Prabhat Kumar, Kanai Lal Barik, Anindya Dasgupta
Post Graduate Student, Department of Pediatric Medicine, Burdwan Medical College And
Hospital, Burdwan
Hyperlipidemia is a common findings in Nephrotic syndrome. There is increase in total
Cholesterol, LDL cholesterol, VLDL cholesterol, TG and low or normal HDL cholesterol (1)
.There are only few studies on derangement of serum lipid with nephrotic syndrome in Indian
children. Hyperlipidemia is usually observed during the active phase of disease and
disappears with resolution of proteinuria. But in relapsing cases, it may persist and may
increase risk of atherosclerosis in later life (2). Hence serial monitoring of lipids is required to
predict atherosclerosis risk in future . There are also only few studies on serial estimation of
lipids in children with nephritic syndrome. Our study is an attempt to know derangement of
serum lipids in Indian children with nephrotic syndrome and to study serial estimation of
lipids to assess, when these levels return to normal. Review Of Literature: - Nephrotic
syndrome is primarily a pediatric disorder, Incidence is 2 – 3 / 100,000 chidren per year ( 3 ).
Majority of affected chidren have steroid sensitive minimal change disease. The characteristic
features of nephritic syndrome are heavy proteinuria ( > 40 mg/m2/ hr ) , hypoalbuminemia (
<2.5 g/dl ), edema and hyperlipidemia. Cause of the increase permeability is not well
understood. In minimal change disease T cell dysfunction may alter level of cytokines, leads
to loss of negatively charged glycoproteins within glomerular capillary wall. Serum lipid
levels are elevated for two reasons. Hypoalbuminemia stimulates generalized hepatic protein
synthesis, including synthesis of lipoproteins. Lipid catabolism is decreased, as a result of
reduced plasma levels of lipoprotein lipase, related to increased urinary losses of this enzyme.
In children with the Nephrotic syndrome, there is an inverse relationship between the rate of
urinary excretion of protein & the degree of hypoalbuminemia. The rate of albumin synthesis
in nephrotic syndrome in a steady state is not decreased, it is either increased or normal. In
general there is inverse correlation between conc. Of serum albumin and that of cholesterol.
The level of TG is more variable and may even be normal in patients with mild
hypoalbuminemia. The conc. Of VLDL chol & LDL chol are increased ( 4). HDL chol are
usually normal or decreased (1) in child with nephrotic syndrome , although the ratio of
HDL chol to Total chol may still be low.(5,6,7,8) Some children with lesions other than
minimal change may have decreased HDL chol. Complications due to hyperlipidemia..risk of
cardiovascular disease AIMS AND OBJECTIVES:- Lipoprotein play an important role in
the transport of plasma lipids; Their elevation or alteration in various fractions may be
responsible for hypercholesterolemia in nephrotic syndrome .There is increased total
cholesterol, LDL cholesterol, VLDL cholesterol, and Triglycerides and normal or low
HDL(4). However in Indian children the degree of hyperlipidemia is not as high as in western
children. Our study is designed to study the derangement of serum lipids in nephritic
syndrome, and to know whether any correlation exist between serum lipid & serum albumin.
