Renal Diseases Flashcards
(46 cards)
1
Q
What is filtered through the glomerular capillary walls?
A
plasma
2
Q
What does ultrafiltrate contain?
A
- Contains electrolytes, glucose, phosphate, urea, creatinine, peptides, low molecular weight proteins
- Do not contain proteins having a molecular weight of ≥68kd e.g. albumin and globulins
- cell free
3
Q
What happens to filtrate?
A
is collected in Bowman’s space and enters the tubules, where its composition is modified by tightly regulated secretion and absorption of solute and fluid, until it leaves the kidney as urine.
4
Q
2 factors restricting filtration of macromolecules?
A
- Size selective barrier of the GBM
- Strong negative ionic charges (endothelial cell, basement membrane, and epithelial cell)
- Blood proteins are negatively charged, and are repelled by the negatively charged sites in the glomerular capillary wall, thus restricting filtration
5
Q
What is glomerular blood hydrostatic pressure?
A
it pushes water and solutes in blood plasma through the glomerular filter promoting filtration
- modified by the tone of the afferent and efferent arterioles
6
Q
What is glomerular capillary oncotic pressure?
A
blood flowing into the glomerulus contains plasma proteins and blood cells that displace water content of the blood
- as water outside the capillaries seeks to equalize with the water inside the capillaries through osmosis
7
Q
Filtration is modified by?
A
- the rate of glomerular plasma flow
- the hydrostatic pressure within Bowman’s space
- the permeability of the glomerular capillary wall
8
Q
Classification of causes of nephrotic syndrome?
A
- primary
- secondary
- idiopathic
9
Q
Primary causes of NS?
A
- Minimal change disease (the most common)
- Focal segmental glomerulosclerosis
- Membranoproliferative glomerulonephritis
- C3 glomerulopathy
- Membranous nephropathy
10
Q
Secondary causes of NS?
A
- Vasculitides (SLE, HSP)
- malignancy [lymphoma and leukemia]
- infections [hepatitis, HIV, and malaria]
- Hereditary mutations - protein components of the glomerular filtration apparatus
11
Q
Idiopathic causes of NS?
A
Henoch-Schönlein Purpura
12
Q
Pathophysiology of NS?
A
- Increased permeability of the glomerular capillary wall
- Massive proteinuria and hypoalbuminemia
13
Q
Biopsy results in NS?
A
extensive effacement of podocyte foot processes
14
Q
Pathogenesis of oedema in nephrotic syndrome?
A
- urinary protein loss
- hypoalbuminemia
- decrease in plasma oncotic pressure
- transudation of fluid from the intravascular compartment
- decrease in intravascular volume (stimulating antidiuretic hormone release causing the leading to oedema)
- decrease in renal perfusion pressure
- activation of renin-angiotensin-aldosterone system
- stimulation of tubular reabsorption of sodium
- OEDEMA
15
Q
Role of antidiuretic hormone in pathogenesis of oedema in NS?
A
causes the kidneys to release less water, decreasing the amount of urine produced
16
Q
Role of renin-angiotensin-aldosterone system in pathogenesis of oedema in NS?
A
- increasing sodium reabsorption
- increasing water reabsorption
- increasing vascular tone (degree to which blood vessels narrow or constrict)
17
Q
What is the underfill hypothesis?
A
- loss of protein
- reduced intravascular volume
- increased secretion of vasopressin and atrial natriuretic factor - along with aldosterone
- result in increased sodium and water retention by the tubules
Note: Sodium and water retention therefore occur as a consequence of intravascular volume depletion
18
Q
What is the overfill hypothesis in NS?
A
primary sodium retention, with subsequent volume expansion and leakage of excess fluid into the interstitium
19
Q
What lipids are elevated in NS?
A
cholesterol and triglycerides
20
Q
2 reasons why serum lipid levels are elevated in NS?
A
- Hypoalbuminemia stimulates generalized hepatic protein synthesis, including synthesis of lipoproteins
- Decreased lipid catabolism due to reduced plasma lipoprotein lipase levels (urinary loss)
21
Q
Complications of nephrotic syndrome?
A
- increased risk of infections
e.g. sepsis, peritonitis, pyelonephritis
- especially with encapsulated organisms such as Streptococcus pneumonia, Haemophilus influenza, E. Coli - hypercoagulable state
22
Q
Causes of increased risk of infections in NS?
A
- Loss of complement factor C3b, opsonins such as properdin factor B, and immunoglobulins in the urine.
- The use of immunosuppressive medications to treat nephrotic syndrome
23
Q
Causes of a hypercoagulable state in NS?
A
- Vascular stasis (immobility, hemoconcentration)
- Increase in hepatic production of fibrinogen and other clotting factors (stimulated by hypoalbuminemia)
- Decreased fibrinolytic factors (antithrombin III, proteins C and S)
- Increased plasma platelet production (as an acute phase reactant)
24
Q
The coagulopathy of NS manifest with?
A
thromboembolic events
1. renal vein thrombosis
2. pulmonary embolus
3. sagittal sinus thrombosis
4. thrombosis of indwelling arterial and venous catheters
25
Indications of hypovolemia?
Its management?
Indications
1. A low urinary sodium (<20 mmol/L)
2. high packed cell volume of red blood cells
Clinical features
3. complains of abdominal pain and may feel faint
Note: There is peripheral vasoconstriction and urinary sodium retention
Management
4. intravenous albumin
- as the child is at risk of vascular thrombosis and shock
26
Epidmiology of minimal change nephrotic syndrome?
