypt, whereas glomerulonephritis is common in Nigeria and South Africa. Late referral of cases explains the preponderance of unknown diagnoses among Egyptian children who already have atrophic kidneys at their first visit to a pediatric nephrology unit.
Signs of CRF in African children are aggravated by three distinct elements: infection (whether causing CRF or acquired during dialysis), malnutrition (especially deficiencies of iron, vitamin D, and trace elements), and late diagnosis and poor management (which aggravate anemia, growth retardation, and bone disabilities).
DIALYSIS AND TRANSPLANTATION
Acute peritoneal dialysis is the most common type of dialysis in Africa and is more readily available than acute hemodialysis. Chronic intermittent peritoneal dialysis is the most common technique used in CRF cases in developing countries in Africa. The use of continuous cycling peritoneal dialysis is less common. In developed areas such as Cape Town in South Africa, however, use of CAPD is predominant. Efficiency of dialysis varies among pediatric nephrology centers in Africa. It depends on availability of funds as well as trained staff. African children on regular dialysis demonstrate lack of compliance with the regimen because of psychosocial and economic factors, and most of them experience poor quality of life. Factors that contribute to their poor outcome include deficient dialysis, undernutrition, infection, and lack of appropriate interdialytic care due to nonavailability of erythropoietin, iron, active vitamin D, and growth hormone (1).
Although renal transplantation is more cost effective than dialysis, it is not available in most African countries.
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Reported centers are concentrated in the northern region and in South Africa. Ethical and religious factors in each country determine whether cadaveric or living donor grafts are used. In South Africa, cadaver organ–based programs are widely used, whereas in Egypt, only living related donor–based programs are permitted. Morbidity and mortality of patients undergoing renal transplantation are higher in Africa than in developed countries.
Most African countries lack national kidney foundations as well as medical insurance systems. Therefore, funding for ESRD therapy remains a significant handicap for most African countries. Prevention of ESRD is the best strategy when approaching the problem of CRF in Africa. Simple measures include health education to combat unhygienic habits and use of traditional remedies, many of which are nephrotoxic. Additional measures include infection control through antischistosomal and antimalarial campaigns and obligatory vaccination against tuberculosis and hepatitis. Screening for renal diseases among schoolchildren might identify patients early in the disease course and maximize appropriate intervention.
The development of the African Pediatric Nephrology Association (AFPNA) in 1999 with its affiliation to the International Pediatric Nephrology Association carries new prospects for upgrading the practice of pediatric nephrology in Africa. Training programs supported by the IPNA to increase the number of trained pediatric nephrologists are now planned to cover northern, central, and southern regions of Africa. Shortage of specialists and trained staff as well as restricted financial resources remain a major handicap in many areas. Development of regional pediatric nephrology societies such as the Egyptian Society of Pediatric Nephrology and the South African transplantation and pediatric nephrology groups as well as improved education offer promise for dramatic improvements in pediatric nephrology care in Africa over the next decade.
ACKNOWLEDGMENTS
The authors would like to thank Prof. M. Adhikari (Durban) and Dr. M. McCulloch and Dr. P. Sinclair (Red Cross Children’s Hospital, Cape Town) for providing valuable data from their centers. The authors also offer special thanks to colleagues in different pediatric nephrology units throughout the continent for their assistance in data collection and collation.
REFERENCES
1. Moustafa B. Mapping of pediatric nephrology in Africa. 1st Congress for African Pediatric Nephrology Association (A.F.P.N.A.), February, 2000:P9.
2. Eke FU, Eke NN. Renal disorders in children: a Nigerian study. Pediatr Nephrol 1994;8:383–386.
3. Musa AR, Veress B, Kordofani AM, et al. Pattern of the nephrotic syndrome in Sudan. Ann Trop Med Parasitol 1980;74:37–44.
4. Moustafa B, El Zawahry K, El Kolally S. Epidemiological profile of nephrotic syndrome in Egypt. Gaz Egypt Paediatr Assoc 1984;32:39–45.
