Acute Glomerulonephritis Flashcards

1
Q

What is Glomerulonephritis?

A

Glomerulonephritis means inflammation of the glomeruli
Glomerulonephritis (GN) is a spectrum of renal diseases of varied etiology and clinical presentations that are characterized by clinical and histological evidence of glomerular damage.
GN are mostly immunologically-mediated and also largely respond to immunosuppressive therapy.
GN is an important cause of both acute and chronic kidney diseases worldwide
GN is a leading cause of ESRD in Africa, while in developed countries, it ranked 3rd (after DM and HTN)

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2
Q

Basic anatomy of the kidney (location, weight, dimensions and structure)

A

A paired organ located retroperitoneally Weight = 120-200g
Dimensions –vertical – 10 to 14cm
transverse – 5 to 6cm
anteroposterior – 3 to 4cm
STRUCTURE OF THE KIDNEY:
Outer cortex
Inner medulla

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3
Q

What is a Nephron? How many nephron per kidney? What do they consist of?

A
  • functional unit of the kidney
  • each kidney has about a million nephrons
  • Each nephron consists of – renal corpuscles, proximal and distal convoluted tubules, loop of Henle, and terminally, the collecting ducts.
    The renal corpuscle is made up of:
    glomerulus
    bowman’s capsule
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4
Q

What is the Glomerulus?

A

a tuft of capillaries surrounded by bowman’s capsule, serves as the filtration barrier. It filters the blood based on particle size and charge.
The glomerular tuft is held together and regulated by mesangial cells. It allows filtrate from plasma to move into the urinary (Bowman’s) space

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5
Q

Discuss the The filtration barrier of the glomerulus
Filtration of molecules across the barrier depends on what?

A

The filtration barrier is composed of:
1. Fenestrated endothelium
2. Glomerular basement membrane
3. Podocytes and their foot processes
Filtration of molecules across the barrier depends on:
*Hydrostatic pressure difference
*Size of the molecule
*Charge on the molecule

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6
Q

Whar are the types of Glomerular diseases?

A
  • Focal: some, but not all, glomeruli show the lesion
  • Diffuse (global): most of the glomeruli (>75%) contain the lesion
  • Segmental: only a part of the glomerulus is affected (most focal lesions are also segmental, e.g. focal segmental glomerulosclerosis)
  • Global: all of the glomerulus is symmetrically involved
  • Proliferative: an increase in cell numbers due to hyperplasia of one or more of the
    resident glomerular cells with or without inflammation
  • Membrane alterations: capillary wall thickening due to deposition of immune deposits or alterations in basement membrane
  • Crescent formation: epithelial cell proliferation with mononuclear cell infiltration in Bowman’s space
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7
Q

How can Glomerular diseases be classified?

A

Aetiology: primary or secondary
According to period: acute or chronic
Histologic pattern: focal, diffuse, segmental or global
Number of cells: non-proliferative or proliferative
Immunofluorescence: Immune or pauci-immune

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8
Q

Primary cause of glomerular diseases?

A
  1. Minimal change disease (MCD)
  2. Membranous nephropathy
  3. Focal segmental glomerulosclerosis
  4. Mesangiocapillary GN now called Mesangioproliferative GN
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9
Q

What are some secondary causes of glomerular disease? Give examples under each

A
  1. Medications: NSAIDs, pamidronate, rifampicin, gold, lithium, interferon alpha.
  2. Allergens: Pollens, serum sickness, vaccines, bee sting
  3. Infections
    Bacterial: Endocarditis, syphilis, tuberculosis, mycoplasma infections
    Viral: HIV, HBV, HCV, EBV, CMV, VZV
    Protozoal: Toxoplasmosis, malaria
    Helminthic: Schisostomiasis, trypanosomiasis, filariasis
    Systemic illnesses: Systemic lupus erythematosus (SLE), Rheumatoid polyarthritis, amyloidosis, Henoch-Schonlein purpura, ANCA positive vasculitis.
  4. Neoplasia: Solid tumours, Haematological malignancies (lymphomas, leukaemias), Multiple myeloma
  5. Metabolic diseases and heredofamilial: Pregnancy-associated, Chronic allograft failure, Obesity
  6. Miscellaneous:Pregnancy-associated, Chronic allograft failure, Obesity
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10
Q

What is the Clinical presentation of GN?

