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NDT Advance Access originally published online on December 2, 2005
Nephrology Dialysis Transplantation 2006 21(3):672-676; doi:10.1093/ndt/gfi297
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Original Articles: Clinical Nephrology

Nephrotic syndrome in African children: lack of evidence for ‘tropical nephrotic syndrome’?

James Yao Doe1, Matthias Funk1, Michael Mengel2, Ekkehard Doehring3 and Jochen H. H. Ehrich3

1 Battor Hospital, Paediatrics, PO Bx 25, Jirapa, Ghana, 2 Medizinische Hochschule, Institute of Pathology, Carl Neuberg Str.1, 30625 Hannover and 3 Medizinische Hochschule Hannover, Pediatric Nephrology, Children's Hospital, Hannover Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany

Correspondence and offprint requests to: Jochen H. H. Ehrich Medizinische Hochschule Hannover, Pediatric Nephrology, Children's Hospital, Hannover Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany. Email: ehrich.jochen{at}mh-hannover.de



   Abstract
Top
 Abstract
Introduction
 Patients and methods
 Results
 Discussion
 References
 
Background. Infections such as malaria, schistosomiasis, hepatitis B and HIV have been suggested as major causes of the nephrotic syndrome (NS) in African children. We retrospectively analysed the course of the NS in 32 children from Ghana and reviewed the literature on NS from 18 different African countries for the presence of ‘the tropical nephrotic syndrome’.

Methods. Thirty-two children (22 boys, 10 girls, median age 12 years, range 1–18 years) with NS were treated from 2000–2003 at Battor Hospital, Ghana. Thirteen out of 32 children underwent a renal biopsy which was investigated by light, immune and electron microscopy. All 32 patients were initially treated with oral prednisone (PRED) therapy (29 with standard therapy for 8 weeks and three individually tailored), and steroid-resistant children received also intravenous methylprednisolone pulses (three children) or oral cyclophosphamide (two children).

Results. All patients fulfilled the clinical and laboratory criteria of a NS. The initial median serum creatinine was 65 µmol/l (range 44–133 µmol/l). Renal biopsy was performed in 13/32 children and revealed focal and segmental glomerulosclerosis (FSGS) in 10 patients, minimal change disease (MCNs) in two and no conclusive result in one patient. Glomerular immune complex deposition was absent in all biopsies. After treatment with PRED, oedema disappeared in 24/32 patients; however, proteinuria normalized in 16/32 patients only. The NS relapsed in 9/16 steroid-sensitive patients after cessation of PRED therapy, and two children were frequent relapsers. The steroid-resistant NS did not respond to an intensified immunosuppression in 5/16 children receiving methylprednisolone or cyclophosphamide. Five out of 32 children died, all were steroid resistant.

Conclusions. There was no evidence for a dominating role of steroid-resistant ‘tropical glomerulopathies’ in children with a NS in Ghana. Similar to South Africa, focal and segmental glomerulosclerosis (FSGS) and minimal change disease were the most frequent findings on histology. Contrary to Nigeria, membrano-proliferative glomerulonephritis was not found in these patients. We conclude from this data and from the literature that the histological pattern of NS may vary between different African countries. Concerning therapy of NS under tropical conditions, we emphasize that despite the limited therapeutic facilities half of these patients may benefit from corticosteroids; however, steroid resistance and FSGS resulted in a high mortality.

Keywords: Africa; nephrotic syndrome; focal and segmental glomerulosclerosis; tropical nephropathy



   Introduction
Top
 Abstract
 Introduction
Patients and methods
 Results
 Discussion
 References
 
In the late 1960s and early 1970s, Kibukamusoke and Hutt [1] in East Africa as well as Hendrickse et al. [2] in West Africa intensively studied the association of nephrotic syndrome with quartan malaria, suggesting an immune complex pathogenesis. Later on, Barsoum [3] summarized the findings on the association of Schistosomiasis and nephrotic syndrome in Egyptian children. In the late 1990s, Bhimma et al. [4] showed that membranous nephropathy dominated in black South Africans and that it was often correlated with hepatitis virus antigens. There may be changing patterns of the underlying causes of nephrotic syndrome (NS) in the past 30 years and the question has never really been answered to what extent the African continent harbours a ‘tropical nephrotic syndrome’, a term that was first created by Liliane Morel-Maroger in 1975 [5]. In the present retrospective clinical study, we describe the course of an NS in 32 children in Ghana at the beginning of the new millenium.



