Kidney International, Vol. 16 (1979), pp.
23-29
Schistosomal glomerulopathy
ZILTON A. ANDRADE and HEONIR ROCHA
Departments of Pathology and Medicine, University of Bahia Medical School, Salvador, Bahia, Brazil
Historical background
For some time clinicians in Brazil have suspected
that renal involvement may occur in Schistosoma
mansoni infection [1, 2]. In 1964, Lopes noted ab-
normal concentrations of protein and leucocytes in
the urine of 26.7% of patients with the hepatosplen-
ic form of schistosomiasis, as compared with 3.8%
of patients with milder forms of the disease [1].
Moreover, Machado demonstrated that in the most
advanced forms of schistosomiasis, large amounts
of beta and gamma globulins, as well as lipopro-
teins, were present in the urine [21.
When a cirrhotic glomerulosclerosis" [3, 41 or
"hepatic glomerulosclerosis" [5] was described in
the literature, it seemed plausible that at least some
similar glomerular changes could be present also in
advanced schistosomiasis, a chronic liver disease
with prominent portal hypertension. A comparative
histologic study then showed that glomeruloscierot-
ic changes were indeed even more marked and fre-
quent in hepatosplenic schistosomiasis than they
were in active hepatic cirrhosis [6]. Membranous
glomerular changes with fibrillar thickening and cel-
lular proliferation of the mesangium were observed
in the kidneys of patients who had died of hepato-
splenic schistosomiasis. The results of this study
stimulated an investigation of the renal lesions in a
larger number of patients. Histologic examination
of 80 cases revealed that renal glomeruli were fre-
quently altered in advanced schistosomiasis [7].
There were a variety of changes that included me-
sangial cell proliferation, increased mesangial ma-
trix, focal sclerosis, and several types of glomerulo-
nephritis.
Reproduction of this glomerular involvement in
S. mansoni-infected experimental animals came lat-
er. Renal lesions were demonstrated in several spe-
cies of monkeys [8—li], mice [12—14], rabbits [15],
and hamsters [161 heavily infected either with S.
mansoni or S. japonicum. The appearance of these
lesions seemed to be similar to those found in hu-
mans. The prevalence of renal involvement in en-
23
demic areas of schistosomiasis has yet to be deter-
mined. In one study, an attempt was made to corre-
late S. mansoni infection with proteinuria [17].
Higher concentrations of urinary protein were en-
countered in individuals with infections compared
to those without infection. Because these authors
only related spleen size with proteinuria, however,
they were unable to assess the importance of ad-
vanced hepatic disease with portal hypertension to
proteinuria. They found that 35.4% of infected indi-
viduals had splenic enlargement, a rate which ex-
ceeds the 4% of cases that normally go on to de-
velop the hepatosplenic form [18, 19].
It has been demonstrated recently that schisto-
somal glomerulopathy is mediated via the glomeru-
lar deposition of immune complexes. Circulating
specific schistosomal antigen has been demon-
strated in the serum [20], as well as in the urine, of
heavily infected animals [21, 22]. Also, circulating
immune-complexes have been detected in patients
with S. mansoni infection [24]. More recently, some
authors have identified specific schistosomal anti-
gens deposited in glomerular capillary loops of ani-
mals [11, 13, 14] and patients [25, 26] with glomeru-
lonephritis.
Several questions, however, still remain to be an-
swered. The true prevalence of renal involvement,
the clinical course of the glomerulopathy, the na-
ture of the antigen or antigens, as well as the nature
of the immunologic factors rendering the host sus-
ceptible to this renal involvement are not well un-
derstood.
Clinical manifestations
Most patients diagnosed as having schistosomal
glomerulonephritis are young adults who come
from an endemic area for schistosomiasis and ex-
Received for publication July 12, 1978
0085-2538/79/0016-0023 $01.40
© 1979 by the International Society of Nephrology
24 Andrade and Rocha
hibit hepatosplenomegaly on physical examination.
