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Nephrol Dial Transplant (1996) 11: 535-536
Case ReportNephrologyDialysisTransplantation
A case of non-Hodgkin lymphoma presenting primarily withrenal
failureS. M. Wood1, S. M. Boyd2, J. E. Taylor2 and J.
Savill1'University Hosp ital, Queens Medical Centre, Nottingham;
2City Hospital, Nottingham, UK
Ke y words: Non-Hodgkin lymphoma; renal failure
IntroductionLymphomatous invasion of the kidneys is a
relativelycommon occurrence and may precipitate acute renalfailure.
It is extremely unusual, however, to find non-Hodgkin lymphoma
(NHL) apparent only in the kid-neys, with no evidence of
disseminated disease. Arecent review of primary renal extranodal
NHL foundonly nine cases since 1980 [1]. We detail a case
whichseems to fit suggested diagnostic criteria: (1) presenta-tion
with renal failure; (2) non-obstructive renalenlargement with no
other organ/nodal involvement;(3) diagnosis made on renal biopsy;
(4) absence ofother causes of renal failure; (5) improvement of
renalfunction on therapy [2,3].Case reportA 61 year old man
presented with a 9-week history ofmalaise, anorexia, weight loss of
3.5 kg, and nightsweats. He also reported a dry cough that had
notresponded to erythromycin from his general practi-tioner. His
past history included rheumatic fever at theage of three, and
long-standing dyspepsia. He was onno medication, had worked as an
industrial cleaner,and had smoked 40 cigarettes a day for 40
years.
On examination he was pyrexial (38C), had twoperipheral splinter
haemorrhages and no palpablelymphadenopathy. He had a regular pulse
of 72, bloodpressure of 132/84, normal venous pressure, normalapex
and a mitral regurgitant murmur with normalheart sounds. The murmur
was unchanging during hisadmission. His chest was clear and
abdominal exam ina-tion revealed only a palpable 1-cm liver edge.
His skin,fundi, and neurology were normal.Investigations were as
follows. Haemoglobin wasCorrespondence and offprint requests to: Dr
M. Wood, ErythropoietinGroup, Room 420, Institute of Molecular
Medicine, University ofOxford, John Radcliffe Hospital, Hedley Way,
Oxford OX3 9DU,UK.
8.2g/dl, platelets. 322x lO 9/l, white count 8.6xlO 9/lwith 1.45
x 109/l lymphocytes (1.5-4.0x109/1) andotherwise normal
differential. The CD4 count wasappropriate for the degree of
lymphopenia. A bloodfilm showed a normochromic, normocytic
anaemiawith rouleaux formation. B12, RBC folate, reticulo-cytes and
serum haptoglobins were normal, as wereclotting studies.
Electrolytes were normal, uric acidwas 465 umol/1 (100-400 umol/1),
urea 9.3 mmol/1,and creatinine 144 umol/1 (on admission). The trans
-aminases were normal, as was the bilirubin andgamma-GT; however,
the lactate dehydrogenase was1727 u/1 (350-700 u/1). Serum ferritin
was 2500 ug/1,in keeping with other raised inflammatory markers(CRP
162 and ESR 90mm/h). The IgA was slightlyraised at 4.39 g/1
(0.7-3.9 g/1), and the other immuno-globulins were normal.
Electrophoresis of serum andurine was normal. An autoimmune screen
(includingANA , AN CA, and anti-GBM ) was negative. Serologyfor
legionella, influenza A & B, psittacosis, coxiella,RSV,
mycoplasma, brucella, VDRL, TPHA, hepatitisA & B, VZV, EBV,
CMV, and HSV did not showinfection on repeated samples. Antibodies
to tox-oplasma were suggestive of infection at least 18
monthspreviously. Frequent culture of urine, sputum, andblood
revealed only proteus in the urine on admissionand Haemophilus
influenzae in sputum a fortnightlater, both sensitive to
ampicillin. Microscopy andculture of sputum, urine, and blood for
mycobacteriumwere all negative. Urine analysis showed 3 + protein
,2 + blood and only a few red cells on microscopy. A24-h urine
collection had 2.77 g protein. Bone marrowaspirate and trephine
were normocellular, and cellularmorphology was normal.
