Nigerian Journal of Paediatrics

6Acute glomerulonephritis mimicking nephrotic syndrome

Niger J Paediatr 2016; 43 (2):95 – 98

CASE REPORT

Adedoyin OT

Acute glomerulonephritis

Afolayan FM

mimicking nephrotic syndrome

Buhari MO

Abdulkadir MB

Ibrahim OR

Akintade OO

Abdualzeez TA

DOI:http://dx.doi.org/10.4314/njp.v43i2.6

Accepted: 4th January 2016

Abstract :

Background:

Acute

(130/80mmHg and 150/100mmHg

post infectious glomerulonephritis

respectively) both systolic and

Adedoyin OT (

)

(APIGN) describes a wide range

diastolic blood pressure were

Afolayan FM, Abdulkadir MB

of glomerulonephritis character-

greater than 99 percentile. Labora-

Ibrahim OR, Akintade OO

Abdualzeez TA

ized by an immunologic response

tory investigations revealed mas-

Department of Paediatrics and

of the kidney to varieties of infec-

sive proteinuria of 4+ and 3+ re-

Child Health

tious agent commonly bacteria. It

spectively, haematuria, hypoalbu-

University of Ilorin Teaching Hospital,

is characterized by an abrupt on-

minemia, and hyperlipidemia. The

Ilorin, Kwara State, Nigeria

set of haematuria, moderate

histology of

their renal tissues

Email: ooadedoyin@yahoo.com

oedema, hypertension and pro-

revealed features in keeping with

teinuria usually < 2g/dl.

How-

acute glomerulonephritis.

Buhari MO

ever, between 2013 and 2015, we

Conclusion:

Acute

glomeru-

Department of Pathology,

managed two children who had

lonephritis may present with fea-

University of Ilorin Teaching Hospital,

Ilorin, Kwara State, Nigeria.

histological diagnosis of post in-

tures of nephrotic syndrome in-

fectious glomerulonephritis but

cluding nephrotic range proteinu-

presented with full complement

ria. Hence in the event of the pres-

of features of nephrotic syndrome

entation of a mixed feature of

including nephrotic range protein-

nephrotic-nephritis as obtained in

uria in addition to the features of

the case of these two children,

nephritis.

management should first be in the

Case reports: A 5year old boy

line of AGN while awaiting the

and an 8 year old girl were admit-

renal hisotology outcome before

ted to our Paediatric Unit with

considering the commencement of

history of generalized body swell-

steroid.

ing, reduction in the volume of

urine and cough. There was no

Keywords: Acute post infectious

antecedent sorethroat or skin rash.

glomerulonephritis, post strepto-

At presentation, both patients had

coccal glomerulonephritis, massive

mild dyspnea, anasarca, massive

proteinuria.

ascitis, and hypertension

Introduction

remained an important public health problem.³

The incidence of APIGN in the developing countries is

Acute post infectious glomerulonephritis (APIGN)

on the increase but has however declined in the industri-

describes a wide range of glomerulonephritis character-

alized world. Globally, the incidence of acute PSGN

ized by an immunologic response of the kidney to varie-

was estimated at 472,000 cases per year, out of which

456,000 occurred in developing countries . The inci-

ties of infectious agent commonly bacteria

1,2,3

.It is char-

acterized by intra glomerular inflammation with cellular

dence of PSGN in the less developed world was re-

proliferation from an immunologic response to bacteria,

ported at 24.3 cases per 100,000 person/ year whereas in

viruses and protozoa. The most common form of

the industrialized countries, its estimated prevalence was

0.3 cases per 100,000 person/ year. Thus, it is a disease

APIGN is the post streptococcal glomerulonephritis

(PSGN) caused by nephritogenic strains of group A

of underdeveloped and developing countries commonly

beta hemolytic streptococcus infection of the throat and

seen in children under the age of 15.

skin.

3,4

It is an important cause of acute kidney injury in

children. Though, the true incidence of APIGN is not

The typical clinical presentation of PSGN which is a

known due to the frequency of subclinical form, it has

representative of a larger group of APIGN is an abrupt

onset of microscopic haematuria, oedema, hypertension,

showed massive proteinuria(4+), haematuria(3+). Serum

oliguria, azotemia, and proteinuria. The urinary excre-

creatinine was 57µmol/l. Lipid profile revealed hyper-

tion of protein varies widely in PSGN but the rate is

cholesterolemia (7.1mmol/l) and hypertriglyceridaemia

generally less than 3g/ days which is what is found in

(2.2mmol/l). Serum albumin(18g/l) and protein (20g/l)

nephrotic syndrome. The oedema in PSGN is due to

were markedly reduced.

