Glomerulonephritis

Glomerulonephritis

1. GLOMERULONEPHRITIS
MR.SACHIN GADADEMR.SACHIN GADADE
M.SC(N) PEDIATRICSM.SC(N) PEDIATRICS

5. Review of Anatomy & Physiology of Review of Anatomy & Physiology of
NephronNephron
The nephron is the anatomical and functional unit of
kidney. There are about 1 million nephron’s in each
kidney. The nephron consists of a tubule closed at one
end & other end opening into a connecting tubule. The
closed end indented to from a cup shaped glomerular
capsule (Bowman’s capsule

6. It is almost encloses a network of arterial
capillaries, the glomerulas continuing from
the glomerular capsule the remainder of
the nephron is about 3cm long. And it has
3 parts :
-Proximal convoluted tubule
-Loop of Henle’s
-Distal convoluted tubule

7. The glomerulas has 3 types of membrane :
1.The Endothelial.
2.Basement Membrane.
3.Epithelial Membrane.

8. These are the filtering membranes of the
glomerulas. The nerve supply of the
kidney consists of sympathetic &
parasympathetic nerves. The presence
of both autonomic nervous system
controls the renal blood flow pressure.

9. FILTRATION: Filtration takes place through the
membranes of the glomerulas. Water & other
large number of molecules passes through,
although some of reabsorbs later. Blood cells,
plasma proteins & other large molecules are
unable to filtrates through & remain in the
capillaries.

10.  The volume of filtrates formed by both
kidneys is called glomerular filtration rate.
The normal GFR is 125ml/min or
180lit/day. Most of the filtrate is
reabsorbed about 1-1.5ml of fluid is
excreted per minute as urine.

12. DEFINATION-Acute glomerular nephritis:
It is the inflammation of the
glomeruli of both kidneys caused by
antigen-antibody reaction with respect to
streptococci, which produces damage to
the glomeruli, the filtrating bed of the
kidney characterized by decrease in the
GFR rate accumulation of organic salts,
water & other nitrogenous wastes into the
body.

13. CAUSES:
There is initially URTI or skin infection,
usually 1-3 weeks before the onset of
symptoms. The most frequent &
commonest causative organism is Group
A beta hemolytic streptococci.

14. PATHOPHYSIOLOGY:
The streptococcal infection from throat or elsewhere
from body
Attacks the immune system, the immune system
produces antibodies against streptococcal antigen.
Antigen- Antibody reaction takes place, with complex
formation.

15.  It gets trapped in the basement membrane of
glomerulas
the complexes combines with complement.(leucosomal
enzyme)
 Destruction of cell occurs.

16. Inflammatory changes occurs in glomerulas.
Decreased in the GFR & increased permeability of
glomerular walls.
Edema, proteinuria & microscopic Hematuria

18. CLINICAL MANIFESTATION:
Fever & chills
Weakness
Generalized Edema
Weight gain.
headache

G.I. disturbances
-Nausea/ vomiting.
-Anorexia
-Ascites
-Abdominal pain

19. Cardiac disturbances:
-Pulmonary edema
-CCF
Ophthalmic disturbances:
-Visual acuity is reduced

20. Renal disturbances:
-Proteinuria
-Oliguria
-Hematuria
-HTN
-Decreased P
H
of urine

21. Diagnostic Evaluation:
-Physical Assessment:
1. Observation of the child.
2. Observation of edema over face,
periorbital area, over feet.
3. Observation for oliguria, anuria &
hematuria.

22. 4. Observation of any visual impairment due
to retinal edema.
5. Monitor B.P for evidence of HTN.
6. Observation of any respiratory infection.

23. Urine Analysis:
It shows 1+ to 2+ protein. There are RBC, WBC cast which
indicates inflammation of glomeruli.
Blood Analysis:
ESR is elevated. There is normocytic anemia due to
heamodilution.
The blood levels of urea creatinine is elevated.
Serum Potassium and sodium is elevated if oliguria
contenous.

24. X-ray shows prominent vascular markings
due to hypervolemia.
Throat swab culture which may show
hemolytic streptococci organism.
Increased antistreptolysin titre.
Biopsy:
Kidney biopsy.
Serum complement level is decreased

25. Differential DiagnosisDifferential Diagnosis
Hypersensitivity reaction.
Hemolytic uremic syndrome.
SLE.
Nephrotic syndrome.

26. Complications Complications
Chronic glomerular nephritis.
Left ventricular failure.
Pulmonary edema.
Renal failure.
Encephalopathy.

27. Medical managementMedical management
Bed rest.
Antibiotics.
Antihypertensive.
Diet.
Restriction of fluid.
Weight monitoring.
Diuretics.
Rx of prolonged oliguria.

28. Chronic glomerulonephritisChronic glomerulonephritis
It is an advanced irreversible
impartment of renal function with or
without symptoms.
It may develop as a primary
Glomerular disease or may occur
secondary in SLE,drug induce
nephropathy or polyarteritis.

30. Etiological factorsEtiological factors
Repeated attacks of streptococci.
SLE
Drugs induced Nephropathy.
Thickening of basement membrane.
Glomerulo-sclerosis.
Polyarteritis.

31. PATHOPHYSIOLOGYPATHOPHYSIOLOGY
Due to etiological factors
Diffuse thickening of glomerular basement
membrane
Glomerular sclerosis takes place

32. Deposition of immunoglobulin,
complement & fibrin
In late stage glomeruli become sclerosis
with tubular, interstitial& vascular changes.

34. Clinical manifestationClinical manifestation
The condition remains a symptomatic
and may be diagnosed during
accidental urine examination.
The presenting features includes edema
severe hypertension, hematuria,
anemia, nocturia, bone pain, bone
deformity, failure to thrive.

35. Diagnostic evaluation Diagnostic evaluation
Urine Analysis:
It shows 1+ to 2+ protein. There are RBC, WBC cast
which indicates inflammation of glomeruli.
Blood Analysis:
ESR is elevated. There is normocytic anemia due to
heamodilution.
The blood levels of urea creatinine is elevated.
Serum Potassium and sodium is elevated if oliguria
contenous..

36. X-ray shows prominent vascular
markings due to hypervolemia.
Throat swab culture which may show
hemolytic streptococci organism.
Increased antistrptolysin titre.
Biopsy:
Kidney biopsy.
Serum complement level is
decreased

37. Management Management
No specific treatment.
Steroid & other immunosuppessrasive
drugs are helpful.
Antibiotics.
Antihypertensive.
Symptomatic & supportive treatment.

38. Nursing management.Nursing management.
Providing care during hospitalization.
Administration of medicines.
Maintaining proper fluid balance & assessing
edema.

39. Providing nutritious diet.
Preventing infections.
Emotional & psychological
support.
Education to family.

40. NURSING DIAGNOSISNURSING DIAGNOSIS
Hematuria R/T dysfunction of glomeruli
due to infection.
Alteration in body temperature R/T
infection.
Activity intolerance R/T edema.

41. Fluid volume excess R/T glomerular
dysfunction.
Disturbed body image R/T physiological
changes secondary to edema.

42. Impaired nutritional status less than body
requirement.
Risk of impaired skin integrity R/T edema.

43. Thank youThank you