The liver is usually hard, with a prominent left lobe,
and has an irregular surface and sharp edge. The
spleen is hard and rarely tender. The majority of
patients have edema of the legs and some have as-
cites. In a study of 100 consecutive patients with
hepatosplenic S. mansoni admitted to a general hos-
pital in an endemic area, 9 patients had nephrotic
syndrome, 6 had only proteinuria, and 3 patients
had arterial hypertension. The urinary protein of
these patients had low selectivity [271 or was non-
selective [281; this corresponds to the detection of
1gM, alpha-2 macroglobulins, and lipoproteins in
the urine. A peculiarity of the nephrotic syndrome
observed in association with schistosomiasis is the
concomitant finding of increased plasma globulin
concentrations and normal cholesterol concentra-
tions in one-third of such patients. The 15% in-
cidence of overt renal disease in hepatosplenic
schistosomiasis observed in this study [291 may not
reflect the true prevalence of this condition. This
survey was conducted in a hospital with an interest
in schistosomal nephropathy, and this fact might
have been responsible for selection of patients. This
figure, however, is similar to the 12% incidence of
glomerulonephritis described in patients with hepa-
tosplenic schistosomiasis autopsied in the same
hospital [71.
Very little is known about the natural history of
schistosomal glomerulopathy. In an endemic area,
some patients with hepatosplenic S. mansoni admitted
for splenectomy or ligation of esophageal varices ex-
hibited only proteinuria and microscopic hematuria,
but they developed the nephrotic syndrome, with or
without arterial hypertension, 10 to 12 years later.
Of 15 patients with hepatosplenic S. mansoni who
had no clinical evidence of glomerular disease when
subjected to renal (surgical) biopsy at the time of
splenectomy, 6 patients had glomerular lesions [301.
The lesions were usually mild, but 1 patient had
membranoproliferative glomerulonephritis, and an-
other had focal glomerular sclerosis. These findings
suggest that glomerular lesions antedate overt clini-
cal manifestations and that the evolution of the gb-
merular disease is slow and probably takes years to
become clinically apparent. Thus far, there is no
conclusive test to detect preclinical renal in-
volvement in this disease. Recently, however, it has
been demonstrated that low levels of f3-l-C are cor-
related with the histologic finding of glomerulone-
phritis in hepatosplenic patients without clinical
renal involvement, but this finding is still prelimi-
nary (Martinelli et al, to be published).
Diagnosis
Several factors should be considered in the clini-
cal diagnosis of schistosomal glomerulopathy: (1)
Patients are usually young adults, more frequently
male than female (2:1), and come from an endemic
area for schistosomiasis. The finding of viable worm
eggs in stool specimens is diagnostic of the parasitic
infection. Rarely is the stool examination negative,
and in such cases, the diagnosis can be made by
rectal and/or liver biopsy. In the biopsy specimens,
granulomas containing the eggs are seen. (2) Pa-
tients exhibit an enlarged liver with a prominent left
lobe, and in most cases, an enlarged spleen; the ma-
jority have esophageal varices. (3) Nephropathy is
usually manifested by a nephrotic syndrome. The
only peculiarity is the finding of high serum globulin
levels and normal serum cholesterol levels in a third
of such cases. Some patients may show only a mild
persistent proteinuria. (4) Other causes of nephrotic
syndrome, such as disseminated lupus erythema-
tosus, malaria, syphilis, diabetes mellitus, strepto-
coccal glomerulonephritis, and any indication of
previous episodes of gbomerulonephritis should be
considered in the differential diagnosis. Although
there is no reliable way to rule out unrelated renal
pathology, it is reasonable to assume, however,
with the accumulated evidence available, that the
major etiology of the glomerular disease in these
cases is related to the S. mansoni infection.
Pathologic features
In good correlation with the clinical picture of
nephrotic syndrome, the majority of human cases
studied histologically conform to a diagnosis of
chronic diffuse membranoproliferative glomerulo-
nephritis, frequently with lobular accentuation [7,
27, 30, 31]. This picture is also in keeping with the
observation that the mesangium is the area that is
most altered in schistosomal gbomerubopathy. Since
the initial studies, both in humans [6, 7, 27, 30, 31J
and in experimental animals [8, 9, 121, the most
prominent finding has been mesangial expansion,
which is seen best at the glomerular vascular pole.
This was described as a fibrillar, PAS-positive
thickening, with a mild to moderate increase in cel-
lularity. In what appeared to be very early cases of
renal involvement and with no clinical manifesta-
tion of renal disease, mesangial cell proliferation
was so outstanding that a diagnosis of mesangial
glomerulonephritis seemed justified [31]. On the
other hand, Brito et al [301 refer to a patient who
progressed from a predominant membranous type
 Schistosomal glomerulopathy 25

of lesion to a definite lobular pattern during a period
of 7 years.
