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RENAL DATA FROM THE ASIA - AFRICA |
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| Year : 2008 | Volume
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| Issue : 3 | Page : 470-474 |
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| Lupus Nephritis in Senegal: A Study of 42 Cases |
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A Niang1, EF Ka1, D Dia2, A Pouye2, A Kane3, MT Dieng3, MM Ka2, B Diouf1, B Ndiaye3, T Moreira-Diop2
1 Service de Nephrologie, Centre Hospitalier Universitaire Aristide Le Dantec de Dakar, Senegal
2 Service de Medecine Interne, Centre Hospitalier Universitaire Aristide Le Dantec de Dakar, Senegal
3 Service de Dermatologie, Centre Hospitalier Universitaire Aristide Le Dantec de Dakar, Senegal
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 Abstract | | |
Renal involvement determines the prognosis of systemic lupus erythematosus (SLE). The aims of this study were to assess the clinical, laboratory and therapeutic aspects of lupus nephritis (LN) in Senegal in order to improve its management. We included all patients presenting with SLE followedup in the Internal Medicine and Dermatology Clinics of the Aristide Le Dantec University Teaching Hospital of Dakar, from January 1993 to December 2002. Patients with SLE without evidence of LN (defined by proteinuria more than 0.5 g/24 hours and/or hematuria) were excluded. A total of 74 patients with a diagnosis of SLE were studied, 42 of whom (56.75%) had features of LN. Their mean age was 29.6 years and male-female ratio was 0.13. The nephrotic syndrome was seen in 45.23% of the cases and renal insufficiency in 37.71%. Renal biopsy was performed in 52.38% of the cases, which showed predominantly WHO classes IV and V lesions. The main treatment modality employed was corticosteroids, while immunosuppressive drugs in addition were used in 35.71% of the patients. The short-term prognosis was favorable but in the middle-term, many patients were lost to follow-up. We conclude that early diagnosis by systematic urine screening, good patient information, percutaneous renal biopsy and use of appropriate immunosuppressive therapy will help improving the prognosis of LN in Senegal. Keywords: Lupus nephritis, Renal biopsy, Senegal
How to cite this article:
Niang A, Ka E F, Dia D, Pouye A, Kane A, Dieng M T, Ka M M, Diouf B, Ndiaye B, Moreira-Diop T. Lupus Nephritis in Senegal: A Study of 42 Cases. Saudi J Kidney Dis Transpl 2008;19:470-4 |
How to cite this URL:
Niang A, Ka E F, Dia D, Pouye A, Kane A, Dieng M T, Ka M M, Diouf B, Ndiaye B, Moreira-Diop T. Lupus Nephritis in Senegal: A Study of 42 Cases. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2022 Dec 1];19:470-4. Available from: https://www.sjkdt.org/text.asp?2008/19/3/470/40517 |
| Introduction | |  |
Lupus Nephritis (LN) is one of the most frequent visceral forms of systemic lupus erythematosous (SLE) and occurs in 50 to 80% of the cases. [1] It represents, in order of frequency, the third visceral manifestation after cutaneous and articular involvement; however, it constitutes the main prognostic factor. [2] Since there are no publications from Senegal on this important entity, we conducted this study to report the epidemiological, clinical, laboratory, therapeutic and prognostic data in order to try and improve the management of patients with LN.
| Patients and Methods | | |
This retrospective survey was conducted between the period from January 1993 to December 2002 in the Departments of internal medicine, nephrology and dermatology at the Aristide Le Dantec University Teaching Hospital, Dakar, Senegal. Lupus nephritis was defined by the presence of proteinuria greater than 0.5 gm per 24 hours and/or hematuria in a patient with SLE. Epidemiological, clinical, laboratory, therapeutic and prognosis-related data were collected and analyzed with version 6 EPI INFO software. Epidemiological, clinical and laboratory data were recorded as they were at the time of diagnosis while therapeutic and evolution-related data were collected during the whole period of the survey. Two therapeutic assessments were performed, one in the sixth month (shortterm assessment) and another in the twentyfourth month of diagnosis (middle-term assessment).
| Results | | |
There were 74 patients diagnosed to have SLE during the study period. Of them, 42 had features of LN, yielding a prevalence of 56.75%. We focused our analysis on these 42 patients. Their mean age was 29.6 years (range, 5 to 60 years); patients aged from 20 to 40 years represented 83.30% of the cases. There were five males and 37 females, with a male-female sex ratio of 0.13.
