Nephrol Dial Transplant (2005) 20: 1275
3
Fig. 1. Magnetic resonance angiogram demonstrating kinking of
left renal artery.
computed tomography (CT) scan revealed a 9.5  9.4 cm
haematoma extending from the lower pole of the left kidney
into the left pelvis. Surgical evacuation of the haematoma
was not advised due to the high risk for infection. The
patient’s hospitalization was marked by continued bleed-
ing and transient acute renal failure with a peak Scr of
3.8 mg/dl. The patient was discharged on the ninth day of
hospitalization, at which time his Scr was 3.1 mg/dl. His
blood pressure had increased to 177/89 mmHg for which
hydralazine and metoprolol were prescribed. Findings on
the renal biopsy suggested tacrolimus nephrotoxicity and
diabetic glomerulosclerosis.
Three weeks later, the patient was readmitted with
oedema, dyspnoea and somnolence. The Scr had increased
to 5.3 mg/dl, urinalysis demonstrated 4þ blood and 4þ
protein, and microscopic analysis was unremarkable. Renal
sonogram demonstrated a 26  14 cm retroperitoneal haema-
toma extending caudally from the left kidney with no
hydronephrosis. Renal replacement therapy with intermittent
haemodialysis was initiated.
Work-up included a MAG3 renal scan showing an
asymmetric decrease in renal blood flow and function in the
left kidney (split function: 16% left, 84% right). Subsequent
magnetic resonance angiography revealed anterior and sup-
erior displacement of the left kidney by the haematoma with
kinking of the left renal artery at the level of the ostium
(Figure 1). Vascular surgery consultation advised against
surgical revascularization because of the high risk for
infection. The patient was discharged with the continued
requirement for renal replacement therapy. A CT scan
4 months after the biopsy demonstrated an evolving left
retroperitoneal hematoma unchanged in size or anatomic
location with continued cephalad displacement of the left
kidney.
In conclusion, this case demonstrates a new complication
ascribed to percutaneous kidney biopsy; anatomic displace-
ment of the kidney from a haematoma resulting in torsion and
kinking of the ipsilateral main renal artery and subsequent
ischaemic nephropathy.
Conflict of interest statement. None declared.
1
Renal Section, Medical Service, Steven D. Weisbord1,3
2
Radiology Service Mohan Ramkumar1,3
VA Pittsburgh Healthcare System Scott A. LaPidus2,4
1275
Renal-Electrolyte Division David J. McBride2
Department of Medicine Paul M. Palevsky1,3
VA Pittsburgh Healthcare System
4
Department of Radiology
University of Pittsburgh School of Medicine
Pittsburgh, PA
USA
Email: steven.weisbord@med.va.gov
1. Parrish AE. Complications of percutaneous renal biopsy:
a review of 37 years’ experience. Clin Nephrol 1992; 38: 135–141
2. Whittier WL, Korbet SM. Timing of complications in
percutaneous renal biopsy. J Am Soc Nephrol 2004; 15: 142–147
3. Korbet SM. Percutaneous renal biopsy. Semin Nephrol 2002;
22: 254–267
4. Wijeyesinghe EC, Richardson RM, Uldall PR. Temporary loss
of renal function: an unusual complication of perinephric
hemorrhage after percutaneous renal biopsy. Am J Kidney Dis
1987; 10: 314–317
doi:10.1093/ndt/gfh828
Downloaded from http://ndt.oxfordjournals.org/ by guest on November 14, 2015
Advance Access publication 12 April 2005
Renal toxicity of Oxaliplatin
Sir,
Oxaliplatin is an antitumoral agent derived from platinum
(trans-1,2-diammino-cylo-hexane-platinum) with cytotoxic
activity against a number of solid tumours, including
colorectal cancer and metastatic ovarian carcinoma. Renal
side-effects are unclear. We report the second case of acute
renal failure following the use of oxaliplatin.
A 69-year-old woman was referred to our nephrology
unit because of anuric acute renal failure. She had a history
of ovarian adenocarcinoma treated in June 2001 by hyster-
ectomy, ovariectomy and chemotherapy. Carboplatin and
paclitaxel (six cycles) had been stopped in November 2001.
In November 2002, oxaliplatin (85 mg/m2) and gemcitabine
(1.5 g) were introduced. Three months before presentation,
serum creatinine was 73 mmol/l (0.8 mg/dl).
On admission, after 10 cycles of oxaliplatin and gem-
citabine, her blood pressure was 120–70 mmHg and she
weighed 47.5 kg. Physical examination was normal. Serum
creatinine was 1126 mmol/l and blood urea was 44.1 mmol/l.
Haemoglobin was 9.8 g/dl and platelets were 64.000/mm3.
Haptoglobin was 1.27 g/l. Renal sonography finding was
normal. No monoclonal component could be detected in
the blood. Circulating immune complexes, antinuclear anti-
body, rheumatoid arthritis haemaglutinin titre, antitubular
basement membrane antibody and antineutrophil cysto-
plasmic antibody were negative. The patient required three
haemodialysis sessions. On renal biopsy, severe tubular
necrosis was observed with denudation of tubular base-
ment membranes, cell fragments and red cells in the tubular
lumen, and cellular dismorphy (Fig. 1). In the interstitium,
only mild oedema was observed without cellular infiltration.
Most of the glomeruli are ischaemic. Immunofluoresence
study did not show specific deposits. Six weeks after
admission, serum creatinine level was 1.09 mg/dl (120 mmol/l).
Six months later, serum creatinine level was still 89 mmol/l
(1.0 mg/dl).