Specific Objectives: - To analyse pattern of change in the serum lipid profile in nephrotic
syndrome in Indian children. To evaluate whether any correlation exists between serum lipid
level & serum albumin in nephrotic syndrome. To assess when the serum lipids returns to
normal. Materials And Methods:- A)Study Area :- Department of pediatric medicine and
Department of Biochemistry , Burdwan medical college and hospital b)STUDY
POPULATION :- patients with nephrotic syndrome admitted in pediatric ward and attending
pediatric OPD. Inclusion Criteria: - Children aged upto 7 yrs with typical features of
nephritic syndrome. Patients were studied at onset of Nephrotic syndrome, during remission,
and relapses. Exclusion Criteria :- Unwilling of patient Associated Known cardiac disease
Associated Known liver disease Associated Known other kidney disease Associated
Malnutrition Associated Protein losing
enteropathy H/o – Diabetes mellitus H/oHypothyroidism H/o – Familial hypercholesterolemia c)Study Period :- March 2011 To
February 2012 d)Sample Size :- Approximately 50 patients with nephrotic syndrome. e)
Sample Design :- A prospective observational study which include approx 50 children with
Nephrotic syndrome, selected by inclusion and exclusion criteria. They were clinically
examined and lipid profile was done in each case before steroid therapy, after one month of
therapy and at the end of therapy. f)STUDY DESIGN :- Institutional based prospective
study. g)Parameters To Be Studied :- History & clinical examination. Biochemical test of
serum - Total cholesterol By ; CHOD/PAP method. LDL cholesterol
By; Friedwald
equation. VLDL cholesterol By ; Calculation HDL cholesterol By ; Phosphotungstic Acid
By ; GPO/PAP method Albumin By ; BCG method. Urine for Total protein By;
Sulphosalicylic acid method. h) Study Tools: - Patient proforma Case record form, OPD
ticket, & BHT. Weighing machine Laboratory equipments & chemical reagentsRelated
articles, books, journals.Consent form. i) Study Techniques: - Consents should be taken from
the parents of the cases Record of history & clinical examination. Relevant laboratory
investigations J) Plan For Analysis Of Data:-Data will be compiled, tabulated, & analysed
with appropriate statistical methods, and subsequently P value is to be measured . P value <
0.05 will be taken as significant.
Prince Parakh, Mishra OP, Prabhakar R , Shah GS, Bhatta NK, Singh RR
Dept.of Pediatrics,BPKIHS,Dharan
Introduction-Acute Postinfectious glomerulonephritis(APIGN) is the commonest cause of
severe acute glomerulonephritis in children. Children with PIGN present in different ways
and with different lab pictures. Aims and Objectives: 1) To study various clinical presentation
(symptoms &signs) and laboratory profile of Acute Post Infectious Glomerulonephritis. 2) To
know the prognosis and outcome of the children suffering from APIGN. Materials and
Methods: This Retrospective study was conducted studying the case reports of 54 children
admitted to BPKIHS Pediatric Ward over a period of one year with features suggestive of
APSGN. The information relating to the children included age, sex and presenting
complaints, complete physical examination, investigation, treatment and outcome of the
disease. Results - Acute PIGN constituted 22% of all renal cases admitted. Edema(85%),
Hematuria(gross-74%,microscopic-6%),hypertension(83%),Abdominal pain (46%) ,Acute
infections(40%),Fluid overload(47%) and Hypertensive encephalopathy(7.4%) were the chief
presentations.94.4% patients required diuretics and 72.2% required antihypertensives.87%
patients were discharged within 10 days whereas 13% patients required hospital stay > 10
days. There was no mortality. Conclusions- Prompt diagnosis in patient with mild renal
compromise, hypertension, and urinary abnormalities is vital, as these patients could lose
kidney function without urgent treatment. PIGN frequently presents with Acute kidney Injury
and fluid overload which should be promptly recognized and treated to have better outcomes.
Key Words-APIGN,Children,AKI.
Rameshwar Gore, Santosh Kondekar, Surbhi Rathi, Shruti Hule, Priti Tamhankar, Sahebrao
Pediatric Resident, Department of Pediatrics, 1st Floor, College Building, TNMC & BYL
Nair Hospital, Mumbai Central, Mumbai-400008
Email id:
Abstract- Introduction-MPGN commonly occurs in older children and young adults and
presents with nephrotic or nephritic syndrome. Unlike any other nephritic or nephrotic
conditions, MPGN may not be predictable from clinical history and examination. Hereby we
present a series of 4 cases of type I MPGN that presented with totally different clinical
history and some related complications. Case History- Case 1- A 4 1/2 year old girl case of
frequently relapsing steroid responsive nephrotic syndrome admitted with 7th relapse.