Imaging was also non-diagnostic. Repeated echocar-diography,
including via the transoesophageal route,showed mildly thickened
aortic cusps and a jet ofmitral regurgitation with no vegetations.
The initialchest radiograph had clear lung fields and a
mildlyenlarged heart shadow; later the patient developedbilatera l
small pleural effusions (prote in 15 g/1 andnormal chemistry,
cytology and culture). Abdominalultrasound was normal. CT scan of
the abdomen andthorax showed an enlarged liver, bilateral pleural
effu-sions and patchy inflammatory changes in both lowerlobes, but
no lymphadenopathy.
1996 European Dialysis and Transplant Association-European Renal
Association
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S. M. Wood et al.
Fig. 1. Renal biopsy showing a proliferative glomerulonephritis
subsequently found to be due to numerous atypical lymphoid cells
withinglomeruli. H & Ex 105.Over the following month the renal
function deteri-orated gradually to a urea of 20.1 mmol/1 and
creat-inine of 386 umol/1, and hence a renal biopsy wasperformed;
45 glomeruli were obtained, of which threewere sclerosed. An
initial diagnosis of focal and seg-mental proliferative
glomerulonephritis was made(Figure 1), but immunohistology
subsequently showedthat the proliferation within renal glomeruli
was in
fact due to the presence of highly atypical lymphoidcells with
positive staining for CD20. The final dia-gnosis was that of renal
involvement by a high-gradelarge B cell non-Hodgkin lymphoma of
angiotrophictype. The lymphoma cells were almost entirely
locatedwithin glomeruli with only an occasional interstitialtumour
cell identified on immunostaining.The patient was treated with
cyclophosphamide andmethylprednisolone. His renal function improved
onthis regime, and 10 days later his urea was 13.0 mmol/1and
creatinine 168 umol/1. However, at this time hedeveloped left
inguinal lymphadenopathy, and a biop-sied node confirmed the
presence of lymphoma.
Unfortunately his condition deteriorated soon afterand he died
20 days after his diagnostic renal biopsywith respiratory distress,
hypotension, and resistantventricular fibrillation. A t auto psy,
nodes, liver, spleen,lungs, marrow, a nd kidneys were found to be
infiltratedwith NHL. The renal involvement was diffuse ratherthan
primarily glomerular as in the biopsy. The causeof death was ARDS
secondary to non-Hodgkinlymphoma.
DiscussionOur patient had primarily renal B-cell NHL; hence
thecase fits with diagnostic criteria of primary renal
extranodal NHL as stated above. He presented withrenal failure,
other causes were excluded, and thediagnosis was made on renal
biopsy. Contrary toreports in the literature, ultrasound and CT
were non-contributory and the patient's kidneys were noted tobe
enlarged only at post-mortem. His renal functionresponded to
chemotherapy for a few days; however,this did n ot prevent the
development of fatal dissemin-ated disease. Of the nine cases of
primary renalextranodal lymphoma taken from the literature
byMalbrain et al. [1], five were followed up to death,and only two
of these did not have disseminated NHL(post-mortem showed only
renal involvement). Itremains unclear as to whether primary renal
extranodalNHL is a distinct diagnosis.Acknowledgements. Dr A.
Cowley and Dr R. P. Burden are thankedfor permision to report a
patient under their care. S. M. Wood iscurrently a Wellcome
Clinical Training Fellow.
References1. Mlbrain MLN G, Lambrecht GL Y, Daelemans R, Lins
RL,Hermans P, Zachee P. Acute renal failure due to
bilaterallymphomatous infiltrates. Primary extranodal
non-Hodgkin'slymphoma of the kidneys: does it really exist? Clin
Nephrol 1994;42: 163-1692. Glicklich D , Sung MW, Frey M. Renal
failure due to lymphomat-ous infiltration of the kidneys. Report of
three new cases andreview of the literature. Cancer 1986; 58:
748-7533. Truong LD, Soroka S, Sheth AV, Kessler M, Mattioloi C,
SukiW. Primary renal lymphoma presenting as acute renal
failure.Case reports. Am J Kidney Dis 1987; 9: 502-506
Received for publication: 23.10.1995Accepted in revised form:
27.10.1995
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