The second most common type of glomerular le-
sion observed in biopsy material is focal glomerular
sclerosis [7, 27, 31]. In necropsy material, however,
almost all histologic types of glomerulonephritis can
be observed in patients dying with renal disease and
advanced hepatic schistosomiasis [7]. In our own
patients' biopsy specimens, although the membrano-
proliferative form occurs in about 50% of the total,
there are cases of acute diffuse proliferative gb-
merulonephritis, rapidly progressive glomerulone-
phritis, focal glomerular sclerosis, membranous
gbomerulopathy, and end-stage kidney disease. In a
case of membranous glomerubopathy, observed in a
13-year-old boy with massive schistosome infection
[32], there was a moderate mesangial cell prolifera-
tion besides the basement membrane thickening
with silver-positive 'spikes."
Electron microscopic studies [9, 12, 18, 29, 33,
34] have shown the presence of electron-dense de-
posits both in the basement membrane near the
mesangial cells and in the mesangial area itself
(Figs. 1 and 2). In this area, the presence of large,
laminated, electron-dense bodies was sometimes
noted.
Patho genesis and immunopathology
There is good evidence that schistosomal glomer-
ubopathy results from deposition of immune com-
plexes in the glomeruli of the affected host. Immu-
nofluorescent studies have revealed IgG, 1gM, IgE,
occasionally IgA and -1-C protein in glomerular
deposits along the glomerular basement membrane

-
CL I.

tt$1.

Fig. 1. Electron-dense deposits (D) in basement membrane (BM) and especially in the mesangium (M) in the glomerulus of a 23-year-old
woman with glomerulopathy and schistosomal hepatosplenic disease (X12,000).
26
Fig. 2. A picture similar to Fig. 1, with electron-dense deposits in mesangial area (probably immune-complex deposits), in the renal
glomerulus of a mouse infected 64 days before with 100 S. mansoni cercariae (x25,650).
and mesangial areas of heavily infected experimen-
tal animals [9, 11-14] and humans [25, 26, 30, 33,
34J. Also, electron micrography of the glomerular
lesions reveal electron-dense deposits within the
mesangium and along the endothelial side of the
basement membrane. This latter finding supports
the concept that the renal damage of schistoso-
miasis is of immunologic origin. The true nature of
these immune complexes, and more important, of
their antigenic component, however, is not under-
stood. Initially it was thought that they were formed
by antigens from the worm or its products and anti-
bodies produced by the host. This hypothesis pro-
gressively received strength from several studies.
More than 60 immunogenic constituents have been
extracted from adult worms, cercariae, and schis-
tosomula [35j. Only few of them, however, appear
on exposed sites of the adult worms, such as the
Andrade and Rocha
tegument or the intestinal lining. In 1961, Okabe
and Tanaka [21j documented the presence of a
dialyzable and thermostable schistosome antigen in
the urine of rabbits and humans. Later, a schisto-
some antigen was detected in the serum [201 and
urine [221 of mice and hamsters heavily infected
with S. mansoni. This antigen was later character-
ized as a high-molecular-weight polysaccharide [36]
and was found only in the intestinal lining of the
adult worm [371. This location is important because
the worm regurgitates the antigen along with ingest-
ed blood into the circulation of the host. This anti-
gen also has been demonstrated in the primordial
esophagus of cercarie and in the developing in-
testinal tube of the schistosomule [381, and this find-
ing may explain the early detection of this material
in the serum of infected animals. Several other cir-
culating worm antigens have been well character-
 Schistosomal glomerulopathy
ized in infected animals. Recently, Deelder et al [39]
characterized a low-molecular-weight substance in
the serum and urine of hamsters heavily infected
with S. mansoni as well as in secretory products of
the adult worm. Thus far, this purified poly-
saccharide antigen could not be made immunogenic
for rabbits, and its role in the pathogenesis of the
glomerulopathy is unknown. It may be related to
the M antigen detected in the urine of infected pa-
tients [231. Besides the adult worm antigens, the
eggs are another important source of schistosomal
antigens. A soluble egg antigen (SEA) plays a major
role in the periovular granulomatous reaction, but
so far SEA has not been implicated in the pathogen-
esis of the glomerular lesions in schistosoma-infect-
ed hosts.
