Q J Med 2003; 96: 382-384
© 2003 Association of Physicians
Correspondence |
Proteinuric renal disease in children in South-Western Uganda
Department of Paediatrics, Mbarara University of Science and Technology, Mbarara, Uganda University of Bristol, Bristol, UK e-mail p.mathieson{at}bris.ac.uk
Sir,
Proteinuric renal disease is common in Africa in both children and adults: in the 1960s it accounted for 2–3% of medical admissions.1 The condition is more severe than nephrotic syndrome in developed countries, incurring high mortality and typically being resistant to corticosteroids or antimitotic agents. Admission rates with nephrotic syndrome are higher during periods of intense malaria transmission, and an association has been reported with Plasmodium malariae infection.2,3 Most literature on this subject pre-dates the epidemic of human immunodeficiency virus (HIV) infection in sub-Saharan Africa. HIV nephropathy is increasingly recognized in the developed world,4 but renal manifestations of HIV have not been studied in Africa.
Thirty-six children (20 males, 16 females, age range 1.5–14 years, median 6 years) were admitted to Mbarara University Hospital with proteinuric renal disease in the first 11 months of 1999: approximately 160/million population/year, or eight times the UK incidence of childhood nephrotic syndrome. The most common clinical diagnosis was acute nephritic syndrome (impaired renal function and/or hypertension and/or active urine sediment, 18 cases, 50%); ‘pure’ nephrotic syndrome (isolated proteinuria, normal blood pressure, normal serum creatinine) was rare (five cases, 14%), but mixed pictures were common (13 cases, 36%). Median serum albumin was 15.5 g/dl, median serum creatinine was 129 µmol/l. Malaria data were collected in a separate study by Médicine Sans Frontieres: 307/541 children (57%) were Plasmodium-positive; 94% of isolates were P. falciparum, P. malariae being rare (5%). The seroprevalence of HIV and hepatitis B were assessed by anonymous analysis of 77 consecutive paediatric in-patients: 16/77 (20%) were HIV-positive, but only 2/77 (3%) had antibodies to hepatitis B. Of the 36 children with proteinuric renal disease, only one had proven HIV infection, and none had evidence of hepatitis B. Overall outcome for these 36 children is shown in Table 1
. Treatments included diuretics, anti-hypertensives, and dietary modifications whenever possible (increasing protein intake, removing salt). Eleven children received corticosteroids; two subsequently also received cyclophosphamide. Mean duration of hospital admission was 11 days (range 1–90). There was some improvement in 69%. Six children died (17% mortality). ‘Pure’ nephrotic syndrome carried the best prognosis (all improved, none lost to follow-up, no deaths), but this was the least common subtype, accounting for only 14% of cases. In the group with acute nephritic presentation, overall mortality was 28%, and may have been even higher if additional deaths occurred among children lost to follow-up.
|
The assumption that P. malariae is the major cause of proteinuric renal disease in Africa has dominated literature on this subject for 40 years, but seems unlikely to be the explanation for the high rate of acute renal disease we observed in Mbarara, SW Uganda. In Mbarara in 1999, only 5% of malarial infections amongst children were due to P. malariae. Nor did we find any evidence that HIV infection is an important cause: only one proteinuric child had proven HIV infection and the mean age of affected children (6.7 years) is against a role for HIV, since vertically transmitted HIV infections are usually manifest at a younger age. The explanation we favour is that the majority of these patients have infection-related glomerulonephritis (GN). The most typical form of this entity is acute proliferative GN complicating streptococcal infection. Each of these possible explanations can only be adequately tested by prospective studies: we have embarked on such a study in Mbarara. Intriguingly, our preliminary findings in a small number of renal biopsies do not show the typical lesion of post-streptococcal GN, but instead an eosinophil-rich mesangiocapillary GN picture (Peat et al., unpublished observations) which may represent GN complicating parasitic infections.
Acknowledgments
We thank the children and their families, the medical and nursing staff of Mbarara University Hospital and Professor Eldryd Parry of the Tropical Health Education Trust, UK who has facilitated the link with University of Bristol, UK.
References
1. Kibukamusoke JW. The nephrotic syndrome in Lagos, Nigeria. W Afr Med J 1966; 15:213–17.
2. Kibukamusoke JW, Hunt MSR, Wilks NE. The nephrotic syndrome in Uganda and its association with quartan malaria. Q J Med 1967; 143:393–408.
3. Hendrickse RG, Adeniyi A. Quartan malarial nephrotic syndrome in children. Kidney Int 1979; 16:64–74.[Web of Science][Medline]
4. Winston JA, Burns GC, Klotman PE. The human immunodeficiency virus (HIV) epidemic and HIV-associated nephropathy. Semin Nephrol 1998; 18:373–7.[Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  Nephrology Arch. Dis. Child., April 1, 2005; 90(suppl_2): A29 - A32. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||