Open Journal of Nephrology, 2013, 3, 181-183
Published Online December 2013 (http://www.scirp.org/journal/ojneph)
Open Access OJNeph
Alarming Presentation of a Seemingly Common
Condition in a Patient with Renal Impairment
Mohammad Budruddin1*, Muhammad Yasir Khalil2, Issa Al Salmi2, Ramaiah Shilpa2
1Nephrology Department, Tawam Hospital, Al Ain, UAE
2Nephrology Department, Royal Hospital, Muscat, Oman
Received August 8, 2013; revised September 9, 2013; accepted October 2, 2013
Copyright © 2013 Mohammad Budruddin et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
We received a 23-year-old male, working in the Army for 18 months, with advanced renal impairment, haemoptysis
and hyperkalemia. An impression of the pulmonary renal syndrome was made and he was managed aggressively with
haemodialysis, plasma exchange and pulsing with methyl p rednisolon e. His condition improv ed, but the rena l functions
did not. The vasculitic workup including Extractable Nuclear Antigen (ENA) and Anti-Neutrophil Cytoplasmic Anti-
body (ANCA) which were sent on admission came out to be negative. As he apparently responded to the initial man-
agement protocol, he was subjected to renal biop sy which did not reveal any vasculitis but was consisten t for end-stage
renal disease. Subsequently he was subjected to lung biopsy which also was not supportive for vasculitis. However, we
concluded that the initial pointers for Wegener’s granulomatosis were misleading. The haemoptysis entirely subs ided as
the congestion improved. He was maintained on Haemodialysis three times per week schedule and discharged to the
peripheral health care facility.
Keywords: Haemoptysis; Renal Impairment; Pulmonary Renal Syndrome; Haemodialysis; ENA; ANCA; Vasculitis;
Pulmonary oedema is not an unusual presentation in pa-
tients with end-stage renal disease. This may be associ-
ated with haemoptysis. Radiological imaging of the chest
may at times be very confusing, mimicking alveolar
haemorrhage. We had a young patient who presented
acute onset advanced renal failure with haemoptysis. In
the course of his management, we concluded that his
haemoptysis was secondary to pulmonary oedema and
not pulmonary renal syndrome .
2. Case Summary
Mr. IRS, a 23-year-old Omani male was referred from a
peripheral Hospital with advanced renal failure and
haemoptysis. He was not know to have any medical pro-
blems in the past and was not on any medications before
this presentation. Neither was he ever told in any health
care facility to be having renal impairment. He presented
with the advanced renal failure with serum creatinine
more than 2000 mmol/l and urea 84 mmol/l. He was in
severe respiratory distress (tachypnoeic RR of 35/m, de-
saturating to 78% on room air) and developed massive
frank haemoptysis immediately after admission. The
chest X-ray Figure 1 on admission and urgent high res-
olution CT (HRCT) Figure 2 done after two sessions of
Haemodialysis with good ultrafiltration showed exten-
sive alveolar haemorrhage with perivascular nodules.
This concurred with our initial impression of pulmonary
renal syndrome (Wegener’s granolomatosis). Further CT
of the sinuses did show the polypoidal thickening of the
mucous membrane of the right frontal sinus. The com-
plements level done were normal.
His condition was critical with severe drop in Hb to 4
gm/dl. He was started on emergent aggressive treatment
for Wegner’s granulomatosis with 7 sessions of plasma
exchange and methylprednisolone 1 gm pulse daily for
three days. His haemoptysis subsided after the forth ses-
sion of plasma exchange and his general condition also
improved with improvement in the pulmonary conges-
tion and uremia following several sessions of haemodi-
alysis and ultrafiltrations.
M. BUDRUDDIN ET AL.
The vasculitic workup subsequently came out to be
negative for Extactable Neuclear antigens (ENA), Anti-
Neutrophil Cytoplasmic Antibody but equivocal for An-
ti-glomerular basement membrane antibody (Anti GBM).
Serology for HBV, HCV and HIV were negative. Repeat
radiology showed improvement in the alveolar shadows.
Ultrasound estimation of kidney size was normal with
increased ecogenicity. The urine analysis was bland (no
active sediments) showed <2 RBC, <2 WBC, of 25 mg/L
After stabilizing he was subjected to renal biopsy in
order to get the tissue diagnosis. The histopathology did
not show any evidence of vasculitis, tubulointerstitial
compartment showed marked sclerosis of the interstitium
and scattered moderate inflammatory cells, tubular atro-
phy with dilatation. The features were consistent with the
end stage renal disease (Figure 3)
Even the lung tissue biopsy done did not reveal any
granuloma, pneumonic changes and evidence of vascu-
litis. However there were findings of scanty recent and
Figure 1. Chest X-ray showing nodular opacities (indicated
by small and big arrows).