5. El Zouki AY, Amin F, Jaiswal OP. Primary nephrotic syndrome in Arab children. Arch Dis Child 1984;59:253–255.
6. Maiz HB, Moussa FB, Abderrahim E, et al. N.S. in childhood, study of 381 cases. The 25th annual meeting of the European society of Pediatric Nephrology. Pediatr Nephrol 1991;5:C26(abst).
7. Sarhan AA, Baker AM, Hammad AM, et al. Pattern of NS in P.N. unit Mansoura University, Egypt in the last 5 years. The 33rd annual meeting of the European Society of Pediatric Nephrology. Pediatr Nephrol 1999;13:C61(abst).
8. Moustafa B, Zahran M, Francis M, et al. Pathological profile of glomerulopathies among Egyptian children. JAC 1996;7(1):25–46.
9. Moustafa B. Schistosomal nephropathy. Egyptian experience. 1st Congress of A.F.P.N.A., Cairo, February, 2000:P9.
10. Barsoom R. Schistosomal glomerulopathies. Kidney Int 1993;44:1.
11. Alsherbiny MM. New schistosomal vaccine. WHO/TDR program supported by the Schistosomiasis Vaccine Development Project (SVDP). A.F.P.N.A. Newsletter September, 2001.
12. Farid F, Moselhy S, Rafik, M, et al. Hepatitis B virus related glomerulopathies in Egyptian children. 1997;18(2):437–448.
13. Moselhy S, Gaffar A, Hememy N. Hepatitis C associated glomerulopathies in Egyptian children. New Egypt J Med 1997;17(3):267–274.
14. Saadi MG, Abdallah S, Fadel F, et al. Prevalence of okra toxin OT among Egyptian children and adults with different renal diseases. Med J Cairo Univ 1996;64(2):497–506.
15. Gbadoe AD, Atakouma DY, Napo-Koura G, et al. Primary nephrotic syndrome in the black African child. Arch Pediatr 1999;6:985–989.
16. Hendrickse RG, Adeniyi A, Edington GM, et al. Quartan malarial nephrotic syndrome. Collaborative clinicopathological study in Nigerian children. Lancet 1972;1:1143–1149.
17. Abdurrahma MB. The role of infectious agents in the etiology and pathogenesis of childhood nephrotic syndrome in Africa. J Infect 1983;8:100–109.
18. Odiit A, Tindyebwa D. Selective protein index and clinical features of childhood nephrotic syndrome in Kampala. East Afr Med J 1997;74:207–209.
19. Pakasa M, Mangani N, Dikassa L. Focal and segmental glomerulosclerosis in nephrotic syndrome: a new profile of adult nephrotic syndrome in Zaire. Mod Pathol 1993;6:125–128.
20. Eke, FU. Nephrotic syndrome in Port Harcourt—clinical presentation and response to steroids. Nig J Paediatr 1990;17:59–63.
21. Mbakop A, Youmbissi TJ, Gonsu JD, et al. [Renal puncture biopsy in nephrotic syndrome in Cameroonian children, adolescents, and adults: histopathologic profile according to age]. Arch Anat Cytol Pathol 1990;38:104–107.
22. Seggie J, Nathoo K, Davies PG. Association of hepatitis B (HBs) antigenaemia and membranous glomerulonephritis in Zimbabwean children. Nephron 1984;38:115–119.
P.1505

23. Bhimma R, Coovadia HM, Adhikari M. Nephrotic syndrome in South African children: changing perspectives over 20 years (1976–1995). Pediatr Nephrol 1997;11:429–434.
24. Adhikar M, Coovadia HM, Morel-Margoer L. Absence of true minimal change nephrotic syndrome in African children in South Africa. J Trop Med Hyg 1993;88:223–228.
25. Coovadia HM, Adhikari M, Morel-Maroger L. Clinico-pathological features of the nephrotic syndrome in South African children. QJM 1979;48:77–91.