In this case, oxaliplatin is very likely to have been
responsible for acute renal failure. There was a close tem-
poral relationship between the onset of renal failure and
1276
Fig. 1. Severe tubular necrosis and red cells in the tubular lumen.
oxaliplatin administration. Renal biopsy showed severe
tubular lesion necrosis, which corresponds to the spectrum
of adverse effects reported on primary cultures of rabbit
proximal tubular cells [4] and also in the first case report [1].
Besides oxaliplatin, the patient had been taking gemcita-
bine — drugs implicated in thrombotic microangiopathy
[3], a diagnosis that was ruled out by the renal biopsy.
This case report points out that the spectrum of oxaliplatin
side effects also includes reversible acute renal failure with
tubular necrosis. Factors predisposing to nephrotoxicity
are unknown; they would include concomitant administra-
tion of a nephrotoxic drug, but the patient had previously
received oxaliplatin with gemcitabine without any renal
damage. Gemcitabine was always given before oxaliplatin.
An animal study [5] suggested that the administration of
gemcitabine prior to cisplatin aggravates cisplatin-induced
nephrotoxicity. Pinotti [1] also suggests that the renal damage
could have been caused by a cumulative dose of oxaliplatin
(in our case 1210 mg).
Internists, oncologists and nephrologists must be aware
of this possible complication and we recommend monitoring
of renal function in these patients.
Conflict of interest statement. None declared.
1
Armed Forces Hospital of
Val de Grâce Jacques Labaye1
Paris Damien Sarret1
France Christan Duvic1
2
INSERM U507 Michel Hérody1
Hôpital Necker (AP-HP) Francis Didelot1
Paris Georges Nédélec1
France Laure-Hélène Noël2
Email: jah.labaye@wanadoo.fr
1. Pinotti G, Martinelli B. A case of acute tubular necrosis due
to oxaliplatin. Ann Oncol 2002; 13: 1951–1952
2. Aapro MS, Martin C, Hatty S. Gemcitabine—a safety review.
Anticancer Drugs 1998; 9: 191–201
3. Gietema JA, Groen HJM, Meijer S, Smit EF. Effects of
gemcitabine on renal function in patients with non-small cell
lung cancer. Eur J Cancer 1998; 34: 199–202
4. Legallicier B, Leclere C, Monteil C, Morin JP, Fillastre JP.
Action toxique de deux agents antitumoraux dérivés du
platine, le cisplatine et l’oxaloplatine sur des cultures primaires
de cellules tubulaires proximales de rein de lapin. Pathologie
Biologie 1993; 41: 873–880
Nephrol Dial Transplant (2005) 20: 1276
5. Saad SY, Najjar TA, Noreddin AM, Al-Rikabi AC. Effects
of gemcitabine on cisplatin-induced nephrotoxicity in rats:
schedule-dependent study. Pharmacol Res 2001; 43: 193–198
doi:10.1093/ndt/gfh826
Advance Access publication 22 March 2005
Fatal renal and hepatic failure following silver nitrate
instillation for treatment of chyluria
Sir,
Toxic acute tubular necrosis (ATN) accounts for the largest
number of cases of acute renal failure (ARF) after ischaemic
ATN. We discuss here a case of fulminant hepatic and
renal failure following instillation of silver nitrate. This
patient underwent silver nitrate instillation in the renal pelvis
for treatment of chyluria. The exact quantity and concentra-
Downloaded from http://ndt.oxfordjournals.org/ by guest on November 14, 2015
tion were not available since the patient was transferred to
our institute from another hospital. He developed severe
hepatic and renal failure within 24 h of instillation. All other
causes of liver and renal failure were ruled out by appro-
priate laboratory investigations and imaging techniques.
He was given a trial of N-acetyl cysteine in view of severe
toxic hepatitis. He was treated with haemodialysis for renal
failure. His course was complicated by the development of
epistaxis despite reasonably acceptable coagulation param-
eters. He underwent ligation of the nasal septal artery in
view of the same, but this did not stop the bleeding and
post-operative ventilatory support was required. In light of
a progressive deterioration in liver function, we decided to
add an activated charcoal cartridge to the haemodialysis
circuit to remove protein-bound toxins secondary to liver
failure, e.g. bilirubin, bile acids, etc. We first processed
dialyzed blood through a plasma filter, which separated
plasma-containing protein-bound toxins. This process
avoided thrombocytopaenia, which can occur with the use
of a charcoal cartridge. This plasma with protein-bound
toxins was subsequently processed through activated char-
coal. Blood from the plasma filter and plasma from the
charcoal cartridge were returned to the body. Low-dose
heparin was used throughout the procedure. With this
extracorporeal circuit there was no thrombocytopaenia
secondary to the charcoal cartridge and no loss of albumin.
Neither was there a need for albumin as a dialysate as
required in a molecular adsorbent recycling system [1].
With the above management, the patient’s general condi-
tion and epistaxis improved. His liver function tests also
showed improvement. He was extubated and started on
oral feeds; however, 2 days later the patient had a sudden
cardiorespiratory arrest from which he could not be revived.
Probable cause of death was thought to be pulmonary
embolism or aspiration pneumonia.
Chyluria is a common problem in India, Hong Kong,
Taiwan and Japan [2]. Although silver nitrate instillation
(0.5–1%) for the treatment of chyluria is a relatively safe
procedure with a 70–80% success rate [3], two case reports
have described ARF following silver nitrate instillation
[4,5]. Possible mechanisms for ARF in these patients were
ATN and acute papillary necrosis. In the present case,
an unknown quantity of silver nitrate was used. This was
possibly absorbed systemically through larger lymphatic
channels, which resulted in fulminant hepatic and renal
failure. Silver nitrate causing both hepatic and renal failure