From the Department of Nephrology, Nizam’s
Institute of Medical Sciences, Panjagutta, Hyderabad 500 082, India.
Correspondence to: Dr. M. Ahmed, B 61/3 Manak
Nagar, Lucknow 226 011, India.
E-mail:
[email protected]
Manuscript received: March 11, 2002; Initial
review completed: April 18, 2002; Revision accepted: January 27,
2003.
Acute renal failure (ARF) is a well known but an
alarming complication of nephrotic syndrome. Smith and Hayslett have
reported that ARF is common in elderly patients with minimal change
disease, who have severe proteinuria and hypoalbuminemia and that most
of these patients had complete recovery of renal function(1). ARF is
uncommon in children with nephrotic syndrome(2,3). Protracted
idiopathic ARF in childhood minimal change disease necessitating
dialysis is extremely rare(2,3). Most of the time ARF in these
patients is due to sepsis, interstitial nephritis or renal vein
thromboasis(3).
Our search of the published literature till date
revealed only few case reports(4-6). We a child with minimal change
nephrotic syndrome who presented with oliguric ARF requiring dialysis.
Case Report
A 9-year-old boy presented with oliguria and
anasarca of 3 days duration, without any history suggestive of
hematuria, dysuria, sore throat, skin rash, fever, joint pains, flank
pain, hypotension, hypertension or nephrotoxic drug intake.
Examination revealed anasarca and mild dehydration. His weight was 28
kg, blood pressure 100/60 mm of Hg, pulse rate 78 per minute, all
peripheral pulses were equally felt and the respiratory rate 18 per
minute. There was no fever, pallor, icterus, lymphadenopathy, rash or
vascular throm-bosis.
Investigations showed blood urea level of 121 mg/dL,
creatinine 5.9 mg/dL, which increased further to 141 mg/dL and 7.8 mg/dL
respectively after one week. He also had severe metabolic acidosis pH
7.30, bicarbo-nate 15 Eq/L. Urine examination showed 4+ proteinuria.
Microscopic examination of fresh urine sample was unremarkable. His
hemo-globin was 13 g/dL total leukocyte counts 10,200/cu mm, with
polymorphs 69%, lymphocytes 25%, eosinophils 4%, and monocytes 2%. The
blood sodium level was 136 mEq/L, potassium 3.5 mEq/L, calcium 9.2 mg/dL,
phosphorus 3.6 mg/dL, total proteins 5.6 g/dL, albumin 2.9 g/dL, total
cholesterol 337 mg/dL and triglyceride 345 mg/dL. Serum complement
levels (C3, C4) were within normal limits. 24-hr urine protein
excretias was 2.9 g, serology for hepatitis B, C and HIV, ANA and ANCA
were negative. Ultrasound of the abdomen showed normal sized kidneys
with normal echogenicity without any evidence of urinary tract
obstruction. Colour doppler ultrasound scanning of the renal vessels
did not show any evidence of vascular occlusion.
The patient was hospitalized and managed with
adequate hydration in the form of intravenous normal saline 30 mL/kg
body weight in one hour, followed by intravenous frusemide at a dose
of 2 mg/kg stat.
In view of anuria and azotemia, he was taken up for
dialysis (acute intermittent peritoneal dialysis initially followed by
hemodialysis). Even after two weeks of dialytic and supportive therapy
patient continued to be remain oliguric and dialysis dependent, so a
percutaneous kidney biopsy was performed to determine the cause of ARF.
Light microscopy of kidney biopsy showed 22
glomeruli, all of which wee apparently normal; tubules, interstitium
and blood vessels were also normal, without any evidence of
interstitial fibrosis or arterio-sclerosis. There was no evidence of
intra-tubular obstruction, acute tubular necrosis, interstitial
nephritis or interstitial edema. Immunoflorescence was negative for
IgG, IgM, IgA, C3 and C1q. Electron microscopy showed effacement of
the foot processes of the podocytes. The biopsy features were
suggestive of minimal change disease.
In view of nephrotic range proteinuria, patient was
treated with prednisolone according to the extended APN protocol(7).
The urine output gradually improved and renal failure recovered in
four weeks. The patient achieved remission from proferuria within four
weeks of prednisolone therapy. He continues to be in remission at six
months follow up.
Discussion
ARF can arise simultaneously with nephrotic
syndrome following administration of NSAIDs, foscarnet, and interferon
alfa therapy. It can also complicate preexisting nephrotic syndrom due
to rapid progression of glomerulonephitis, hypotension, acute tubular
necrosis, interstitial nephritis, renal vein thrombosis, intratubular
obstruction by proteineous cast or interstitial edema(2).
Sakarcan, et al. described four pediatric
patients, in whom reversible ARF developed due to mild acute tubular
necrosis, during relapse of All the four patients required dialysis,
but had complete recovery of renal function(4). Varada, et al.
reported a 15-year-old girl with steroid resistant nephrotic syndrome,
who developed reversible ARF due to severe intersitial edema and
fusion of foot processes. This patient required dialysis and
aggressive nutritional therapy for one year before recovery(5).
Steele, et al. reported 2 patients in which one presented with
ARF at the time of onset of nephrotic syndrome, while other patient
developed ARF at the time of relapse. Both patients had complete
recovlery following peritoneal dialysis and oral prednisolone
therapy(6).
In our patient, we tried to exclude pre-renal
azotenia as a contributory factor for ARF by adequate hydration.
Kidney biopsy showed Minimal change disease without any evidence of
acute tubular necrosis, interstitial nephritis, interstitial edema or
intratubular obstruction by proteinecious casts. The cause of renal
failure could not be determined despite adequate investigations.
Childhood idiopathic nephrotic syndrome can present as eversible ARF.
The cause of renal failure may be difficult to determine even after
kidney biopsy. These patients can be managed successfully with proper
dialytic and suppor-tive measures. Response to prednisolone therapy is
satisfactory in such cases.
Contributors: MA managed the patient and
drafted the manuscript. He would act as the guarantor for the paper.
Funding: None.
Competing interests: None stated.
