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Title: seminar


1
  • Nephrotic/Nephritis Management
  • From Paediatrics ward
  • By Shimelis Engida (PG )

2
Presentation outlines
  • Introduction
  • Epidemiology
  • Risk factors Aetiology
  • Pathophysiology
  • Clinical presentation
  • Complications
  • Treatment
  • Evaluation and monitoring

3
Introduction
  • The nephrotic syndrome is caused by renal
    diseases that increase the permeability across
    the glomerular filtration barrier.
  • Nephrotic range proteinuria -Urinary protein
    excretion greater than 50 mg/kg per day
  • Hypoalbuminemia - Serum albumin concentration
    less than 3 g/dL (30 g/L)
  • Oedema
  • Hyperlipidaemia

4
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5
Cont..
  • The nephritic syndrome is a clinical syndrome
    that presents as-
  • Haematuria
  • elevated blood pressure
  • decreased urine output, and oedema.
  • The major underlying pathology is inflammation of
    the glomerulus that results in nephritic syndrome

6
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7
Epidemiology
  • As per the final report by the National Center of
    Health Statistics, nephritis syndrome, along with
    nephrotic syndrome, is the 9th leading cause of
    death in the USA in the year 2017.
  • The reported number of combined deaths due to the
    nephritic syndrome, nephrotic syndrome, and renal
    diseases was 50,633 out of a total of 2,813,503
    deaths in the year 2017

8
Risk factors
  • Risk factors of development of minimal change
    disease include
  • Children within the Age gt1 year but lt8 years
  • Hodgkin lymphoma
  • Leukemia
  • Recent viral illness
  • Toxins such as mercury, gold, bee stings, fire
    coral exposure.
  • Medication

9
Co
  • The following are considered risk factors for the
    development of focal segmental glomerulosclerosis
    (FSGS)
  • Male gender
  • Black race
  • Family history
  • Heroin abuse
  • Drugs known to be associated with FSGS
  • Chronic viral infection
  • Single kidney status
  • Obesity

10
Etiology
  • 90 - are primary glomerular abnormality
  • Other are involvement of other disease (10)
  • We can classify based on etiology
  • Primary
  • Secondary
  • congenital and infantile nephrotic syndrome

11
Conti.....
  • Based on pathological
  • Minimal change disease (MCD)
  • Focal segmental glomerulosclerosis (FSGS)
  • Membranous glomeruli nephropathy
  • Membranoproliferative glomerulonephritis (MPGN)
  • Mesangial proliferation
  • Focal and global glomerulosclerosis

12
Tendencies of Glomerular Diseases to Manifest
Nephrotic and Nephritic Features
13
CLASSIFICATION
  • Primary nephrotic syndrome, which refers to
    nephrotic syndrome in the absence of an
    identifiable systemic disease.
  • Secondary nephrotic syndrome, which refers to
    nephrotic syndrome in the presence of an
    identifiable systemic disease.
  • Congenital and infantile nephrotic syndrome,
    which occur in children less than one year of age
    and can be either secondary (mostly due to
    infection) or primary.

14
Pathophysiology
  • Damaged glomerular capillary membrane
  • Increase permeability of glomerular capillary
    wall which leads to massive proteinuria, and
    hypoalbuminemia
  • Decrease oncotic pressure
  • Generalized edema
  • Activation of RAAS
  • Sodium retention edema

15
Con..
16
Clinical presentations
  • Nephrotic
  • Edema
  • Weight gain
  • Fatigue
  • BP normal/raised
  • Leukonychia
  • Breathlessness
  • Pleural effusion, fluid overload, AKI
  • DVT/PE/MI
  • Eruptive xanthomata/ xanthalosmata
  • Nephritic
  • Haematuria (E.g. colacoloured)
  • Proteinuria
  • Hypertension and edema as renal function declines
  • Oliguria
  • Flank pain
  • General systemic symptoms
  • Post-infectious 2-3 weeks after
    strep-throat/URTI

17
Complications
  • Malnutrition
  • Nephrotic edema
  • Infection of NS
  • Thromboembolic complication
  • Lipid abnormality
  • Acute renal failure
  • Chronic kidney disease

