Rapidly progressive renal failure - PowerPoint PPT Presentation

Loading...

PPT – Rapidly progressive renal failure PowerPoint presentation | free to view - id: 5134a4-NzYwY



Loading


The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
About This Presentation
Title:

Rapidly progressive renal failure

Description:

Rapidly progressive renal failure Dr. HRS: Treatment (Contd) Spcific measures Renal vasodilators Systemic vasoconstrictors TIPS Renal replacement therapy Liver/renal ... – PowerPoint PPT presentation

Number of Views:350
Avg rating:3.0/5.0
Slides: 47
Provided by: Ani93
Category:

less

Write a Comment
User Comments (0)
Transcript and Presenter's Notes

Title: Rapidly progressive renal failure


1
Rapidly progressive renal failure
Dr.
2
Overview
  • Introduction
  • Etiology
  • Pathology
  • Clinical features
  • Management
  • Conclusions

3
Introduction
  • Rapidly progressive renal failure (RPRF)
  • Deterioration of the GFR, associated with the
    accumulation of wastes such as urea and
    creatinine (azotemia) within weeks to months
  • Note Acute renal failure (ARF) duration is
    hours to weeks

GFR Glomerular Filtration Rate
4
Etiology
  • RPRF may be due to various causes
  • Pre-renal
  • Renal
  • Post-renal

5
Etiology
  • Acute Nephritis
  • Rapidly progressive glomerulonephritis (RPGN)
  • Acute on chronic renal failure

6
RPGN
  • Characterized clinically by
  • A rapid decrease in the GFR of at least 50 over
    a short period, from a few days to 3 months

7
RPGN History
  • The term RPGN was first used to describe a
  • Group of patients who had an unusually fulminant
    poststreptococcal glomerulonephritis and a poor
    clinical outcome
  • Several years later,
  • The anti-GBM antibody was discovered to produce a
    crescentic glomerulonephritis in sheep, and,
    following this discovery,
  • The role of anti-GBM antibody in Goodpasture
    syndrome was elucidated

Anti GBM antiglomerular basement membrane
8
RPGN History (Contd)
  • Soon afterward,
  • The role of the anti-GBM antibody in RPGN
    associated with Goodpasture disease was
    established
  • In the mid 1970s,
  • A group of patients was described who fit the
    clinical criteria for RPGN but in whom no cause
    could be established

9
RPGN History (Contd)
  • Many of these cases were
  • Associated with systemic signs of vascular
    inflammation (systemic vasculitis), but some
    cases were characterized only by renal disease
  • A distinct feature of these cases was
  • The virtual absence of antibody deposition after
    immunofluorescence staining of the biopsy
    specimens, which led to the label pauci-immune
    RPGN

10
RPGN History (Contd)
  • More than 80 of patients with pauci-immune RPGN
    were subsequently found to have
  • Circulating antineutrophil cytoplasmic antibodies
    (ANCAs), and,
  • Thus, this form of RPGN is now termed
    ANCA-associated vasculitis

11
RPGN Causes
  • Abscess of any internal organ
  • Anti- GBM antibody disease
  • Blood vessel diseases such as
  • Vasculitis or polyarteritis
  • Collagen vascular disease such as
  • Lupus nephritis and Henoch-Schonlein purpura
  • Goodpasture syndrome
  • IgA nephropathy History of cancer
  • Membranoproliferative GN
  • Blood or lymphatic system disorders
  • Exposure to hydrocarbon solvents

12
RPGN Pathology
  • The main pathologic finding is
  • Extensive glomerular crescent formation
  • Focal rupture of glomerular capillary walls that
    can be seen by light microscopy and electron
    microscopy

13
RPGN Classification
  • Immunological classification based on the or
    - of ANCAs
  • The disorders are also classified based on their
    clinical presentation

14
RPGN Classification (Contd)
  • Anti-GBM antibody (Approx. 3 of cases)
  • Goodpasture syndrome (lung and kidney
    involvement)
  • Anti-GBM disease (only kidney involvement)
  • Note 10-40 of patients may be ANCA positive