Screening for secondary causes of nephrotic syndrome was negative. Renal biopsy was done
due to age of onset being 1 year age , Electron microscopy(EM) and immunoflorescence
(IF)was suggestive of type I MPGN. Case 2 –A 10 yr old boy presented as chronic
glomerulonephritis (Nephritic features along with hypertension for 8 months), serum C3
being low, ASLO titer-normal, secondary workup was negative. Renal biopsy EM&IF
performed in view of CGN was suggestive of type I MPGN. Case 3-A 5yr old girl presented
as acute glomerulonephritis with hypertensive encephalopathy. on investigation urine
albumin 3+,serum C3 was low, other secondary workup negative. Biopsy was performed in
view of presentation with a complication. Renal biopsy finding was suggestive of type I
MPGN. Case 4 –An 8 yr old girl presented with features of acute glomerulonephritis without
hypertension. Though clinical diagnosis was PSGN due to ASLO being 800; persistence of
cola hematuria for more than 4 weeks indicated an unusual course. Renal biopsy EM &IF
shows type I MPGN. Discussion: There is enough literature to state that MPGN cannot be
suspected from clinical presentation and it has always been a surprise diagnosis. Although the
four cases looked straightforward, each had an unusual feature. It becomes crucial to keep a
watch for unusual features in each case of nephrotic or nephritic syndrome.MPGN prognosis
and therapy depends on the histopathological pattern. Hence timely histopathological
diagnosis can help predict the prognosis. Conclusion-Early index of suspicion and early
biopsy in case of atypical presentation; will stop us from starting empirical therapy for AGN
and or nephrotic syndrome which may give overestimated better prognosis.
Rameshwar Gore, Varun Bansal,Radha Ghildiyal, Poonam Sankhe, Jane David.
Dept. of Pediatrics, BYL Nair Ch. Hospital and TN Medical College, Mumbai-8
Introduction: Membranoproliferative Glomerulonephritis(MPGN) type II is also known as
Dense deposit Disease,is a rare entity.The incidence being 2-3/10,00,000.It is usually seen in
older children , the mean age of onset being 10 year with slight female preponderance. Case
history: 11 year old girl, diagnosed as a case of atypical nephrotic syndrome at 9 years of age,
was admitted with third relapse of nephrotic syndrome. screening for secondary cause of
nephrotic syndrome was negative.As serum C3 level was low renal biopsy was done.
Electron Microscopy and Immunoflorenscence examamination was suggestive of Dense
deposit disease.Child required extended course of steroids in high doses along with
Cyclophosphamide and antihypertensive drugs. Discussion: MPGN type II is a caused by
uncontrolled activation of alternate pathway of.complement cascade. The condition may arise
as an inherited disorder with factor H deficiency. Factor H dysfunction is due to presence of
C3 Nephritic Factor (C3 Nef),which is an Ig G antibody that binds to C3 convertase of
alternate complement pathway,preventing cleavage of C3bBb and permiting breakdown of
C3. It is characterized by proteinuria, hematuria ,nephrotic syndrome, acute nephritic
syndrome ,recurrent gross hematuria or azotemia. Long term administration of alternate day
predniolone (1-1.5 mg/kg) combined with Angiotensin converting enzyme inhibitor is
considered standard therapy. Cyclophosphamide, Mycophenolate have been tried with little
success. Almost all cases progress to end stage renal diseae with in 10 years of diagnosis.
Conclusion: MPGN type II should be suspected in a case of atypical nephrotic syndrome,
with low C3 level. Early treatment with long term steroid may induce remission in these
Shivani Deswal, Pradeep Debata, Murtaza Kamal, K.C Aggarwal.
Department of Pediatrics, Safdarjung hospital & V.M.M.C, New Delhi
Renal tubular acidosis (RTA) is a group of tubular transport disorders characterised by
inability to appropriately acidify urine, a normal anion gap (hyperchloremic) metabolic
acidosis in the setting of normal or near-normal glomerular filtration rate. DRTA defect is
usually secretory, characterised by an inability of the tubular cells to secrete H+ ions leading
to inappropriately alkaline urine (urine ph>6) despite systemic acidosis (bloodpH<7.2).