   Patients and methods
Top
 Abstract
 Introduction
 Patients and methods
Results
 Discussion
 References
 
Thirty-two children with an NS were treated from 2000–2003 at Battor Hospital, Ghana. Twenty-two boys and 10 girls with a median age of 12 years (range 1–18 years) were included in the retrospective study. All children underwent a clinical investigation and a laboratory diagnosis including serum protein, creatinine, cholesterol, quantitative urinary protein and semiquantitative dip stix for haematuria. Thirteen out of 32 children were biopsied and the renal biopsy was investigated at Hannover Medical School by light microscopy, immunohistology and electron microscopy in 12 biopsies, and at a local pathological institute by light microscopy only in one biopsy. A renal biopsy was performed in children who did not respond to the initial prednisone therapy. Initial therapy in 29 patients was oral prednisone (PRED) therapy (60 mg/m2/d for 4 weeks followed by 40 mg/m2 every other day for 4 weeks) [6]. Three patients received an individually tailored oral PRED treatment. Of those children who did not respond to oral PRED three children received three intravenous methylprednisolone pulses (300 mg/m2/d) and two children were treated with oral cyclophosphamide (2 mg/kg/d for 8 weeks).

All children lived in an area where almost every child experienced once or twice per year an infection with falciparum malaria. At the time of nephrological investigations, none of the patients suffered from acute malaria. The prevalence of schistosoma haematobium infections was high among school children and praziquantel therapy was available for patients. The hepatitis B and HIV status were unknown in the patients. None of them had sickle cell disease or any other overt disease which may have caused a secondary NS, such as diabetes, systemic lupus or amyloid disease.



   Results
Top
 Abstract
 Introduction
 Patients and methods
 Results
Discussion
 References
 
All 32 children had an overt NS with oedema. On admission, all children had a proteinuria above 2 g/l and the median serum protein was 41 g/l (range 30–46 g/l). Median serum cholesterol was 9.6 mmol/l (range 8.0–17.7 mmol/l). Median serum creatinine was 65 µmol/l (range 44–133 µmol/l); six children had an elevated serum creatinine between 97 and 133 µmol/l. Six children [three steroid-resistant focal and segmental glomerulosclerosis (FSGS), three steroid-sensitive NS] had arterial hypertension with both systolic (range 130–150 mmHg) and diastolic blood pressure (range 80–120 mmHg) ranging above age-matched normal values of casual blood pressure measuring in European children. Four children (all steroid sensitive) had elevated diastolic blood pressure (range 80–100 mmHg). No patient suffered from hypertensive crises. There are no data available on the follow-up of hypertension. Haematuria of 1+ to 3+ was detected by the use of dip sticks in 17 children (3+ haematuria referring to approximately 1000 erythrocytes per µl was found in five children, 2+ in nine children, 1+ in three children). Erythrocyturia was neither verified nor characterized by microscopy. Haematuria was found in two-thirds of children with steroid-sensitive nephrotic syndrome and in one-third of children with FSGS. There is no follow-up data on haematuria.

Renal biopsies were performed in 13 patients (nine patients with steroid-resistant NS and four with relapsing NS).

Renal biopsy revealed FSGS in 10 patients and minimal change disease in two patients. Pathognomonic glomerular immune complex deposition was absent in all the investigated biopsies. No conclusive result was found in one biopsy undergoing light microscopy only. In the ultrastructural examination of 12 patients no electron dense deposits or tubuloreticular structures as hints to an infectious genesis (hepatitis, HIV) of FSGS were detectable.