- more common in boys than in girls (2 : 1)
- Most commonly appears between the ages of 2 and 6 yr
- MCNS is present in 85-90% of patients <6 yr of age
- 20-30% of adolescents who present for the first time with nephrotic syndrome have MCNS
27
Clinical manifestations of MCNS?
1. Oedema (around the eyes and lower extremities)
2. Later generalized oedema
e.g. ascites, pleural effusions, and genital edema
3. Anorexia, irritability, abdominal pain, and diarrhea
4. Absence of hypertension and gross hematuria
28
Differential diagnosis of oedema in NS?
1. Protein-losing enteropathy
2. Hepatic failure
3. Heart failure
4. Acute or chronic glomerulonephritis
5. Protein malnutrition
29
MCNS should not be considered a diagnosis when which clinical manifestations are present?
1. children <1 yr of age
2. a positive family history of nephrotic syndrome
3. presence of extrarenal findings (e.g., arthritis, rash, anemia)
4. hypertension or pulmonary edema
5. acute or chronic renal insufficiency
6. gross hematuria.
30
Children with features that make MCNS less likely?
1. Gross hematuria
2. Hypertension
3. Renal insufficiency
4. Hypocomplementemia
5. Age <1 yr or >8 yr
6. considered for renal biopsy before treatment
31
Expected urinalysis of NS?
1. 3+ or 4+ proteinuria (>3.5g/dL)
2. Microscopic hematuria in 20% of children
3. Serum albumin <2.5 g/dL
4. Serum cholesterol and triglyceride levels are elevated - increased LDL and VLDL
5. Renal biopsy not routinely performed if clinical picture fits MCNS
6. The serum creatinine value is usually normal, but it may be abnormally elevated if there is diminished renal perfusion from contraction of the intravascular volume
7. granular and fatty casts in urine microscopy
32
Management of NS?
1. Education of parents
The child’s parents must be able to recognize the signs and symptoms of the complications of the disease and its treatment and must be taught how to use and interpret the results of urinary dipstick testing for protein
2. Prednisone (after a negative PPD test)
33
Dosage of prednisolone?
2mg/kg maximum 80 mg/day
Duration of Rx is 4-6 wk
Taper dose to 1 mg/kg/day given every other day as a single daily dose for at least 4 wk.
The alternate-day dose is then slowly tapered and discontinued over the next 1-2 mo
34
Management of severe symptomatic edema?
1. Sodium restriction
2. Fluid restriction if hyponatremic
3. Elevate swollen scrotum with pillows
4. Augment diuresis with loop diuretics (furosemide) with extreme caution
Note: Aggressive diuresis can lead to intravascular volume depletion and a significantly increased risk of intravascular thrombosis.
35
What is considered as severe symptomatic edema?
1. large pleural effusions
2. ascites
3. severe genital edema
36
Clinical Course in Steroid-Responsive Nephrotic Syndrome?
1/3 resolve directly
1/3 infrequent relapses
1/3 frequent relapses - steroid dependent
37
What is a nephritic syndrome?
a clinical syndrome that presents as hematuria, elevated blood pressure, decreased urine output and edema
- underlying pathology is inflammation of the glomerulus
38
Common pathogenic causes of acute post-streptococcal glomerunephritis?
1. infection of the throat or skin by certain “nephritogenic” strains of GAS
2. streptococcal pharyngitis (cold weather)
3. Streptococcal skin infections or pyoderma during warm-weather months
39
Epidemiology of post-strep GN?
Common 3 – 15year of age
40
Mechanisms of immune injury that cause post-strep GN?
1. streptococcal antigens in blood stream
2. antistreptococcal antibodies
3. molecular mimicry with glomerular antigens
41
Clinical manifestations of APSGN?
Most common in children aged 5-12 yr
Uncommon before the age of 3 yr
Symptoms develop 1-2 wk after a streptococcal pharyngitis or 3-6 wk after a pyoderma
42
Clinical manifestations of APSGN?
1. be asymptomatic microscopic hematuria
In severe cases:
2. Oedema, hypertension, and oliguria
3. Encephalopathy and/or heart failure secondary to hypertension or hypervolemia
4. Hypertensive encephalopathy must be considered in patients with blurred vision, severe headaches, altered mental status, or new seizures
Note:Encephalopathy can also result from the direct toxic effects of streptococcal antigens on the central nervous system
43
Complications of glomerunephritis?
Hypertension (60% of patients)
Hypertensive encephalopathy in 10% of cases
Neurologic sequelae
Intracranial bleeding
Heart failure, hyperkalemia, hyperphosphatemia, hypocalcaemia, acidosis, seizures, and uremia
Acute renal failure - treat with dialysis
44
Acute complicatios are a result of?
hypertension and acute renal dysfunction
45
Prevention of complications includes?
Early systemic antibiotic therapy for streptococcal throat and skin infections does not eliminate the risk of GN
46
Management of APSGN?
Treat acute effects of renal insufficiency and hypertension
A 10-day course of systemic antibiotics
Sodium restriction
Diuresis with intravenous furosemide
Calcium channel antagonists, vasodilators, or angiotensin-converting enzyme inhibitors for hypertension
