Glomerulonephritis is an inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste from the blood. There are two main types - acute glomerulonephritis, which has a sudden onset typically in children following a streptococcal infection, and chronic glomerulonephritis, which develops over time and can lead to long-term kidney damage. Acute glomerulonephritis causes kidney dysfunction seen as edema, high blood pressure, reduced urine output, and blood in the urine. Treatment focuses on rest, fluid management, antibiotics, and controlling blood pressure. Chronic glomerulonephritis can develop from acute or other causes and may cause few symptoms initially

1. GLOMERULONEPHRITIS
BY;
ANUSHRI SRIVASTAVA

2. Introduction
• The kidneys contain many coils of tiny blood vessels. Each of these is called a glomerulus. Glomeruli
filter substances from the blood into the urine. Glomerulonephritis is a type of kidney disease where
these coils become inflamed. This makes it hard for the kidneys to filter the blood.
• Glomerulonephritis is an inflammation of the glomeruli within the kidneys.
• It is of two type acute glomerulonephritis and chronic glomerulonephritis

3. Definition
• Glomerulonephritis is defined as an inflammation of the glomerulus of the nephron in the kidney
• Glomerulonephritis is defined as an inflammation or infection of the glomeruli

4. Types
Glomerulonephritis is divided into two types:-
• Acute glomerulonephritis
• Chronic glomerulonephritis

5. Acute glomerulonephritis
• Acute glomerulonephritis is an acute or sudden inflammation of the glomeruli within the kidneys
• It is an immune mediated inflammatory disease of the capillary loops in the renal glomeruli. the
antigen antibody complex deposition within the glomeruli results in glomerular injury which is
manifested as hematuria, oliguria, edema and hypertension
• abrupt onset
• commonly seen in preschool are in early school age group of male children
 Incidence
• twice more common in males
• mostly seen in children between five and eight years of age
• peak incidence is seen at seven years of age

6.  Etiology and risk factor
• Nephritogenic strains of Group A beta streptococcus hemolyticus (type 12)
• Initial infection of upper respiratory tract on a skin usually one to three weeks before the onset of symptoms
• Systemic autoimmune diseases. With these types of diseases, the body’s immune system attacks healthy cells by mistake.
Systemic means that many parts of the body are affected. An example of this is systemic lupus erythematosus (SLE or lupus).
• Polyarteritis nodosa. This is an inflammatory disease of the arteries.
• Granulomatosis with polyangiitis. This is a progressive disease that leads to widespread inflammation of all of the body's
organs.
• Henoch-Schönlein purpura. This disease causes small or large purple lesions (purpura) on the skin and internal organs. It
causes other symptoms in several organ systems.
• Alport syndrome. This is a form of inherited glomerulonephritis that affects both boys and girls. But boys are more likely to
have kidney problems. Treatment focuses on preventing and treating high blood pressure and preventing kidney damage.
• Hepatitis B. This infection can be passed from mother to baby or rarely contracted through a blood transfusion.
• Other infections like bacterial endocarditis , viruses , HIV ,etc.
• IgA nephropathy

7.  Pathogenesis
due to etiological factors like Group A beta streptococcus hemolyticus (type 12)
produces an antigen antibody complex
Antigen- antibody complex trapped in the glomerular loops
causes inflammatory reaction due to activation of complement
Proliferation, swelling and increase permeability of endothelial cells of glomeruli
diminish amount of glomerular filtrate and allow the passage of blood cells and protein into the filtrate
due to decreased glomerular filtration, sodium and
water are retained
Resulting edema and hypertension
damage of glomerular basement membrane
progressive renal failure

8. •Pathological Changes
• HISTOLOGICAL and PATHOLO CHANGES:
1. minimal change disease: fatty alteration in tubules. PCT exhibit lipid
vacules and hyaline droplets.
2. Focal segmental glomerulosclerosis : collagenous sclerosis in centre.
3. Membranous nephropathy: subepithelial Ig accumulates along the
Glomerular basement membrane (GBM). Diffuse thickening in basement
membrane.
4. Membranoproliferative glomerulonephritis or mesangiocapillary
glomerulonephritis (MCGN): Proliferation of cells and thickening of
glomerular basement membrane
5. Mesangial proliferative nephritis: IgA nephropathy