After oral therapy with PRED, oedema disappeared in 24/32 patients; however, proteinuria normalized in 16 patients only and persisted in eight (one patient also receiving cyclophosphamide) of these 24 patients at lower levels. The NS did not respond to treatment at all in eight patients (including three patients with methylprednisolone pulses and two patients receiving cyclophosphamide) and five of these died. Causes of death were acute renal failure in two children (‘nephrotic crisis’), severe anaemia in one, bacterial peritonitis in one and unclear in one). There are no follow-up data on serum creatinine. Eight out of 10 children with FSGS were PRED resistant, two were steroid-sensitive and one of these two had a relapse. One child with steroid resistance had minimal changes on renal biopsy, ad did one child with frequently relapsing NS.

The NS relapsed in 9/16 steroid sensitive patients after cessation of PRED therapy. Two patients were frequent relapsers.



   Discussion
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
References
 
In the mid 1970s a ‘tropical nephropathy’ was described in Senegalese patients with an NS showing a ‘curious progressive and segmental glomerulosclerosis characterized by a flaking or fibrillary splitting of the capillary wall, seen in quartan malarial nephropathy’ [5]. Barsoum [7] concluded that glomerular immune complex deposition in a variety of parasitic diseases may lead to ‘mild and self limiting glomerulo-nephritis (GN), reflecting the critical balance of concomitant immunity’. This author proposed that some other additional autoimmune pathogenetic mechanisms may be superimposed to the parasitic process inducing progression to an NS [7].

Thus, the question of a possibly distinct renal pathology diagnostic of a tropical NS may be raised. In fact, the pattern of childhood nephrotic syndrome in Africa varied according to geographical, racial, environmental and even historical and methodological factors.

In most North African countries the literature on geographical pathology of NS shows a profile which seems to be similar to that in Europe [8,9], with the exception of Egypt [10] where schistosomal–salmonella associated glomerulopathy was described.

The situation is less clear in West Africa. We describe mainly FSGS and MCNS in children from Ghana. These findings are supported by Adu et al. [11] reporting in the early 1980s MCNS in 14/25 children and FSGS in 12/61 patients of all age groups. By contrast, Nigerian children had a high proportion of cases with MPGN and quartan malaria nephropathy in the 1980s and MPGN in the 1990s [12,13]. In the early 1970s Hendrickse et al. [2] had described a peculiar type of quartan malaria nephropathy with lacunae in the glomerular basement on electron microscopy; however, these latter findings were never confirmed and may have been due to an artefact during fixation (R.H.R.White, personal communication). In Nigeria, the response of the NS to corticosteroids was poor [2]; however, 20 years later 52% of patients responded to PRED [14]. There was also a relatively high corticosteroid sensitivity in children from Togo [15] and in our patients from Ghana. In the late 1960s, 17/25 nephrotic patients from the Ivory Coast showed a peculiar type of glomerulopathy, with focal and segmental lesions due to hyalinosis of some glomerular loops probably affecting some more than others [16]. Today, there seems to be a high proportion of patients in the Ivory Coast suffering from secondary NS due to systemic lupus and amyloidosis [17,18]. The HIV glomerulopathy was found in patients from Benin [19]. The analysis of 55 cases with NS in Senegal revealed 27% with MCNS, 14% with FSGS and 10% with MPGN as the most frequent histological types [20]. The literature on NS in the Sudan is scarce [21]. In our own study on renal function in 218 Sudanese school children and 58 adults, we failed to detect a significant number of patients with schistosomal glomerulopathy [22,23].

Concerning East Africa, John Kibukamusoke and Michael Hutt were pioneers in the study of NS in Uganda in the 1960s; however, recent studies in this country are scarce, showing a high rate of nephrotic patients with a low selective protein index in the urine, thus suggesting a low sensitivity to steroids [24]. Nephrotic children and young adults in Kenya showed a high rate of mesangioproliferative glomerulonephritis (25%), MCNS (18%) and FSGS (15%) [25].

There are few reports on NS from Central Africa, e.g. in Cameroon 38% of patients had MCNS, 31% membranous glomerulo-nephritis (GN) and 24% proliferative GN [26]. In Zaire, 22% of nephrotic children had MCNS, 18% amyloidosis, 16% proliferative GN, 14% MPGN and 10% membranous GN. The FSGS was found in 6% only [27].

