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PRESENTED BY
DR SHASHANK AGRAWAL
(MEDICINE)
 Glomerular disease includes
glomerulonephritis, i.e. inflammation of the
glomeruli and glomerulopathies when there
is no...
 Nephrotic syndrome.
 Acute glomerulonephritis (acute nephritic
syndrome).
 Rapidly progressive glomerulonephritis.
 A...
Primary – confined to the kidney
Secondary – due to a systemic
disease
5
 Proteinuria – asymptomatic
 Haematuria – asymptomatic
 Hypertension
 Nephrotic syndrome
 Nephritic syndrome
 Acut...
6
 Presence of glomerular disease as opposed to
tubulointersititial or vascular disease is suspected from
history
 Haema...
Immune complex disease
 Neutrophils:
Protease GBM degradation
O₂ free readicals cell damage
AA metabolites ↓ GFR
Compleme...
 Named according to
 etiology
 microscopic findings
 clinical syndrome
 Most common clinical presentations
 acute ne...
 Autoimmune injury initiated by beta-hemolytic
streptococcus
 aka acute proliferative glomerulonephritis
 Presents as a...
 Unknown causes or secondary to
poststreptococcal
glomerulonephritis
 Autoimmune
 aka crescentric
glomerulonephritis
 ...
 Autoimmune
 Most common cause of
nephrotic syndrome in
adults
 About 10% proceed to
renal failure within 10
yrs, 25% r...
 Incidental discovery of occult proteinuria or
HTN
 Usually presents as chronic renal failure or
occult proteinuria
 Gl...
 Diabetes most common cause
 most common cause of renal failure
 glycoproteins deposit in basement membrane
 Vascular ...
Heavy
proteinuria
Proteinuria &
haematuria
Predominant
haematuria
Minimal Change Lupus nephritis Acute post strep
Focal sc...
 Acute glomerulonephritis is the
inflammation of the glomeruli which causes
the kidneys to malfunction
 It is also calle...
 Infectious
 Streptococcal
 Nonstreptococcal postinfectious
glomerulonephritis
▪ Bacterial
▪ Viral
▪ Parasitic
 Noninf...
Previously M-protein of the organism was
felt to be responsible for PSGN.
Recently, nephritis-associated
streptococcal cat...
Diffuse proliferative GN (PGN)
 proliferation of cells within the glomeruli, accompanied
by leukocyte filtrate
 typical ...
 Fever
 Headache
 Malaise
 Anorexia
 Nausea and vomiting
 High blood pressure
 Pallor due to edema and/or anemia
 ...
 Hematuria: dark brown or smoky urine
 Oliguria: urine output is < 400 ml/day
 Edema: starts in the eye lids and face t...
 urinary (haematuria, proteinuria),
 nephritic (edemas, hypertension, gross
haematuria, proteinuria),
 nephrotic (edema...
 Abrupt onset of:
glomerular haematuria (RBC
casts or dysmorphic RBC).
non-nephrotic range
proteinuria (<2 g in 24 hrs)...
Base line measurements:
- ↑ Urea
- ↑ Creatinine
Urinalysis (MSU):
a) Urine microscopy (red cell cast)
b) proteinuria
COMPL...
Treat the underlying infections when acute GN is associated with chronic infections.
 Antimicrobial therapy
 Antibiotics...
Post streptococcal GN
- Has a GOOD prognosis.
- Supportive measures until spontaneous recovery.
- Control HT.
- Fluid bala...
The condition is characterized by
irreversible and progressive glomerular and
tubulointerstitial fibrosis.
-> ultimately l...
Nearly all forms of acute glomerulonephritis have a
tendency to progress to chronic glomerulonephritis.
The progression fr...
Reduction in nephron mass from the initial injury
reduces the GFR.
This reduction leads to hypertrophy and
hyperfiltration...
fusion of podocytes
on electron microscopy
Segmental areas of
glomerular sclerosis,
hyalinization of
glomerular capillaries
large glomeruli with mesangial
proliferation and ‘double’ BM. 2 histological
types: type I (subendothelial deposits) type ...
thickened BM, IF +ve
for IgG & C3 and
subepithelial deposits
on EM
Hypercellularity, mesangial proliferation,
inflammatory cell infiltrate, positive IF for IgG
and C3 and subepithelial depo...
 Most common cause of GN in Asia but uncommon in Sth
America or Africa
 15-40% of all biopsy proven GN
 Male > Females
...