Hypercalciuria, hypocitraturia and hypokalemia are also usually present. A four year old
unimmunised boy of average growth presented with lower limb weakness that had
progressed slowly to involve his upper limbs over a period of 12 hours without history of
preceding upper respiratory tract infection, diarrhoea , intramuscular injection and
seizures.The patient did not have any weakness of the cranial nerves or respiratory muscles,
or any sphincteric disturbance.Had similar history one year back, for which he was treated as
a case of GBS and received IVIG for two days. Vitals were stable with a fairly normal
general physical examination. Power was 2/5 in bilateral lower limbs and 3/5 in upper limbs,
with normal tone and deep tendon reflexes, flexor plantars , normal sensory and cranial nerve
examination. The investigations showed normal hemogram and counts, ABG (pH
=7.178,HCO3- 9.8meq/L).Electrolytes- Na+ 142meq/L,K+ 2.2meq/L, Ca+ 10.1meq/L,PO4 very high, ALP 1307,Blood urea- 26mg/dl, S.creatinine 0.5mg/dl, TSH 5.09IU, ECGhypokalemic changes, NCV normal study, CPK 92IU/L ,urinary ph 7,Urine anion gap –
raised-106meq/L (urinary Na+ 143meq/L,K+ 49.5meq/L,Cl-67meq/L, Ca+ 13.4meq/L),
Ultrasonography KUB –normal.Alkali solution(urilizer) and potassium supplements were
started and the patients weakness improved completely and on follow up blood bicarbonates
improved to near normal with normal serum electrolytes. The diagnosis of DRTA in our
patient was made from his inability to acidify urine in the face of metabolic acidosis with
hypokalemia. Thus, an important presentations of distal renal tubular acidosis (DRTA) is
recurrent hypokalaemic weakness, which can be life threatening if not suspected and treated
Girish Chandra Bhatt, Devki Nandan,Vivek Dewan, Nirmaljeet Kaur
Associate Professor, Pediatrics, PGIMER & Associated Dr RML Hospital New Delhi, India
Abstract: Introduction: Acute glomerulonephritis occurring during the course of enteric fever
is a rare entity and only few cases are reported in the literature. Two interesting cases of acute
glomerulonephritis occurring in twin siblings are described. Case 1: Ten years old, first of
twin siblings presented with complaints of moderate grad fever for last 7 days, pain abdomen
from last 2 days and passing dark coloured urine on the day of admission. There was no
history of oliguria, swelling over body, pyoderma or sore throat. Examination revealed
temperature of 102.80C, heart rate of 98/minute and blood pressure of 108/60mm of mercury.
Per abdomen examination revealed soft non tender enlarge liver (4cm below subcostal
margin with smooth surface) and enlarged spleen 2 cm below subcostal margin. which was
further confirmed by ultrasonography. Urinary examination showed proteinuria of 1.1
gm/day, with presence of 70-80 red blood cells(RBC’s) with more than 75% dysmorphic
RBC’s. Phase contrast microscopy further confirmed the presence of dysmorphic RBC’s.
Blood culture was sent which was positive for Salmonella typhi and widal was positive (TH
and TO ;1:340). Rest of the work up was inconclusive. Case 2: Second of twin sibling
presented with fever for last seven days and pain abdomen for last 2 days. Examination
revealed a temperature of 102.60F, heart rate of 92/min, respiratory rate of 20/min and normal
blood pressure (104/62mm of mercury). Per abdomen examination revealed
hepatosplenomegay. Urinary examination showed proteinuria of 960mg/d with 20-30 RBC
cast which were further confirmed on phase contrast microscopy. S.typhi was grown in blood
culture and widal was positive(TH and To;1:240). Rest of the work up was inconclusive.
Renal biopsy was refused by the parents. A diagnosis of acute glomerulonephritis due to
S.typhi was made and patient was commenced on ceftriaxone therapy. Hematuria
disappeared in both cases during 4th week on follow up. Conclusion: Enteric fever may
sometime present with rare clinical manifestations, such as acute glomerulonephritis as in our
case. Early treatment of typhoid fever with intravenous antibiotics and fluid management
prevents further progression of the disease. Furthermore, familial occurrence of this rare
complication may be an incidental finding in this case, it is indeed intriguing and requires
further research.