retention of fluid and electrolyte (sodium). Unlike

There was no bacteria growth in both throat and urine

nephritic syndrome, nephrotic syndrome is characterized

culture. He was managed as a case of nephrotic-

by massive proteinuria, hypoalbuminemia, hyperlipide-

nephritic syndrome and commenced on intravenous

mia and anasarca (generalized oedema).

frusemide, ceftriaxone, nifedipine. Blood pressure had

However, there can be an atypical presentation of

normalized by the fourth day on admission. There was

resolution of the edema by the 8 day on admission and

nephritic syndrome characterized by symptoms of both

nephritic and nephrotic syndrome. When this occurs,

by day 12, proteinuria and haematuria were 1+ respec-

the glomerular lesion is at the mesangium and the mem-

tively. Renal biopsy revealedendocapillary proliferation

brane. Patients with nephrotic range proteinuria in post

with infiltration of neutrophils and mesangial cellular

streptococcal glomerulonephritis has poor prognosis and

proliferation consistent with diffuse proliferative lesions

tend to develop hypertension and can also progress to

highly suggestive of post-infectious glomerulonephritis

chronic glomerulonephritis. We describe two children

(Figure 1).

who had histological diagnosis of post infectious glome-

rulonephritis but with full complement of features of

Fig 1: Endocapillary prolif-

nephrotic syndrome including nephrotic range proteinu-

eration with infiltration of

ria in addition to features of nephritis.

neutrophils and mesangial

cellular proliferation consis-

tent with diffuse prolifera-

Case report

tive lesions highly sugges-

Case 1

tive of post-infectious

glomerulonephritis (×400).

A 5year old boy presented at the Emergency Paediatric

Unit with a six day history of generalized oedema and a

four day history of reduction in urinary output. There

Case 2

was progressive body swelling which initially started

from the face and was described as being worse in the

An 8year old girl presented with a seven day history of

morning but disappears as the day goes by which later

generalized body swelling, five day history of cough and

progressed to involve both legs and the abdomen and

a three day history of difficulty with breathing. The

then became generalized. Four days after onset of body

swelling started from the face and progressed to involve

swelling, his parents noticed a reduction in urine pro-

the lower limb and abdomen. Swelling was worse early

duction in both volume and frequency. There was no

in the morning and progressively resolved as the day

passage of coke colored or frothy urine and no prior

went by. There was no antecedent history of sore throat

history of a preceding sore throat or skin rash before

or rash, though urine volume and frequency were re-

onset of symptoms. There was history of occasional

duced. There was no pain on micturition or passage of

cough but no difficulty in breathing or orthopnea. No

coke colored urine. No history of use of mercury con-

history of use of mercury containing soap, waddling in

taining soap, insect bite or ingestion of herbal remedies.

streams or recent blood transfusion. No family history of

Cough started two days after the onset of body swelling,

renal disease. Parents also attested to the use of herbal

was insidious in onset andnon paroxysmal. It was pro-

remedies. He was treated for malaria a month before

ductive of whitish sputum and not blood stained. Asso-

symptoms. There was no history of headache, convul-

ciated difficulty in breathing started a day after the onset

sion or loss of consciousness.

of cough with worsening on lying supine. There was no

cyanosis

Physical examination revealed anasarca with platysma

lock and mild respiratory distress evidenced by flaring

Physical examination revealed anasarca and mild pallor

of the alar nasi. He Weighed 21kg (expected 18kg),

(26%). She was in respiratory distress, respiratory rate;

height: 104cm, heart rate 84/min, respiratory rate:

42cpm with intercostal and subcostal recession. There

24cpm, blood pressure was 130/80 mmHg. There were

was a reduced breath sound with bilateral coarse basal

wide spread basal crepitations bilaterally, breath sounds

crepitations. Pulse rate; 122bpm, blood pressure was

were normal. There was no added heart sound. The ab-

150/100 mmHg. Abdomen was uniformly distended

domen was uniformly distended with flank fullness with

(girth-71 cm measured 15cm from the xiphisternum),

no organ enlargement. Moderate ascitis was demonstra-

The liver was enlarged measuring 8cm below right cos-

ble by shifting dullness and the abdominal girth was

tal margin with a span of 16cm. There was massive as-

63.8cm measured 14cm from xiphisternal junction.

citis demonstrable by fluid thrill. There was no neuro-

There was also scrotal edema. There was no neurologi-

logical deficit.

cal deficit.

Initial laboratory test included complete blood counts

The complete blood counts revealed moderate anaemia

which reveal moderate anaemia(26%). Urinalysis

(PCV-33%)

with reversal of differential. Urinalysis

showed massive proteinuria (3+), haematuria (1+).