 Slowly progressive
 By 20 years, 50% have end stage kidney
disease
 Worse prognosis if >1g/day proteinuria,
hypertensi...
 Uremia-specific findings
 Edemas
 Hypertension
 Jugular venous distension (if severe volume overload is
present)
 Pu...
 Latent (changes in urine)
 Hypertensive (increased blood pressure)
 Hematuric
 Nephrotic (edemas, proteinuria,
hypopr...
 Urinalysis
 Urinary protein excretion
 Serum chemistry
 Serum creatinine and urea nitrogen levels are elevated.
 Imp...
 Renal ultrasonogram
 Obtain a renal ultrasonogram to determine renal
size, to assess for the presence of both kidneys,
...
 The target pressure for patients with proteinuria greater
than 1 g/d is less than 125/75 mm Hg; for patients with
protei...
 Renal osteodystrophy can be managed early by
replacing vitamin D and by administering phosphate
binders.
 Seek and trea...
Minimal change glomerulonephritis (MCGN)
Corticosteroids induce remission in >90% of
children and 80% of adults (slower re...
Focal segmental glomerulosclerosis
Poor response to corticosteroids (10–30%).
Cyclophosphamide or ciclosporin
(=cylosporin...
Mesangiocapillary GN
Treatment: None is of proven benefit.
Prognosis: 50% develop ESRF.
Membranous nephropathy
If renal function deteriorates, consider
corticosteroids and chlorambucil.
Prognosis: Untreated, 15...
Mesangial proliferative GN
Antibiotics, diuretics, and
antihypertensives as necessary. Dialysis is
rarely required.
Progno...
 Management
 Aggressive control of blood pressure and
proteinuria with ACEI’s or AR2B’s
 Corticosteroids +/- azathiprin...
Rapidly progressive glomerulonephritis
(RPGN) is a disease of the kidney that results
in a rapid decrease in the glomerula...
50
 Classic – haemoptysis after upper respiratory infection and
have nephritic urinary sediment
 History of smoking or h...
More than 80% of patients with
pauci-immune RPGN were
subsequently found to have
circulating antineutrophil
cytoplasmic an...
RPGN is classified pathologically into 3
categories:
 (1) anti-GBM antibody disease
(approximately 3% of cases),
 (2) im...
 Symptoms and signs of renal failure,
 pain,
 haematuria,
 systemic symptoms (fever, malaise, myalgia,
weight loss).
 The most important requirement in the diagnosis of antineutrophil
cytoplasmic antibodies (ANCA) ANCA-associated disease ...
High-dose corticosteroids;
cyclophosphamide ± plasma exchange/ renal
transplantation. Prognosis: Poor if initial
serum cre...
THANK YOU
Glomerulonephritis (1)
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Glomerulonephritis (1)

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about types of glomerular disease

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Glomerulonephritis (1)

  1. 1. PRESENTED BY DR SHASHANK AGRAWAL (MEDICINE)
  2. 2.  Glomerular disease includes glomerulonephritis, i.e. inflammation of the glomeruli and glomerulopathies when there is no evidence of inflammation.  Glomerulonephritis is a subset of glomerulopathies
  3. 3.  Nephrotic syndrome.  Acute glomerulonephritis (acute nephritic syndrome).  Rapidly progressive glomerulonephritis.  Asymptomatic urinary abnormality (haematuria, proteinuria or both).