The literature on NS in the Southern parts of Africa, especially in the South African Republic itself, is rich. The patterns of GN in Zimbabwe showed predominantly proliferative GN in 51%, followed by membranous GN and FSGS [28]. Proliferative GN and FSGS were also dominant in Malawi [29]. Namibian children had mainly membranous GN [30]. Glomerulonephritis in South Africa is characterised by a high frequency in Africans, a lesser frequency in Indians and a low frequency in Caucasians [31]. Bhimma et al. [4] reviewed their 20 year experience of 636 children with NS in Durban. Membranous GN was found in 40% of Blacks, mostly associated with hepatitis B. Typical steroid-sensitive NS was uncommon [32]. In Indian children, 47% had MCNS and 21% had FSGS. The FSGS was also frequently found in children from Natal [33].

In summary, there seems to be no unique pattern of the underlying histological types of GN in African children with NS and the term ‘tropical nephrotic syndrome’ could be dropped because there is no unique geographical pathology. We conclude from our own data and from the literature that FSGS may be a frequent cause of steroid-resistant NS in West African children. This hypothesis is supported by the findings that FSGS is also frequently found in adult African North Americans whose ancestors originated mainly from West Africa [34]. Because of a lack of molecular genetic studies on NPHS2 mutations in Africans, it is unclear if there is a genetic explanation for our hypothesis. Preliminary data from African South Americans did not show a high rate of podocin mutations in these patients (E.J. Bellotto Monteiro, personal communication).

In addition to genetic factors, there are a number of environmental factors contributing to the different pathology of childhood NS in African children. There is not much evidence that toxic factors play a major role in African NS [35]. By contrast, the association of NS with parasitic and viral infections has been repeatedly published. The role of Plasmodium malariae in the aetiology of human glomerulonephritis is based on circumstantial clinical and epidemiological evidence [1], and on experimental work suggesting that parasitic antigens and host antibodies could be the culprits of glomerular damage [36]. The quartan malaria nephrotic syndrome story started at a time when the classical concept of immune complex disease was discovered. Almost all patients with malaria develop circulating immune complexes (own unpublished observation); however, it was never shown that the deposition of malaria immune complexes was able to induce severe glomerular disease in humans or in animals. Furthermore, it was never explained why the quartan malaria NS was associated with proliferative glomerular lesions in Ugandan patients, whereas Nigerian patients had a more membranous type of lesions. Last but not least, there is almost no recent data on quartan malaria NS in the literature. Although it cannot be ruled out that an improved nutritional status and a better supply of anti-malarials may have reduced the number of cases with quartan malaria NS, it is more likely that the paradigm of tropical NS induced by quartan malaria is no longer valid [37].

There are a few confounding factors which may have contributed to the incomplete understanding of NS in African children. First of all, many studies have not used triple diagnosis for renal histology and up to 16% of biopsies were invalid [25]. Therefore, mild forms of FSGS may have been overlooked. Secondly, most studies like this one are based on a relatively small number of patients. Thirdly, there is a possible bias due to different indications or availability of renal biopsies over the years.

Regardless of the different causes of African NS, there is a therapeutic dilemma in most tropical countries. A common finding seems to be the larger proportion of African children with steroid resistance if compared with European or North American children with NS. In our own study, 8/32 (25%) of children did not benefit at all from steroid therapy, a result similar to that in non-African countries. We conclude that all African children with an NS should receive standard prednisone therapy for the initial attack, and those children who relapse should be given a standard relapse therapy. However, an unknown proportion of these steroid-responsive children may not have MCNS but FSGS and their course may be characterized by late steroid resistance. There is an ethical dilemma when it comes to the questions if and when African children with steroid resistance should be biopsied, because there is a lack of therapeutic facilities in many African countries concerning expensive immunosuppressive drugs and renal replacement therapy. Even today African children with a steroid-resistant NS have very few chances to survive.

Conflict of interest statement. None declared.



   References
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 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 

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Received for publication: 17. 9.04
Accepted in revised form: 8.11.05


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