9.  Clinical features
• history of sore throat or pyoderma or scabies or impetigo ( present in most of the patients )
• decreased urine output/ oliguria
• presence of blood or brown color urine ( tea colored urine )
• Edema ( manifested as periorbital puffiness found in the morning )
• pedal edema and generalized edema (Anasarca )
• rapid weight gain ( due to presence of massive edema )
• Fever
• Headache
• nausea and vomiting
• anorexia
• abdominal pain
• Malaise
• Hypertension ( more than 50% cases with sudden onset and may appear during four to five days of illness )
• Diplopia oh

10.  Phases Of clinical features
• Phase I: child presents with edema and oliguria which persists for five to 10 days
• Phase II: edema reduces and urinary output increases

11.  Complications
congestive cardiac
failure
acute renal failure
hypertensive
encephalopathy
persistent
hypertension
Anemia growth failure
chronic
glomerulonephritis

12.  Diagnostic evaluation
• history collection
• physical examination
• urine examination – increased specific gravity, Smokey dirty brown color urine with decrease total amount
in 24 hours and mild-moderate or severe albuminuria
• Urine microscopic examination – presence of red cells, WBCs, pus cells, epithelial cells, and granular cast
• blood examination – increase urea, creatinine, ESR, ASO titer, and anti-DNAse ‘B’ ; Decrease hemoglobin
percent and albumin
• hypernatremia and hypokalemia may be occurred in persistent oliguria
• throat swab culture – presence of beta hemolyticus streptococcus in some children
• chest X-ray – pulmonary congestion
• renal biopsy

13.  Management
• severe oliguria and azotemia needs hospitalization
• bed rest till urine is free from RBC
• restrict protein, salt and fluid intake till oliguria and increased blood urea level persist
• fluid intake should be allowed in calculated amount ( that is total amount of previous day urine output in 24 hours + insensible
loss to be allowed to drink on that day )
• daily weight recording due to presence of edema
• pharmacological management –
• Antibiotic –penicillin for seven to 10 days
• antihypertensive drugs like nifedipine and atenolol
• sedative tranquilizers like diazepam (if hypertension conversion and encephalopathy)
• dialysis, if severe electrolyte imbalance and renal failure
• dopamine infusion , steroid therapy and respiratory support (may be required for some patients )
• Diuretic is not usually indicated except in association with pulmonary edema and left ventricular failure
• Frusemide (Lasix) is given as 1-3 mg/kg/dose oral (two to three times a day )and IV (every two to six hours )

14. Chronic glomerulonephritis
• Advanced ,irreversible impairment of renal function with or without symptoms
• it may develop as primary disease or may occur in SLE ,drug induced nephropathies ,and polyarteritis
nodosa
• pathological changes – diffuse thickening of glomerular basement membrane are focal segmental
glomerulosclerosis with variable deposition of immunoglobulin ,complement and fibrin.
• GFR is reduced
• mesangial cells proliferation may occur
• later stages ,most glomeruli become sclerosed with tubular ,interstitial and vascular changes

15.  Clinical features
may remain
asymptomatic and
diagnosed during
routine urinary
examination
Edema severe hypertension Hematuria
Nocturia persistent anemia bone pain Bony deformities
failure to thrive

16.  Diagnosis
Urine examination
Blood examination
Ultrasonography

17.  Management
Corticosteroid
Anti-
hypertensive
drugs
Antiobiotics

18. Chronic renal failure
Complication

19. NURSING MANAGEMENT
Obtain
complete
history of
past illness
and
infections
01
Assess the
child’s weight
urine output
and look for
the presence of
manifestations
of
glomeruloneph
ritis
02
Monitor vital
signs, intake
and output
chart
03
Administer
medication as
prescribed by
physician
educate the
parent and
child about
hygienic
practices
04
prevent skin
breakdown by
frequent
changing
child's position
and provide
back and skin
care
05
meet the
nutritional
needs of
the child
06
provide
emotional
support to
the child
07

20. Bibliography
Datta Parul, Textbook of Pediatric Nursing, edition 4, The medical sciences
publishers, 4838/24 Ansari road, Daryaganj, New Delhi, 110002, India
https://www.stanfordchildrens.org/en/topic/default?id=glomerulonephritis-in-
children-90-P03085