  4. 4. Primary – confined to the kidney Secondary – due to a systemic disease
  5. 5. 5  Proteinuria – asymptomatic  Haematuria – asymptomatic  Hypertension  Nephrotic syndrome  Nephritic syndrome  Acute renal failure  Rapidly progressive renal failure  End stage renal failure
  6. 6. 6  Presence of glomerular disease as opposed to tubulointersititial or vascular disease is suspected from history  Haematuria (especially dysmorphic red cells)  Red cell casts  Lipiduria (glomerular permeability must be increased to allow the filtration of large lipoproteins)  Proteinuria (may be in nephrotic range of >3.5 g/24hours)
  7. 7. Immune complex disease  Neutrophils: Protease GBM degradation O₂ free readicals cell damage AA metabolites ↓ GFR Complement- dependentComplement-leukocyte- mediated mechanism  Activation of the complement pathway Recruitment of neutrophils and monocytes C₅- C₉ (MAC) Epithelial cell detachment.  (+) epithelial & mesangial cells to secrete damaging chemical mediators. Upregulates TGF receptors on epithelial cells, excessive synthesis of extracellular matrix which leads to GBM thickening
  8. 8.  Named according to  etiology  microscopic findings  clinical syndrome  Most common clinical presentations  acute nephritic syndrome  nephrotic syndrome  Most common cause is autoimmune
  9. 9.  Autoimmune injury initiated by beta-hemolytic streptococcus  aka acute proliferative glomerulonephritis  Presents as acute nephritic syndrome  hematuria  HT  increased urea & creatinine  low urine output  edema  Antibodies produced by strep throat deposit in glomerulus  Most fully recover but about 10% evolve into rapidly progressive glomerulonephritis
  10. 10.  Unknown causes or secondary to poststreptococcal glomerulonephritis  Autoimmune  aka crescentric glomerulonephritis  Some present as acute nephritic syndrome & others as renal failure  Caused by deposition of An-Ab complexes  All but a few progress to renal failure
  11. 11.  Autoimmune  Most common cause of nephrotic syndrome in adults  About 10% proceed to renal failure within 10 yrs, 25% recover completely, most progress slowly with proteinuria, HTN, loss of renal function
  12. 12.  Incidental discovery of occult proteinuria or HTN  Usually presents as chronic renal failure or occult proteinuria  Glomerulus has scar tissue  Dialysis & transplant
  13. 13.  Diabetes most common cause  most common cause of renal failure  glycoproteins deposit in basement membrane  Vascular disease  atherosclerosis  HTN  vascultitis
  14. 14. Heavy proteinuria Proteinuria & haematuria Predominant haematuria Minimal Change Lupus nephritis Acute post strep Focal sclerosis Membranous Diabetes Mellitus Amyloidosis Membrano- proliferative Endocarditis Henoch-Schonlein purpura Crescentic (RPGN) Haemolytic uraemic syndrome
  15. 15.  Acute glomerulonephritis is the inflammation of the glomeruli which causes the kidneys to malfunction  It is also called Acute Nephritis, Glomerulonephritis and Post-Streptococcal Glomerulonephritis  Predominantly affects children from ages 2 to 12  Incubation period is 2 to 3 weeks
  16. 16.  Infectious  Streptococcal  Nonstreptococcal postinfectious glomerulonephritis ▪ Bacterial ▪ Viral ▪ Parasitic  Noninfectious  Multisystem systemic diseases  Primary glomerular diseases
  17. 17. Previously M-protein of the organism was felt to be responsible for PSGN. Recently, nephritis-associated streptococcal cationic protease and its zymogen precursor (NAPR) has been identified as a glyceraldehyde-3-phosphate dehydrogenase that functions as a plasmin(ogen) receptor.
  18. 18. Diffuse proliferative GN (PGN)  proliferation of cells within the glomeruli, accompanied by leukocyte filtrate  typical features of immune complex disease : - hypocomplimentemia - granular deposits of IgG & complement on GBM  Implicated antigens seem to be endostreptosin and nephritis – plasmin- binding ptn
  19. 19.  Fever  Headache  Malaise  Anorexia  Nausea and vomiting  High blood pressure  Pallor due to edema and/or anemia  Confusion  Lethargy  Loss of muscle tissue  Enlargement of the liver
  20. 20.  Hematuria: dark brown or smoky urine  Oliguria: urine output is < 400 ml/day  Edema: starts in the eye lids and face then the lower and upper limbs then becomes generalized; may be migratory  Hypertension: usually mild to moderate
  21. 21.  urinary (haematuria, proteinuria),  nephritic (edemas, hypertension, gross haematuria, proteinuria),  nephrotic (edemas, proteinuria, hypoproteinemia, hypercholesterolemia),  mixed.
  22. 22.  Abrupt onset of: glomerular haematuria (RBC casts or dysmorphic RBC). non-nephrotic range proteinuria (<2 g in 24 hrs). oedema (periorbital, sacral). hypertension. transient renal impairment (oliguria, uraemia).
  23. 23. Base line measurements: - ↑ Urea - ↑ Creatinine Urinalysis (MSU): a) Urine microscopy (red cell cast) b) proteinuria COMPLICATION Hypertensive encephalopathy, heart failure and acute pulmonary edema may occur in severe cases Acute renal necrosis due to injury of capillary or capillary thrombosis
  24. 24. Treat the underlying infections when acute GN is associated with chronic infections.  Antimicrobial therapy  Antibiotics (eg, penicillin) are used to control local symptoms and to prevent spread of infection to close contacts.  Antimicrobial therapy does not appear to prevent the development of GN, except if given within the first 36 hours.  Loop diuretic therapy  Loop diuretics may be required in patients who are edematous and hypertensive in order to remove excess fluid and to correct hypertension.  Relieves edema and controls volume, thereby helping to control volume-related elevation in BP.  Vasodilator drugs (eg, nitroprusside, nifedipine, hydralazine, diazoxide) may be used if severe hypertension or encephalopathy is present  Diet:  Sodium and fluid restriction  Protein restriction for azotemic patients  Activity: Recommend bed rest until signs of glomerular inflammation and circulatory congestion subside.
