Renal disease, Glomerulonephritis

1. GLOMERULAR DISEASES
Yjnah D. Lim BMLS III-A
Riverside College Inc.

2. GLOMERULAR DISEASES
➤ Membranous Glomerulonephritis (MGN)
➤ Membranoproliferative Glomerulonephritis (MPGN)
➤ Chronic Glomerulonephritis
➤ Berger Disease

3. GLOMERULUS

4. GLOMERULUS

5. FILTRATION MEMBRANE

6. MEMBRANOUS
GLOMERULONEPHRITIS
(MGN)

7. MEMBRANOUS GLOMERULONEPHRITIS
➤ Pronounced thickening of the glomerular basement
membrane resulting from the deposition of
immunoglobulin G immune complexes in the sub-epithelial
space.

8. MEMBRANOUS GLOMERULUNEPHRITIS

9. MEMBRANOUS GLOMERULUNEPHRITIS
➤ The immune complex serves as an activator that triggers a
response from the C5b - C9 complements, which form a
membrane attack complex (MAC) on the glomerular
epithelial cells.

10. MEMBRANOUS GLOMERULUNEPHRITIS

11. MEMBRANOUS GLOMERULUNEPHRITIS

12. LABORATORY FINDINGS
➤ Proteinuria and microscopic hematuria.
➤ In some cases the protein loss can be large
enough to be associated with water
retention, and swelling of the face, hands or
feet.

13. COMPLICATIONS
➤ High blood pressure may develop. This damages
the kidneys and puts a strain on the heart and the
rest of the circulation.
➤ Kidney failure may sometimes occur.

14. DISEASES ASSOCIATED
WITH MGN DEVELOPMENT

15. SYSTEMIC LUPUS ERYTHEMATOSUS

16. SYSTEMIC LUPUS ERYTHEMATOSUS
➤ Usually arises within 5 years of diagnosis.
➤ Production of autoantibodies directed against nuclear
elements.
➤ These autoantibodies form pathogenic immune complexes
intravascularly, which are deposited in glomeruli.
➤ Alternatively, autoantibodies may bind to antigens already
located in the glomerular basement membrane, forming
immune complexes in situ.
➤ Immune complexes promote an inflammatory response by
activating complement and attracting inflammatory cells,
including lymphocytes, macrophages, and neutrophils.

17. SYSTEMIC LUPUS ERYTHEMATOSUS

18. SJÖGREN'S SYNDROME
➤ Autoimmune disease of salivary and tear glands.
➤ Most patients with Sjögren's syndrome are female.
➤ Primary: Inflammation of the lacrimal glands and parotid
glands leading to dry eyes, dry mouth and lips.
➤ Secondary: Associated with a connective tissue disease, such
as rheumatoid arthritis, systemic lupus erythematosus, or
scleroderma.

19. SJÖGREN'S SYNDROME

20. SECONDARY SYPHILIS
➤ Systemic invasion of Treponama pallidum
➤ Usually marked by a non-itchy rash. The rash might be
confined to one part of your body, or it could spread over
several parts.

21. OTHERS
➤ Hepatitis B: Hepadnaviridae. Liver disease.
Immune complexes on glomerular membrane.
➤ Gold and mercury treatments: Kidney is the
main mercury accumulation and excretion
organ.
➤ Malignancy: Cancerous cells that have the
ability to metastasize or to invade and destroy
locla tissues.
➤ Thrombosis: Decreased antithrombin III.

22. MEMBRANOPROLIFERATIVE
GLOMERULONEPHRITIS

23. MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
➤ Marked by two different alterations in the cellularity of the
glomerulus and peripheral capillaries.
➤ Histopathologic findings:
➤ Proliferation of mesangial and endothelial cells and
expansion of the mesangial matrix.
➤ Thickening of the peripheral capillary walls by
subendothelial immune deposits and/or
intramembranous dense deposits.

24. MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
➤ Type 1 – Increased cellularity in the subendothelial
cells of the mesangium causing thickening of the
capillary walls.
➤ Type 2 – Dense deposits in the glomerular basement
membrane
➤ Type 3 – Subepithelial and subendothelial deposits

25. MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

26. MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

27. MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

28. LABORATORY FINDINGS
➤ Hematuria
➤ Proteinuria
➤ Decreased serum complement levels

29. CHRONIC
GLOMERULONEPHRITIS

30. CHRONIC GLOMERULONEPHRITIS
➤ Caused by slow, cumulative damage and scarring
of the glomeruli.
➤ Scarring of the glomeruli impedes the filtering
process, trapping waste products in the blood while
allowing red blood cells or proteins to escape into
the urine.

31. CHRONIC GLOMERULONEPHRITIS

32. MANIFESTATIONS
➤ Hematuria, proteinuria, glucosuria as a result of tubular
dysfunction, and many varieties of casts, including broad
casts.
➤ A markedly decreased glomerular filtration rate is present in
conjunction with increased BUN and creatinine levels and
electrolyte imbalance.

33. MANIFESTATIONS

34. BERGER DISEASE
Immunoglobulin A Nephropathy

35. BERGER DISEASE
➤ IgA immune complexes are deposited on mesangial region
causing glomerulonephritis and gradually affecting its filtering
ability.
➤ Immunoglobulin A (IgA) is an antibody synthesized in plasma
cells found in mucosal-associated lymphoid tissue.
➤ Most common form of primary glomerulonephritis
worldwide.

36. BERGER DISEASE

37. BERGER DISEASE

38. LABORATORY FINDINGS
➤ A patient with the disorder may remain essentially
asymptomatic for 20 years or more.
➤ Cola- or tea-colored urine following an infection or strenuous
exercise.
➤ Asymptomatic microhematuria and elevated serum levels of
IgA remain.

39. BERGER DISEASE

40. MANIFESTATIONS
➤ High blood pressure. Damage to kidneys from IgA deposits can raise blood
pressure, and high blood pressure can cause further damage to kidneys.
➤ High cholesterol. High levels of cholesterol may increase risk of a heart
attack.
➤ Acute kidney failure. If kidneys lose their filtering ability due to IgA
deposits, waste products build up quickly in the blood.
➤ Chronic kidney disease. IgA nephropathy can cause kidneys to gradually
stop functioning. In such cases, permanent dialysis or a kidney transplant is
needed to sustain life.
➤ Nephrotic syndrome. This is a group of problems that can be caused by
damage to the glomeruli, including high urine protein levels, low blood
protein levels, high cholesterol and lipids, and swelling of your eyelids, feet
and abdomen.