26. Thomson PD. Glomerulonephritis in children: a South African perspective. Specialist Medicine 2000:21–32.
27. Bhimma R, Coovadia HM, Adhikari M. Hepatitis B virus—associated nephropathy in black South African children. Pediatr Nephrol 1998;12:479–484.
28. Gilbert DR, Wiggelinkhulzen J. The clinical courses of Hepatitis B virus nephropathy. Pediatr Nephrol 1994;8:11–14.
29. Adhikari M, Bhimma R, Coovadia HM. Focal segmental glomerulosclerosis in children from KwaZulu/Natal, South Africa. Clin Nephrol 2001;55(1):16–24.
30. Kew MC. Progress towards the comprehensive control of hepatitis B in Africa: a view from South Africa. Gut 1996; 38(suppl 2):S31–S36.
31. Moustafa B. UTIs in Egyptian children. 19th Congress of Egyptian Society of Nephrology and Transplantation, Gona, Egypt, 2000:P27.
32. El-Gamal SA, Saleh LH. Asymptomatic bacteriuria in school children in a rural area, Egypt. J Egypt Public Health Assoc 1991;66:113–121.
33. Anoukoun T, Agbodjan-Djossou O, Atakouma YD, et al. [Epidemiologic and etiologic features of urinary infections in children at the pediatrics service of the CHU-Campus de Lome (Togo)]. Ann Urol 2001;35:178–184.
34. Azubike CN, Nwamadu OJ, Oji RU, et al. Prevalence of urinary tract infection among school children in a Nigerian rural community. West Afr J Med 1994;13:48–52.
35. Eke FU, Eke N. Urinary tract infection in Nigerian children. Nephron 1995;70:132.
36. Moustafa B, Soliman N, Kamalo M, et al. Profile of UTI in Cairo University PN unit through last 8 years. J Egypt Soc Pediatr Nephrol Transplant (in press).
37. Verle P, Stelma F, Desreumaux P, et al. Preliminary study of urinary schistosomiasis in a village in the delta of the Senegal river basin, Senegal. Trans R Soc Trop Med Hyg 1994:88.
38. Cunin P, Griffet A, Poste B, et al. Epidemic Schistosoma mansoni in a known S. Haematobium area. Trans R Soc Trop Med Hyg 2000;94:657–660.
39. Reed RP, Wegerhoff FO. Urinary tract infection in malnourished rural African children. Ann Trop Paediatr 1995;15:21–26.
40. Jeena PM, Coovadia HM, Adhikari M. Bacteriuria in children attending a primary health care clinic: a prospective study of catheter stream urine samples. Ann Trop Paediatr 1996;16:293–398.
41. Quezado ZMN, Natanson C. Systemic haemodynamic abnormalities and vasopressor therapy in sepsis and septic shock. Am J Kidney Dis 1992;20:214.
42. Moustafa B, Baha El-Din H, Shoman M. Acute renal failure among Egyptian children. Causes and outcome. XXI International Congress of Pediatrics, Cairo, Egypt, September 10–15, 1995:P526.
43. Eke FU. Acute renal failure as seen in Port Harcourt over fifteen years. 12th Congress of the International Pediatric Nephrology Assoc, 2001:55.
44. AdelekunTA, Ekwere TR, Akinsola A. The pattern of acute toxic nephropathy in Ife, Nigeria. West Afr J Med 1999;18: 60–63.
45. Bhimma R, Rollins N, Coovadia HM, et al. Post dysenteric hemolytic-uraemic syndrome in children during an epidemic of shigella dysentery in Kwazulu/Natal. Centr Afr J Med 1997;43:152–158.
46. Bhimma R, Nigel CR, Coovadia HM, et al. Post-dysenteric hemolytic uremic syndrome in children during an epidemic of shigella dysentery in Kwazulu/Natal Ped. Nephrol 1997; 11:560–564.
47. Safouh H, El Hetw M. Chronic renal failure in Egyptian children. XXI International Congress of Pediatrics, Cairo, Egypt, September 10 to 15, 1995:P658.