The presenting clinical features of the study patients are depicted in [Table - 1]. Mucocutaneous manifestations were present in 92.85% and joint manifestations were noticed in 66.66% of the patients. The other clinical manifestations (vascular, cardiac, neurological, pleuro-pulmonary, digestive, etc.) occurred in less than five per cent of the patients.
All patients presented with anemia and the mean hemoglobin was 9.4 g/dl. Leukopenia was noticed in 14.28% and thrombocytopenia in 4.76% of the patients. Inflammatory syndrome was found in all patients but the C-reactive protein was elevated in only two patients (4.61%). Renal function was impaired in 15 patients (35.71%) with mild renal failure in nine cases, severe renal failure in four cases and end-stage renal disease in two cases. Proteinuria greater than 0.5 g per 24 hours was noticed in all patients and among them 45.23% had nephrotic range proteinuria. The other abnormallities noticed on urinalysis included leukocyturia (35.71%), microscopic hematuria (2.57%), casts (4.76%) and klebsiella infection (4.76%). The anti-nuclear antibodies were positive in the 35 tested patients and the anti-native DNA anti-bodies, in the two tested ones.
Percutaneous renal biopsy (PRB) was performed in 22 patients (52.38%) and showed the following results: Class II, one case; Class III, two cases; Class IV, seven cases and Class V, 12 cases, according to the WHO classification. [3]
Immunofluorescence revealed the following findings: complement C3 deposits in 21 cases, IgG in 19 cases, C1q in 17 cases, IgM in 14 cases, IgA in 13 cases and albumin and fibrin in eight cases each.
The basic treatment in all patients consisted of oral prednisone. The various protocols used are depicted in [Table - 2]. Bolus methylprednisone and cyclophosphamide were used in patients with Class III or IV LN as well as in patients with Class V LN with heavy proteinuria or renal failure. Hydroxychloroquine was given to patients with muco-cutaneous lesions of acute lupus. Hemodialysis was performed in two patients (4.76%).
At short-term assessment, there was one death in a patient with end-stage renal disease. At middle-term assessment, 12 patients (28.57%) were lost to follow-up; eight patients (19.04%) showed good improvement; in six patients, the disease worsened and among them, two had transformation of their histological lesion (class V and class III lesions in one patient each to Class IV lesion). Five patients died, two due to complications of chronic renal failure, two others due to septicemia and one patient due to hypertensive encephalopathy; 10 patients (23.80%) remained on irregular follow-up.
| Discussion | | |
Our survey was conducted at the main Nephrology Center in Senegal; all patients needing a kidney biopsy, either for SLE or any other disease, are referred to this center.