15
RPGN Classification (Contd)
  • Immune complex
  • Postinfectious (staphylococci/streptococci)
  • Collagen-vascular disease
  • Lupus nephritis
  • Henoch-Schönlein purpura (immunoglobulin A and
    systemic vasculitis)
  • Immunoglobulin A nephropathy (no vasculitis)
  • Mixed cryoglobulinemia

16
RPGN Classification (Contd)
  • Immune complex contd.
  • Primary renal disease
  • Membranoproliferative glomerulonephritis
  • Fibrillary glomerulonephritis
  • Idiopathic
  • Note Of all patients with crescentic immune
    complex glomerulonephritis, 25 are ANCA lt 5
    of patients with noncrescentic immune complex
    glomerulonephritis are ANCA

17
RPGN Classification (Contd)
  • Pauci-immune
  • Wegener granulomatosis (WG)
  • Microscopic polyangiitis (MPA)
  • Renal-limited necrotizing crescentic
    glomerulonephritis (NCGN)
  • Churg-Strauss syndrome
  • Note 80-90 of patients are ANCA

18
RPGN Symptoms
Edema (swelling) of the face, eyes, ankles,
feet, legs, or abdomen Blood in the
urine Dark or smoke-colored urine Decreased
urine volume Abdominal pain Cough
Diarrhea General ill feeling Fever Joint
aches Muscle aches Loss of appetite
Shortness of breath
19
RPGN Signs
  • A physical examination reveals edema (swelling)
  • Abnormal heart and lung sounds may be present
  • Blood pressure may be high

20
RPGN Tests diagnosis
  • Anti-glomerular basement membrane antibody tests
  • Antineutrophil cytoplasmic antibodies
  • BUN and creatinine
  • Complement levels
  • Creatinine clearance Urinalysis

21
RPGN Treatment
  • Depends on the underlying cause
  • Corticosteroids may relieve symptoms in some
    cases
  • Medications that suppress the immune system may
    also be prescribed, depending on the cause
  • Plasmapheresis may relieve the symptoms in some
    cases

22
RPGN Treatment
  • Persons should be closely watched for signs of
    progression to kidney failure
  • Dialysis or a kidney transplant may ultimately be
    necessary

23
RPGN Prognosis
Without treatment, RPGN often worsens rapidly to
kidney failure and end-stage kidney disease in
6 months, although a few cases may just go away
on their own Those who receive treatment may
recover some or rarely all of their original
kidney function The extent of recovery is related
to the degree of kidney function at diagnosis and
degree of crescent formation The disorder may
recur If the disease occurs in childhood, it is
likely that kidney failure will eventually develop
24
RPGN Prevention
The prompt treatment of disorders that can cause
RPGN may prevent the development of this disease
25
RPGNComplications
Congestive heart failure Pulmonary
edema Hyperkalemia Acute renal
failure Chronic renal failure End-stage renal
disease
26
RPRF Other causes
  • Hepatorenal syndrome (HRS)
  • Frerichs (1861) and Flint (1863) first noted
    association of liver disease and oliguria without
    renal histologic changes

27
HRS Types
  • Type 1
  • Rapidly progressive renal failure
  • Doubling of creatinine
  • Precipitating factor frequently identified
  • Type 2
  • Moderate, steady renal failure
  • Milder elevation of creatinine
  • May arise spontaneously

28
HRS Aggravating factors
29
HRS Pathologphysiology
  • Hallmark Intense renal vasoconstriction
  • Starts at an early time point and progresses with
    worsening liver disease

30
HRS Pathophysiology (Contd)
  • Peripheral (splanchnic) arterial vasodilation
    subsequent renal vasoconstriction
  • Stimulation of renal sympathetic nervous system
  • Cardiac dysfunction circulatory derangements and
    renal hypoperfusion
  • Cytokine/mediator action on renal circulation

31
HRS Pathophysiology (Contd)
32
HRS Prognosis
  • Type 1 RPRF
  • 80 2 week mortality,
  • 90 3 month
  • Prognosis worse if precipitating factor exists
  • Severity of liver disease a determinant of
    survival