Serum creatinine was 392 µmol/l, urea was 19.1 mmol/l,

ria, hypercholesterolemia and hypoalbuminemia . How-

hypoalbuminemia (18g/l) , serum cholesterol was

ever, the presence of hypertension, haematuria and oe-

5.7mmol/l, serum triglyceride was 2.1 mmol/l. A diag-

dema which are the three most important triad of PSGN

nosis of nephrotic syndrome complicated by acute renal

makes it a mixed nephritic. The proteinuria and hema-

failure with pulmonary oedema was made.

turia of nephrotic syndrome is due to break in the

glomerular basement membranes, resulting from an in-

She was commenced on oxygen at 3Litre/ min, intrave-

flammatory response due to an immunologic mecha-

nous frusemide at 2mg/kg, then 1mg 8hrly. Intravenous

nism. Unlike nephritic syndrome, massive proteinuria

ceftriaxone was administered. She was given a bolus of

is one of the most important findings in nephrotic

intravenous hydralazin followed by oral hydrochlorothi-

syndrome and it is due to damage to the podocyte within

azide, methyl dopa and captopril. By second day on

the glomerular membrane, leading to loss of negative

admission, respiratory distress had resolved, blood pres-

charge and thus increased permeability of the glomeruli.

sure was still elevated warranting another bolus of intra-

This leads to loss of albumin in urine, resulting in hypo-

venous hydralazin.

albuminemia cumulating into reduction in oncotic pres-

sure and finally oedema. Massive proteinuria is a rare

Blood

pressure

remained

between

140/110-

and atypical presentation in PSGN and when it occurs,

120/90mmHg in the first week on admission before a

it is associated with severe disease and poor prognosis

significant improvement was made. She was maintained

In PSGN, clinical recovery is the rule in 90% of cases.

on the prescribed medication. She had progressive reso-

However with a finding of massive proteinuria, the

lution over the following 14 days into admission;

course of the microscopic proteinuria is likely to be pro-

oedema and ascitis resolved, weight declined, urinary

longed in atypical PSGN leading to chronic renal insuf-

output was within 1.1- 2.5ml/kg/hr and proteinuria and

ficiency. Thus early differentiation between a nephrotic

haematuria were 1+ and 2+ respectively by the 12 day.

-nephritic overlap and a typical nephritic syndrome us-

Renal biopsy done 10 days into admission revealed

ing a renal biopsy as a tiebreaker is important because

features in keeping with diffuse proliferative lesions

their management and prognosis are quite different.

highly suggestive of post-infectious glomerulonephritis

Though, renal biopsy is not often needed in PSGN,

(Figure 1). Child recovered and was discharged for fol-

except in atypical presentation.

low up in the clinic.

Most studies that described an overlap of nephrotic and

nephritic syndrome were in adult population with a dif-

ferent etiology other than group A beta hemolytic strep-

tococcus. Most importantly in resource poor countries

Discussion

where there are few facilities for renal biopsy, most pa-

The

presence of the combination of features of

tient with true PSGN who had atypical presentation

nephrotic and nephritic syndrome results in a clinical

tending towards a nephrotic syndrome might be treated

impression of nephrotic-nephritic syndrome. However,

as nephrotic using steroid which is clearly contraindi-

in view of the presence of nephrotic syndrome, it was

cated in PSGN.

instructive to carry out a renal biopsy to delineate the

histological type. Furthermore renal biopsy was necessi-

tated to differentiate between AGN which would not

require steroid and NS which requires the commence-

Conclusion

ment of steroid to classify whether it was steroid

responsive or resistant. In the two patients , while we

While the presence of a nephrotic picture in a PSGN is

were expecting a non- Minimal change NS such as focal

atypical,

clinicians should not commence steroid in

segmental glomerular sclerosis (FSGS),

meme-

such mixed state until a renal biopsy has been carried

branoproliferative glomerulonephritis (MPGN) e.t.c we

out, hence a nephrotic -nephritic picture makes renal

obtained a diffuse proliferative acute glomerulonephritis

biopsy mandatory. On the other hand in resource poor

most probably post infectious.

setting where renal biopsy may be difficult to procure,

such patients should be managed first as PSGN while

The presence of features of haematuria, hypertension

watching the trend and progress for relapse which would

and indeed azotaemia in children with NS portends a

further confirm nephrotic syndrome as recurrence is rare

poor prognosis as they will likely be non-MCNS. Hence

in PSGN or complete recovery if it is PSGN. In addi-

extra care is deployed once nephrotic syndrome is

tion , follow up for the occurrence of persistent protein-

accompanied by features of nephritic syndrome.

uria, haematuria and hypertension will help prevent long

The concomitant clinical presentation of these two cases

term morbidity and mortality.

was that of nephrotic syndrome with massive proteinu-

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