18
TREATMENT
19
Non-pharmacologic Therapy
  • Restriction of sodium intake to 50 to 100 mEq/day
  • To control edema, hypertension and proteinuria.
  • Restriction of protein intake of 0.8 to 1 g/day
  • To reduce proteinuria and progression of renal
    disease
  • a low-fat diet of lt 200 mg cholesterol/day. Total
    fat should account for lt 30 of daily total
    calories.
  • plasmapheresis or plasma exchange, may be used to
    remove the inflammatory mediators

20
Pharmacological Treatment
  • Initial treatment of NS in children
  • We recommend that oral glucocorticoids be given
    for 8 weeks (4 weeks of daily glucocorticoids
    followed by 4 weeks of alternate-day
    glucocorticoids) or 12 weeks (6 weeks of daily
    glucocorticoids followed by 6 weeks of
    alternate-day glucocorticoids) (1B)

21
  • Immunosuppressive Agents
  • are commonly used to alter the immune processes
    that are responsible for several of the
    glomerulonephritides.
  • Corticosteroids reduce the production and/or
    release of many substances that mediate the
    inflammatory process
  • such as prostaglandins, leukotrienes,platelet-act
    ivating factors, tumor necrosis factors, and
    interleukin-1 (IL-1).
  • Cytotoxic agents, such as cyclophosphamide,
    chlorambucil, or azathioprine, are commonly used
    to treat glomerular diseases.

22
  • The standard dosing regimen for the initial
    treatment of nephrotic syndrome is daily oral
    prednisone/prednisolone 60 mg/m2/d or 2 mg/kg/d
    (maximum 60 mg/d) for 4 weeks followed by
  • alternate day prednisone/prednisolone, 40 mg/m2
    or 1.5 mg/kg (maximum of 50 mg) for other 4
    weeks,
  • or prednisone/prednisolone 60 mg/m2/d (maximum 60
    mg/d) for 6 weeks followed by alternate day
    prednisone/prednisolone, 40 mg/m2 or 1.5 mg/kg
    (maximum of 50 mg), for other 6 weeks.

23
Prevention and treatment of relapses of NS in
children
  • For children with frequently relapsing and
    steroid-dependent nephrotic syndrome
  • If frequent relapse (2 or more relapses in the
    initial 6 months or more than 3 relapses in any
    12 months),
  • prednisolone 60mg/m2 (maximum 80mg) daily until
    urinary protein turns negative or trace for 3
    consecutive days followed by alternate day
    therapy with 0.1-0.5mg/kg for 6 months and then
    taper.

24
  • For children with frequently relapsing nephrotic
    syndrome who develop serio glucocorticoid-related
    adverse effects and for all children with
    steroid-dependent nephrotic syndrome
  • we recommend that glucocorticoid-sparing agents
    be prescribed, rather than no treatment or
    continuation with glucocorticoid treatment alone
    (1B).

25
  • If infrequent relapse (lt 2 relapses in 6 months
    or lt 3 relapses in one year)
  • prednisolone 60mg/m2 (maximum 80mg) daily until
    urinary protein turns negative or trace for 3
    consecutive days followed by alternate day
    therapy with 40mg/m2 (maximum 60mg) for 28 days
    or 14 doses.
  • If the child relapses while on alternate day
    prednisolone,
  • add levamisole 2.5mg/kg on alternate days for
    6-12 months, then taper prednisolone and continue
    levamisole for 2-3 years.

26
Steroid-resistant nephrotic syndrome in children
  • We recommend using cyclosporine or tacrolimus as
    initial second-line therapy for children with
    steroid-resistant nephrotic syndrome (1C).

27
  • Management of complication

28
Diuretics
  • Management of nephrotic edema involves salt
    restriction, bed rest, and use of support
    stockings and diuretics.
  • Large doses (160 to 480 mg of furosemide)may be
    needed for patients with moderate edema.
  • presence of large amounts of protein in the urine
    promotes drug binding, and thereby reduces the
    availability of the diuretic to the luminal
    receptor sites.
  • reduced sodium delivery to the distal tubule
    secondary to decreased glomerular perfusion may
    also alter diuretic effectiveness.
  • thiazide diuretic or metolazone may be added to
    enhance natriuresis.