Thus, our study patients came from all regions of Senegal. The age and sex-ratio of our study patients correspond with the data published so far, which show that SLE, with or without renal localization, is mainly a disease of the young woman in the period of genital activity. [4] The prevalence of LN in our study (56.75%) is also according to most published data. [5],[6] The prevalence of cutaneous and joint manifestations in our patients is similar to that reported in other studies on SLE. In fact, the prevalence of the different manifestations as published are variable and tend to reflect orientation or specialization of the recruiting services. [7] LN was diagnosed at the time of first hospital admission in our patients, as in conformity with the data of Ballow et al, [8] who found that LN occurs concomitantly with extra-renal manifestations or during the first year of evolution in a patient with SLE. Proteinuria was the main mode of expression of LN and was found in all our patients with 45.23% of them having the nephrotic syndrome; in contrast, Frigui et al. have reported a 20% prevalence of the nephrotic syndrome in their patients with LN. [9]
Renal failure rarely occurs in more than 20% of the cases in studies from the West [10] whereas it was seen in 35.7% of our cases; it reflects either delayed diagnosis in the developing countries or the increased severity of renal involvement in black subjects. [11] The frequency of kidney biopsy in our survey (52.38%) is relatively low when compared with that of Northern African studies, where the frequency varies between 82 and 96%; [9],[12] this could reflect a relative lack of adequate renal pathology services in Senegal. Our results showed a predominance of Class IV and V LN whereas in most publications, classes III and IV predominate. [2],[5],[9],[12] The therapeutic protocols that we used [Table - 2] are in conformity with the available data indicating that the basis of treatment consists of corticosteroids [13] and that in acute proliferative forms (Classes III and IV), addition of immunosuppressive drugs improves both life and renal prognosis. [14] The short-term prognosis in our patients was good. At middle-term, difficulties arose in view of the large number of patients that were lost for follow-up. This is probably related to the high cost of the immunosuppressive drugs and the inaccessibility of renal replacement therapies in Senegal. The cause of death was dominated by renal complications in our study while in the developed world, deaths due to renal failure per se are considerably low and have been replaced by cardiovascular and infectious complications. [15]
| Conclusion | | |
LN was seen in 56.75% of patients in Senegal with SLE. Kidney biopsy, performed in about half of the cases, showed predominantly WHO classes IV and V lesions. The short-term prognosis was good whereas at middle-term, follow-up of the patients was irregular. Early diagnosis, liberal use of kidney biopsy, reduction of treatment cost and better patient education would help in improving the prognosis.
| References | | |
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| 2. | Beji S, Kaoroud H, Ben Moussa JE, et al. Lupus nephritis: 211 cases. Rev Med Interne 2005;26(1):8-12. |
| 3. | Meyer O. Acute disseminated lupus erythematosus. Diagnosis, course, principles of treatment. Rev Prat 1997;47 (16):1821-31. |
| 4. | Massot C. Lupus diseases. Rev Prat 1998; 48:640-9. |
| 5. | Tazi-Mezalek D, Harmouche H, Adnaoui M, et al. Characteristics of disseminated lupus erythematosus in Morocco. About 166 cases. Rev Med Interne 2000;21 (S4): 465-6. |
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| 8. | Ballow JE, Buompas DT, Fesler BJ, Austin HA. Management of lupus nephritis. Kidney Int 1996;53:88-92. |
| 9. | Frigui M, Marzouk S, Ben Hmida M, et al. Lupus nephropathy in internal medicine. About 44 cases. Rev Med Interne 2003; 24(S4):433. |
| 10. | Martins L, Rocha G, Rodrigues A, et al. Lupus nephritis: a retrospective review of 78 cases from a single center. Clin Nephrol 2002;57(2):114-9. |
| 11. | Reveille JD, Bartolucci A, Alarcon GN. Prognosis in lupus erythematosus: Negative impact of increasing age at onset, black race and thrombocytopenia, as well as causes of death. Arthritis Rheum 1990;33(1):39-47. |
| 12. | Smiti Khanfir M, Hamzaoui A, Ben Ghorbel I, Braham A, Houman MH. Study of the clinical, paraclinical and evolutionary characteristics of lupus nephropathy in a group of Tunisian patients. Rev Med Interne 2004; 25(S1): 102-3. |
| 13. | Piette JC. Traitement du lupus erythemateux dissemine. Treatment of systemic lupus erythematosus. Rev Prat 1998;48(6):643-7. |
| 14. | Contreras G, Pardo V, Leclerque B, et al. Sequential therapies for proliferative lupus nephritis. N Engl J Med 2004; 350(10):971-80. |
| 15. | Abu Shakra M, Urowitz MB, Gladman DD, Gough J. Mortality studies in lupus erythematosus: Results from a single center. Predictor variables for mortality. J Rheumatol 1995;22(7):1665-70. |
Correspondence Address:
A Niang
B.P. 6548, Dakar Etoile, Dakar
Senegal
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 18445916 
[Table - 1], [Table - 2] |
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