  25. 25. Post streptococcal GN - Has a GOOD prognosis. - Supportive measures until spontaneous recovery. - Control HT. - Fluid balance. - Oliguric with fluid overload. - GN complicating SLE or systemic vasculitides: immunosuppression with prednisolone, cyclophosphamide or azathioprine/MMF.
  26. 26. The condition is characterized by irreversible and progressive glomerular and tubulointerstitial fibrosis. -> ultimately leading to a reduction in the glomerular filtration rate (GFR) and retention of uremic toxins. -> If disease progression is not halted with therapy, the net result is chronic kidney disease (CKD), end-stage renal disease (ESRD), and cardiovascular disease
  27. 27. Nearly all forms of acute glomerulonephritis have a tendency to progress to chronic glomerulonephritis. The progression from acute glomerulonephritis to chronic glomerulonephritis is variable. Whereas complete recovery of renal function is the rule for patients with poststreptococcal glomerulonephritis, several other glomerulonephritides, such as immunoglobulin A (IgA) nephropathy, often have a relatively benign course and many do not progress to ESRD.
  28. 28. Reduction in nephron mass from the initial injury reduces the GFR. This reduction leads to hypertrophy and hyperfiltration of the remaining nephrons and to the initiation of intraglomerular hypertension. These changes occur in order to increase the GFR of the remaining nephrons, thus minimizing the functional consequences of nephron loss. The changes, however, are ultimately detrimental because they lead to glomerulosclerosis and further nephron loss.
  29. 29. fusion of podocytes on electron microscopy
  30. 30. Segmental areas of glomerular sclerosis, hyalinization of glomerular capillaries
  31. 31. large glomeruli with mesangial proliferation and ‘double’ BM. 2 histological types: type I (subendothelial deposits) type II (intramembranous deposits)
  32. 32. thickened BM, IF +ve for IgG & C3 and subepithelial deposits on EM
  33. 33. Hypercellularity, mesangial proliferation, inflammatory cell infiltrate, positive IF for IgG and C3 and subepithelial deposits on EM.
  34. 34.  Most common cause of GN in Asia but uncommon in Sth America or Africa  15-40% of all biopsy proven GN  Male > Females  2nd -3rd decade  Most commonly asymptomatic with serendipitous finding of haematuria and mild proteinuria  Another classic presentation is macroscopic haematuria in conjunction with a viral infection  Renal function is usually normal but occasionally a patient will present with acute renal failure due to acute tubular necrosis secondary to the gross haematuria  Biopsy – mild to moderate mesangial cell proliferation, IgA deposits in the mesangium on immunofluorescence, often with C3 deposition also
  35. 35.  Slowly progressive  By 20 years, 50% have end stage kidney disease  Worse prognosis if >1g/day proteinuria, hypertension, increased creatinine of glomerular fibrosis at biopsy, on presentation
  36. 36.  Uremia-specific findings  Edemas  Hypertension  Jugular venous distension (if severe volume overload is present)  Pulmonary rales (if pulmonary edema is present)  Pericardial friction rub in pericarditis  Tenderness in the epigastric region or blood in the stool (possible indicators for uremic gastritis or enteropathy)  Decreased sensation and asterixis (indicators for advanced uremia)
  37. 37.  Latent (changes in urine)  Hypertensive (increased blood pressure)  Hematuric  Nephrotic (edemas, proteinuria, hypoproteinemia, hypercholesterolemia),  Mixed
  38. 38.  Urinalysis  Urinary protein excretion  Serum chemistry  Serum creatinine and urea nitrogen levels are elevated.  Impaired excretion of potassium, free water, and acid results in hyperkalemia, hyponatremia, and low serum bicarbonate levels, respectively.  Impaired vitamin D-3 production results in hypocalcemia, hyperphosphatemia, and high levels of parathyroid hormone.  Low serum albumin levels may be present if uremia interferes with nutrition or if the patient is nephrotic.