33
HRS Treatment
  • General measures
  • Central venous access
  • Monitor fluid status
  • Volume albumin/furosemide to titrate CVP
  • Nutrition critical avoid high protein low salt,
    free water restriction

34
HRS Treatment (Contd)
  • Spcific measures
  • Renal vasodilators
  • Systemic vasoconstrictors
  • TIPS
  • Renal replacement therapy
  • Liver/renal replacement therapy
  • Liver transplantation

TIPS Transjugular intrahepatic portosystemic
shunt
35
RPRF Other causes
  • Multiple Myeloma

36
Myeloma KidneyEpidemiology
  • In two large multiple myeloma studies, 43 (of
    998 pts) had a creatinine gt 1.5 and 22 (of 423
    pts) had a Cr gt 2.0
  • The one-year survival was 80 in pts with Cr lt
    1.5 compared to 50 in pts with a Cr gt 2.3
  • Prognosis is especially poor in pts who require
    dialysis

37
Meyloma Kidney Causes of renal failure in MM
  • Cast nephropathy
  • Light chain deposition disease
  • Primary amyloidosis
  • Hypercalcemia
  • Renal tubular dysfunction
  • Volume depletion
  • IV contrast dye, nephrotoxic meds

38
Meyloma Kidney Causes of renal failure in MM
Cast Nephropathy
39
Myeloma Kidney Treatment of renal failure in MM
  • Hydration with IV fluids
  • Treatment of hypercalcemia
  • Loop diuretics
  • Caution with bisphosphonates
  • Treatment of myeloma
  • Pulse steroids /- thalidomide
  • VAD chemotherapy
  • Possible role for plasmapheresis
  • Dialysis, as necessary

40
Myeloma Kindey Prevention of renal failure in MM
  • IVF hydration
  • Discontinuation of nephrotoxic drugs (i.e.
    NSAIDs, etc.)
  • Chemotherapy/steroids treatment of multiple
    myeloma to decrease the filtered light chain load

41
RPRF Other causes
  • Drug induced, e.g.
  • Acyclovir
  • Orlistat
  • The increased intraluminal free fatty acids
    complex with intraluminal calcium ions,
    competitively inhibiting the precipitation of
    oxalate with calcium
  • The increase in soluble uncomplexed oxalate
    facilitates oxalate absorption, resulting in
    hyperoxaluria and oxalate stone

42
RPRF Other causes
  • Type 2 Diabetes with renal failure, Factors
    Affecting Progression of
  • hypoalbuminemia, anemia, higher mean blood
    pressure, and lack of use of insulin predict
    rapid progression of renal failure, but HbA1c
    does not, and insulin therapy may be possibly an
    indicator of the delay in progression of renal
    failure

Diabetes Care, May 200326(5)1530
43
RPRF Other causes (Contd)
  • Diabetes Dietary acid load and rapid progression
    to end-stage renal disease
  • High ingestion of nonvolatile acids with food
    increases susceptibility for progression to
    end-stage renal failure
  • These high dietary acid loads lead to
    compensatory increases in renal acid excretion
    and ammoniagenesis.
  • The price paid for maintenance of acid-base
    homeostasis is renal tubulointerstitial injury,
    with subsequent decline in renal function and
    induction of hypertension

J Nephrol. 2010 Sep 24
44
RPRF Other causes (Contd)
  • Causes of acute-on-chronic renal failure
  • Dehydration
  • Drugs
  • Disease relapse/acceleration
  • Infection
  • Obstruction
  • Hypercalcemia
  • Hypertension
  • Heart failure
  • Interstitial nephritis

45
Conclusions
  • RPRF is defined based on duration of decline in
    renal function (weeks to months) with various
    etiologies
  • Patient should be evaluated for the cause and
    treated accordingly
  • RPGN is common group for RPRF
  • Diabetes, HRS, Multiple myeloma may also be the
    reasons for RPRF

46
THANK YOU !
About PowerShow.com