Figure 2. CT scan of the chest showing ground glass ap-
old intra-alveolar haemorrhage (5% of the tissue sample)
Semi-permanent vascular access (Right Internal Jugu-
lar vein tunneled catheter) was inserted for him and he
was put on maintenance haemodialysis three times per
week and radiocephalic fistula was also created for him.
He was discharged to the peripheral health care facility
with dialysis facility, in a stable condition with a plan for
living related renal transplantation from his brother in the
The presentation with pulmonary oedema is very com-
mon in patients on maintenance haemodialysis. These
end stage renal disease patients irrespective of etiology
are at times polyuric before being started on dialysis.
However after initiating on haemodialysis they tend to
decrease their urine output. Little excess of fluid intake
inter dialytic period leads to pulmonary congestion an d at
times frank pulmonary oedema. This is exacerbated by
the concur re nt presenc e of poorly functioning heart.
In our patient the scenario was a bit perplexing as he
presented for the first time with very advanced renal
failure and pulmonary congestion. However his urine
Figure 3. Haematoxylin Eosin stain section shows a core of
kidney tissue with two globally hyalinised glomeruli, (black
arrow heads) marked tubulointerstitial sclerosis and mild
chronic infl a mmation.
Figure 4. Section showing the lung tissue with mild thick-
ening of the alveolar septa and congestion. No vasculitis or
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M. BUDRUDDIN ET AL.
Open Access OJNeph
output was nearly 1500 ml in 24 Hours. The clinical pre-
sence of frank haemoptysis with first time documentation
of grossly deranged renal functions and CT finding of
alveolar haemorrhage was quite suggestive of pulmonary
renal syndrome (Wegener’s Granulomatosis/Good pas-
tures syn drome).
Pulmonary oedema can at times present with haemop-
tysis but again it usually does not show alveolar haemor-
However going through the literature we realized that
radiological findings of pulmonary oedema can present
in several forms .
a) Postobstructive pulmonary edema.
b) Pulmonary edema with chronic pulmonary embo-
c) Pulmonary edema with veno-occlusive.
d) Stage 1 near drowning pulmonary edema manifests
as Kerley lines, peribronchial cuffing, and patchy,
perihilar alveolar areas of airspace consolidation;
e) stage 2 and 3 lesions are radiologically nonspecific.
f) Pulmonary edema following administration of cyto-
g) High-altitude pulmonary edema.
(h) Neurogenic pulmonary edema manifests as bilateral,
rather homogeneous airspace consolidations that pre-
dominate at the apices in about 50% of cases.
i) Reperfusion pulmonary edema.
j) Postreduction pulmonary edema manifests as mild
airspace consolidation involving the ipsilateral lung.
k) Pulmonary edema due to air embolism initially de-
monstrates interstitial edema followed by bilateral, peri-
pheral alveolar areas of increased opacity that predomi-
nate at the lung bases.
The typical alveolar shadows seen in our patients CT
is one of the forms.
Further it is well known that those patients with ob-
structive airway disease who develop congestive heart
failure have much higher pulmonary extravascular vol-
ume. Left ventricular failure due to hypoxia leads to left
atrial hypertension, which could be the patho-physiolo-
gic basis of interstitial pulmonary oedema .
Histological studies in uremic lungs have proven the
presence of proteinaceous oedema fluid though many
have even shown intra-alveolar haemorrhage . Evalu-
ation of the oedema fluid by direct endotracheal aspira-
tion have even shown high content of protein which
could suggest increased pulmonary vascular p ermeability
to plasma proteins in ren al failure . Though a co mmon
feature of pulmonary oedema is increased permeability
of the basement membrane to water and low molecular
weight solutes, this may be attributable to the hemody-
namic factors playing role in the alveolar interstitium and
basement membrane .
Patients with pulmonary edema may present not only
blood tinged frothy sputum but may even present mas-
sive haemoptysis, which may be life threatening and
mimicking serious medical conditions, clinically and ra-
diologically. Keeping this in mind one must deal cau-
tiously with patients presenting pulmonary haemorrhage
(haemoptysis) and advanced renal failure.
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