29
Cont
  • Alternatively, continuous IV infusion of a loop
    diuretic, such as furosemide 160 to 480 mg/day,
    may be employed.
  • For patients with morbid edema, albumin infusion
    may be used to expand plasma volume and increase
    diuretic delivery to the renal tubules
  • However, it may precipitate CHF and may
    alsoreduce therapeutic response to steroids in
    patients with minimal-change nephropathy.
  • For patients with significant edema, the goal of
    treatment should be
  • a daily loss of 1 to 2 lb (0.45-0.9 kg) of fluid
    until the patients desired weight has been
    obtained.

30
Antihypertensive Agents
  • Optimal control of hypertension for patients with
    glomerular disease is important in reducing both
    the progression of renal disease and the risk for
    cardiovascular
  • According to JNC 8 guidelines, the target BP for
    patients with CKD (GFRlt 60 mL/min/1.73 m2 is lt
    140/90 mmHg
  • ACEIs ARBs delay the loss of renal function for
    patients with diabetic and nondiabetic (primarily
    glomerulonephritis)renal diseases.
  • Non-dihydropyridine calcium channel blockers (eg,
    diltiazem and verapamil) reduce proteinuria and
    preserve renal function and could be used as an
    additional agent.

31
Antiproteinuria Agents
  • ACEIs ARBs
  • The antiproteinuric effect of ACEIs is associated
    with a fall in filtration fraction, suggesting a
    reduction in intraglomerular pressure.
  • ACEIs and ARBs may also have direct effects on
    podocytes, resulting in reduction of proteinuria
    and glomerular scarring.
  • ACEI inhibition may also reduce the effect of
    angiotensin II on renal cell proliferation,
    thereby reducing sclerosis.
  • ACEIs ARBs can reduce proteinuria through
    differentmechanisms and combined use has been
    shown to be more effective than monotherapy.
  • However, the risk of combination therapy has
    become a concern recently.

32
Antiproteinuria Agents
  • NSAIDs probably reduce proteinuria through PG E2
    inhibition, resulting in a reduction of
    intraglomerular pressure
  • Indomethacin and meclofenamate, the two most
    evaluated NSAIDs have similar efficacy to ACEIs,
    and combined
  • treatment with an ACEI results in
    additionalproteinuria reduction.
  • Adherence to a low-sodium diet or concurrent use
    of a diuretic is needed to maximize the
    antiproteinuric effect.
  • Because of their potential for nephrotoxicity,
    especiallyfor patients with preexisting CKD

33
Statins
  • (HMG-CoA) reductase inhibitors, also known as
    statins
  • such as lovastatin, pravastatin, simvastatin,
    fluvastatin atorvastatin and rosuvastatin,
  • statins should be used to treat the dyslipidemia
  • Aside from the lipid-lowering effects, statins
    can reduce cardiovascular risk independent of
    serum lipid concentrations.
  • Meta-analysis of published studies showed that
    statins appear to reduce renal function decline
    andslow the progression of proteinuria
    moderately.
  • The beneficial effect may be dose-related
    andduration-dependent

34
Anticoagulants
  • Renal vein thrombosis andpulmonary emboli are
    serious and common complications of nephrotic
    syndrome,
  • patients who have documented thromboembolic
    episodes should beanticoagulated with warfarin
    until remission of nephrotic syndrome,
  • The use of prophylactic anticoagulation is
    controversial.
  • A decision analysis study suggested that
    prophylactic anticoagulation is beneficial for
    patients with membranous nephropathy.
  • Prophylactic anticoagulation is recommended for
    pts at high risk (ie, those with severe
    nephrotic syndrome and a serum albumin
    concentration less than 2-2.5.

35
Monitoring Parameters
  • Renal function
  • Serum creatinine concentration
  • 24-h urine collection for creatinine clearance
    determination
  • 24-h urine collection for urinary protein
    excretion
  • Urine protein-to-creatinine ratio
  • Clinical signs and symptoms
  • Nephrotic syndrome
  • Protein
  • uriaSerum lipid concentrations
  • Edema

36
  • Nephritic presentations
  • Hematuria
  • Urinalysis
  • Complete blood count
  • Blood pressure
  • General well-being appetite, energy levelKidney
    biopsy to assess disease progression and response
    to therapy
  • Assessment of drug therapy adverse reactions and
    toxicities

37
Reference
  • Heron M. Deaths Leading Causes for 2017. Natl
    Vital Stat Rep. 2019 Jun68(6)1-77. PubMed
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