Antibodies to several antigenic fractions of the
schistosome worm or its products can be detected
in infected animals and humans [40, 41]. These
serum antibodies react with several antigenic frac-
tions derived from mature eggs, cercaria, schistoso-
mula, and from living and dead worms. Schistosom-
al antigens and antibodies have been detected in the
milk of mothers with S. mansoni infection [421.
Circulating antigen-antibody complexes have
been demonstrated in experimental animals and hu-
mans with schistosomiasis [24, 43, 441, and the
highest titers of complexes were found in patients
having the hepatosplenic form of the disease or as-
sociated nephropathy [45]. The reasons why the
glomerular involvement in schistosomiasis appears
to be limited to the hepatosplenic form of the dis-
ease deserve a special comment. (1) It seems im-
portant that the polysaccharide antigen described
has been detected only in serum and urine of heavi-
ly infected hosts. Normally, as has been suggested
[9, 14, 461, this polysaccharide antigen is removed
from the circulation by reticuloendothelial cells
(similarly to other high-molecular-weight poiy-
saccharides), and only when the RES is saturated
does the antigen appear in the circulation. In this
respect, it is important that patients with the hepa-
tosplenic form of schistosomiasis generally have a
greater parasitic load. (2) It has been shown that the
induction of colateral portal circulation by partial
portal vein ligation resulted in greater deposition of
immunoglobulins and complement in the glomeruli
of mice infected with S. mansoni [14]. This finding
suggested that diversion of immune complexes from
filtration by the Kupifer cells results in a greater op-
portunity for them to reach the kidneys and other
organs of the systemic circulations. It is of interest
that in hepatosplenic schistosomiasis there is a col-
27
lateral circulation due to pre sinusoidal portal vein
obstruction in practically all cases. (3) Finally, it is
of interest that occurrence of glomerular lesions are
related to the development of the hepatosplenic
form of the disease. It has been shown that baboons
infected with S. mansoni do not develop portal fi-
brosis, and, in this species, even heavy infections
do not result in glomerular lesions [47]. Likewise, in
humans heavily infected with S. haematobium,
liver damage is less severe, and the disease is ac-
companied rarely by glomerulopathy [481.
Definite evidence that schistosome antigen or an-
tigens are present in the immune-complex glomeru-
lar disease observed in humans and animals has ap-
peared only recently. Earlier studies probably failed
to demonstrate specific antigens in the glomeruli,
because of the lack of a potent antischistosomal
sera. More recently, Tada et al [11] were able to
demonstrate the presence of coarse granular depo-
sition of IgG, 1gM, IgA, and IgE, together with
/3-1-C mainly in mesangial area in monkeys heavily
infected with S. japonicum. Schistosoma antigens
were also detected in the mesangium and along the
glomerular capillary wall. The authors pointed out
the unique feature of IgE deposition in this nephri-
tis. All these findings have been duplicated in hu-
man patients [25, 26]. Immunoglobulins which react
with the intestinal lining and tegument of adult S.
mansoni have been eluted from the kidneys of pa-
tients with schistosomal glomerulopathy [49].
Therapy
Treatment of patients with schistosomal glomeru-
lopathy has been disappointing. Patients having the
nephrotic syndrome with membranoproliferative
glomerulonephritis or focal glomerular sclerosis of-
ten do not respond to therapy with corticosteroids
and or cyclophosphamide [50]. The use of anti-
schistosomal drugs alone or in association with cor-
ticosteroids and immunosuppressors also does not
improve the results. The few cases that have re-
sponded well to therapy have been followed for 2
and 3 years, without recrudescence, but more eval-
uation is needed. Thus far, the use of anti-
schistosomal drugs such as oxamniquine or hycan-
thone does not seem to have had any immediate
deleterious effect on renal function of the patients,
as judged by lack of changes in proteinuria, urea
and creatinine levels, and creatinine clearences. In
any case, it seems logical to use antischistosomal
drugs in patients with schistosomal glomerulopa-
thy. Elimination of the worms and their antigens in
28 Andrade and Rocha
early glomerular involvement could be curative, but
this awaits a well-documented proof.
Acknowledgments
This work was supported by grants (SIP 08/126
and PDE 06/2/04) from the Conselho Nacional de
Desenvolvimento Cientifico e Technolçgico CNPq.
Reprint requests to Dr. Z. A. Andrade, Department of Pathol-
ogy, University of Bahia Medical School, Salvador, Bahia, Bra-
zil.
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