  39. 39.  Renal ultrasonogram  Obtain a renal ultrasonogram to determine renal size, to assess for the presence of both kidneys, and to exclude structural lesions that may be responsible for azotemia.  Small kidneys often indicate an irreversible process.  Kidney biopsy
  40. 40.  The target pressure for patients with proteinuria greater than 1 g/d is less than 125/75 mm Hg; for patients with proteinuria less than 1 g/d, the target pressure is less than 130/80 mm Hg.  Angiotensin-converting enzyme inhibitors (ACEIs)  angiotensin II receptor blockers (ARBs)  combination therapy with ACEIs and ARBs.  Diuretics  Beta-blockers,  calcium channel blockers,  central alpha-2 agonists (eg, clonidine),  alpha-1 antagonists  direct vasodilators (eg, minoxidil, nitrates) may be used to achieve the target pressure.
  41. 41.  Renal osteodystrophy can be managed early by replacing vitamin D and by administering phosphate binders.  Seek and treat nonuremic causes of anemia, such as iron deficiency, before instituting therapy with erythropoietin.  Discuss options for renal replacement therapy (eg, hemodialysis, peritoneal dialysis, renal transplantation).  Treat hyperlipidemia (if present)  Expose patients to educational programs for early rehabilitation from dialysis or transplantation.
  42. 42. Minimal change glomerulonephritis (MCGN) Corticosteroids induce remission in >90% of children and 80% of adults (slower response). Indications for immunosuppression: (cyclophosphamide, ciclosporin (=cylosporin)): early/ frequent relapses; steroid SEs/dependence. Prognosis: 1% progress to ESRF.
  43. 43. Focal segmental glomerulosclerosis Poor response to corticosteroids (10–30%). Cyclophosphamide or ciclosporin (=cylosporin) may be used in steroid-resistant cases. Prognosis: 30–50% progress to ESRF.
  44. 44. Mesangiocapillary GN Treatment: None is of proven benefit. Prognosis: 50% develop ESRF.
  45. 45. Membranous nephropathy If renal function deteriorates, consider corticosteroids and chlorambucil. Prognosis: Untreated, 15% complete remission, 9% ESRF at 2–5yrs and 41% at 15yrs.
  46. 46. Mesangial proliferative GN Antibiotics, diuretics, and antihypertensives as necessary. Dialysis is rarely required. Prognosis: Good.
  47. 47.  Management  Aggressive control of blood pressure and proteinuria with ACEI’s or AR2B’s  Corticosteroids +/- azathiprine – varied schools of thought  However if rapidly progressive GN with crescent deposition treatment should be aggressive with high dose steroids and cyclophosphamide  Consult the Nephrologist
  48. 48. Rapidly progressive glomerulonephritis (RPGN) is a disease of the kidney that results in a rapid decrease in the glomerular filtration rate of at least 50% over a short period, from a few days to 3 months.
  49. 49. 50  Classic – haemoptysis after upper respiratory infection and have nephritic urinary sediment  History of smoking or hydrocarbon exposure is common  CXR – pulmonary haemorrhage  Lab- iron deficiency anaemia and renal dysfunction, circulating anti-GBM antibodies  Kidney biopsy crescentic GN with linear staining IgG and C3 along the glomerular basement membrane
  50. 50. More than 80% of patients with pauci-immune RPGN were subsequently found to have circulating antineutrophil cytoplasmic antibodies (ANCA), and thus, this form of RPGN is now termed ANCA-associated vasculitis.
  51. 51. RPGN is classified pathologically into 3 categories:  (1) anti-GBM antibody disease (approximately 3% of cases),  (2) immune complex disease (45% of cases),  (3) pauci-immune disease (50% of cases).
  52. 52.  Symptoms and signs of renal failure,  pain,  haematuria,  systemic symptoms (fever, malaise, myalgia, weight loss).
  53. 53.  The most important requirement in the diagnosis of antineutrophil cytoplasmic antibodies (ANCA) ANCA-associated disease is a high index of suspicion. Rapid diagnosis is essential for organ preservation. Laboratory studies include the following:  Routine chemistry: The most common abnormality is an increased serum creatinine level.  Urinalysis with microscopy:  Antinuclear antibody (ANA) titer:  ANCA .
  54. 54. High-dose corticosteroids; cyclophosphamide ± plasma exchange/ renal transplantation. Prognosis: Poor if initial serum creatinine >600µmol/L.
  55. 55. THANK YOU

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