A
  1. Asymptomatic urinary abnormalities (proteinuria / Or haematuria)
    Proteinuria, accompanied by variable degrees of hematuria, is the hallmark of glomerular disease.
  2. Nephrotic syndrome
  3. Nephritic syndrome (Acute glomerulonephritis)
  4. Nephritic-Nephrotic syndrome
  5. Systemic Hypertension
  6. Rapidly progressive GN
  7. Acute kidney injury
    8.Chronic kidney disease-CKD/ ESKD
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11
Q

Nephrotic syndrome is characterized by

A
  • Proteinuria >3.5g/day
  • Hypoalbuminemia
  • Dyslipidaemia
  • Generalized oedema from salt and water retention
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12
Q

How do you investigate glomerular disease?

A
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12
Q

What are the causes of nephrotic syndrome

A
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13
Q

What is the Management of Glomerular disease?

A

General measures
Dietary sodium restriction
Diuretics
Nephrotic patients may malabsorb diuretics (as well as other drugs) due to gut mucosal oedema
Normal protein diet is advisable. A high-protein diet increases proteinuria and can be harmful in the long term.
Albumin infusion produces only a transient effect. It is only given to patients who are diuretic-resistant
Anticoagulation
Antibiotics if Sepsis.
Statins
ACE inhibitors and/or angiotensin II receptor antagonists

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14
Q

What are some Specific measures to take in the Management of Glomerular disease?

A

Immunosuppressive agents: corticosteroids, calcineurine inhibitors (tacrolimus, cyclosporine), cyclosphosphamide
Treat the underlying cause

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15
Q

What is ACUTE GLOMERULONEPHRITIS aka nephritic syndrome?
What is it characterized by?

A

Acute glomerulonephritis is an inflammation of the renal parenchyma due to immune complex deposition, characterized by:

  • Sub-nephrotic range proteinuria (1–2 g/24h)
  • hematuria with red blood cell casts,
    hypertension,
  • oliguria (Acute renal failure) and fluid retention.
    It is not a disease itself, but the manifestation of an underlying disease
16
Q

Discuss the aetiology of ACUTE GLOMERULONEPHRITIS

A

A) Post infectious
Bacterial eg Group A ß hemolytic streptococci (Post- streptococcal GN), staphylococcus , Pneumococcus ,Salmonella, Legionella
Viral eg Hepatitis B, Hep. C , infectious Mononucleosis
Parasites eg Toxoplasmosis, Malaria, Shistosomiasis
B) GN of undetermined etiology
Membranoproliferative GN
Rapidly progressive GN
C) Connective tissue diseases
SLE
Henoch Schonlein Syndrome
Polyarteritis Nodosa
D) IgA nephropathy
E) Familial Nephropathy eg Alport Syndrome
F) Others eg Shunt Nephritis, Infective Endocarditis, Visceral abscess

17
Q

What is Post-streptococcal glomerulonephritis?
What is it caused by? What is it’s latency period?

A

Post-streptococcal glomerulonephritis (PSGN) is the most common form of acute GN, usually occurs in childhood.

Usually caused by nephritogenic strains of streptococcal infection (group A β-haemolytic streptococcus), pharyngitis or impetigo.

The latency period from infection may vary from 1 to 2 weeks after pharyngitis to 3 to 6 weeks after skin infections.

18
Q

What is the Pathophysiology of Post-streptococcal glomerulonephritis?