Barik Chinmay, Chandan CK,Mohanty Ajay ,Mohanty Niranjan
C/O Narahari Barik, Maitri Vihar, Jagannathpur, Bhadrak, Orissa
A 4 month 1.9kg female child of birth weight 2.5kg born out of nonconsanguinous marriage
presented to our emergency OPD with severe respiratory distress,loosing of weight since
birth. She was very sick looking and cachectic.On enquiry she had two prior similar episode
of chest infection for which hospitalized and relieved. There was history of polyuria,loss of
weight and frequent vomiting. On examination she was dehydrated,skin pinch going
slow,rapid thready pulse,bilateral crepitation in chest,no obvious cardiological abnormality.
She was stabilized and routine investigation done. Hemoglobin-9.6mg/dl, TLC-14,450/cmm.
DC-N-68%, L-30%, E-2%, platelet count - 3.2lac/cmm, serum urea-102mg/dl, serum
creatinine-1.8,serum NA+-149meq / l,S. K+2.9meq/l,s. ca++8.9mg/dl,s.albumin-3.8mg/dl.
Urine sugar, ketone bodies and albumin was negative. Urine c/s-no growth and blood c/s-no
growth. Urinary CA++: Creatine-.28. Urinary Ph-7, not improved with ingestion of
frusemide.Urinary anion gap +30meq/l. Artery blood gas analysis showed Ph
7.080,bicarbonate-6.2mmol/l, base excess-22.5mmol/l. On USG ABDOMEN bilateral
medullary nephrocalcinosis found.serum PTH-46pg/l.chest x ray-bilateral patchy opacities
found. She was treated with intravenous antibiotic for bronchopneumonia . After stabilization
oral syrup potassium citrate ( SOHL SOLUTION),syp calcium given.After 14 days she had
significant general improvement with gain of wieght. ABG showed pH 7.249, bicarbonate18.9, base excess-8.7. Conclusion- Infants presenting with failure to thrive with clinical
picture of sepsis or bronchopneumonia renal causes must be kept on mind. Correct & early
diagnosis and long term treatment required to prevent complication and morbidity of
Dulari Gupta, Indira Agarwal, Swasti Chaturvedi, Sunil Chandy
Department of Pediatrics, Christian Medical College, Vellore
Introduction: Cardiovascular risks are a leading case of mortality and morbidity amongst
children with chronic kidney disease. They are responsible for 20-41% of death in children
with Chronic Kidney disease (CKD). These risks are often ignored during normal clinical
practice. Aims And Objectives: This is a cross-sectional study of the cardiovascular
consequences in children with CKD aged 1-18 years with GFR < 60 ml/min/1.73 m2. The
prevalence of Left Ventricular Dysfunction by ECHO and of hypertension- both manifest
(clinic BP) and latent hypertension (Ambulatory Blood Pressure Monitoring- ABPM) was
studied. Materials And Methods: 37 children with CKD, of which 9 were on dialysis had
ECHO, Clinic BP and ABPM monitoring. LVH was defined as lvmass > 95th centile for age
and sex. ABPM was correlated with clinic BP readings. Results: 8 children had clinic
hypertension (14.2% of CKD, 44.4% on dialysis). Nine more children were found to be
hypertensive using ABPM. The BP load (defined by BP > 25% of 95th centile) was increased
in 18 children (39.2% of CKD, 77.7% on dialysis), with loss of nocturnal BP dipping in 17
children (33.3% of CKD, 88.8% on dialysis). Fourteen children were found to have LVH
(77.7 % of children on dialysis and 25% of children with CKD). Conclusions: LV
Hypertrophy is common amongst children with CKD, especially those on dialysis. APBM
was able to identify more hypertension in children compared to single clinic BP readings
alone. It is important to look for and treat these cardiovascular risk factors to decrease
morbidity and mortality.