A

Post streptococcal GN Follows infection of throat or skin with
Group A ß hemolytic streptococci (usually 1- 4 weeks)
Common strains 12 , 4 , 1 with Pharyngitis
Type 49 with Pyoderma
Mainly involves school age boys
Is an Immune-Complex Disease.
The antibody formed against streptococcus combines with antigen and forms Immune complex
Immune complex deposition along the capillary wall
Activate complement
Inflammatory changes
Glomerular injury

19
Q

Pathology of Post-streptococcal glomerulonephritis on light microscopy

A

Glomeruli are enlarged, hypercellular ,ischemic capillary loops narrowed
Hypercellularity due to Infiltration by leucocytes , both neutrophils and monocytes; Proliferation of endothelial and mesangial cells
In severe cases by crescent formation
Swelling of endothelial cells along with proliferation leucocytic infiltration obliterates the capillary lumen
There may be interstitial edema.
Tubules often contain red cell casts

20
Q

Pathology of Post-streptococcal glomerulonephritis with Immunofluorescence staining

A

Granular deposits of IgG , IgM , C3 along the capillary walls basement membrane

21
Q

Pathology of Post-streptococcal glomerulonephritis on an Electron Microscopy

A

Discrete, amorphous, electron dense deposits on the subepithelial side of capillary basement membrane often shows Lumpy deposits (Subepithelial humps).

21
Q

What is the gold standard to test for Post-streptococcal glomerulonephritis?

A

Renal biopsy

22
Q

CF and atypical presentation of Post-streptococcal glomerulonephritis

A

Most commonly affects children and young adults
Sudden onset of hematuria, with RBC casts in the urine
Proteinuria
Hypertension
edema
urine is smoky, cola-coloured
Impairment of renal function

Atypical presentation
convulsions due to hypertensive encephaclopathy
left ventricular failure (Acute pulmonary edema)
Acute renal failure

22
Q

Laboratory findings of Post-streptococcal glomerulonephritis (urine exam and blood)

A

Urine examination
shows red blood cells (dysmorphic) and rbc casts.
significant proteinuria (1 to 3 plus)
white cells indicative of glomerular inflammation

CBC:Normocytic normochromic anemia
ESR elevated
EUCr: Blood levels of urea and creatinine elevated during early phase (return to normal within 2-3 weeks)
Hyponatremia, hyperkalemia

Chest X-ray
ASO titre (proves a recent streptococcal infection)
Anti hyaluronidase , anti deoxyribonuclease ,

22
Q

Indications for Renal Biopsy in Post-Streptococcal Glomerulonephritis

A

indicated only in patients where clinical features are atypical
* age of onset < 2 yrs
* Presense of systemic features including arthritis, skin rash, hepatosplenomegaly
* absence of elevated ASO titre
* normal C3 (complement 3) levels
* prior h/o renal disease
*oliguria, azotemia (accumulation of nitrogenous waste such as urea and creatinine) rapidly worsen or do not resolve with 2-3 weeks

23
Q

Treatment for Post-Streptococcal Glomerulonephritis

A

Mainly supportive
Diet
intake of protein (0.6 g/kg/body.wt/day)
sodium,Potasium should be restricted
Monitor urine output
fluid intake should be restricted to an amount equal to insensible losses plus 24 hr urine output
Daily weighing (in severe oliguria should lose 0.5 body wt./day)
oral or parenteral penicillin if throat or skin culture reveal Group A streptococcus

24
Q

Which diuretics are used for post-Streptococcal Glomerulonephritis?

A

Diuretics
if pulmonary edema give iv frusemide 2-4 mg/kg
not indicated, since edema is rarely massive and gradually disappears with return of renal function

25
Q

How do you control bp in post-Streptococcal Glomerulonephritis?

A

Control of BP
Mild hypertension- restrict salt water intake
Atenolol, hydralazine or nifedipine are effective
Malignant HT- iv Nitroprusside/ Labetalol

26
Q

When is dialysis indicated in post-Streptococcal Glomerulonephritis?

A

Dialysis is indicated if;
prolonged oligo-anuria
fluid overload
life threatening electrolyte disturbance
Left ventricular failure

27
Q

What is the prognosis of post-Streptococcal Glomerulonephritis?

A

Good prognosis in children
Loss of edema
fall in BP in first week
Gross hematuria and significant proteinuria disappears in two weeks.
Microscopic hematuria, slight proteinuria may remain