ACUTE GLOMERULONEPHRITIS

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ACUTE GLOMERULONEPHRITIS Powered By Docstoc
					      ACUTE
GLOMERULONEPHRITIS
     FATUROTI M.O
             CONTENT
•   INTRODUCTION
•   DEFINATION
•   EPIDERMIOLGY
•   AETIOLGY
•   PATHOPHYSIOLOGY
•   CLINICAL FEATURES
•   INVESTIGATIONS
•   TREATMENT
              INTRODUCTION
• ACUTE GN is the term generally reserved for the variety
  of renal diseases in which inflammation of the
  glomerulus , manifested by proliferation of cellular
  elements, is secondary to an immunologic mechanism.
• In earlier years, AGN often was known inappropriately
  as Bright disease, and almost any clinical presentation of
  gross hematuria was labeled.Most incidents of AGN
  appear to be associated with a post infectious state.
  Several bacterial and viral infections like staphylococcal
  and pneumonococcal infections, coxsackie virus B,
  echovirus type 9, influenza virus, and mumps
• The most commonly recognized clinical picture (i.e,
  PSAGN) follows infection with group A beta hemolytic
  streptococci
          DEFINATION
• ACUTE GLOMERULONEPHRITIS IS A
  NON SUPPRATIVE IMMUNE MEDIATED
  INFLAMATORY LESION OF THE
  GLOMERULUS .
• IT IS USUALLY OF SUDDEN ONSET
• IT IS XTERISED BY ACCUMULATION OF
  NITROGENOUS WASTE IN THE BLOOD
  FLIUD &ELECTROLTE DERANGEMENT
               EPIDERMIOLGY

• IN THE TROPIC,CHILDERN OF THE PRESCHOOL
  AGE ARE COMMONLY AFFECTED,WHILE
  ELSEWHERE CHILDREN OF THE SCHOOL AGE ARE
  COMMONLY AFFECTED
• No racial predilection appears to exist; the condition is
  reported in all ethnic and cultural groups. In urban
  populations, a predilection toward minority populations
  appears to exist; however, this may be related more to
  the socioeconomic factor of overcrowding than to any
  racial predilection
• . The disease is more prevalent in males in all regions of
  the world; the male-to-female ratio range is 1.7-2:1.
          AETIOLGY
• MOST INCIDENTS OF AGN APPEAR TO
  BE ASSOCIATED WITH A
  POSTINFECTIOUS STATE. SEVERAL
  BACTERIAL AND VIRAL INFECTIONS
  HAVE BEEN ASSOCIATED TO BE ITS
  CAUSESUCH AS STAPHYLOCOCCAL
  AND PNEUMONOCOCCAL
  INFECTIONS, COXSACKIEVIRUS B,
  ECHOVIRUS TYPE 9, INFLUENZA
  VIRUS, AND MUMPS
• THE MOST COMMONLY OCCURING IS
  POSTSTRETOCOCCI AGN .THE
  ORGANISM IS THE B HEMOLYTIC
  LANCE FIELD GROUP A
  STEPTOCOCCUS
• IN EUROPE /AMERICA MAY RESULT
  FROM A SORE THROAT INFECTION
• THIS INFECTION MAY PRESENT AS
  IMPETIGO /2 SCABIETIC INFECTION.
 PATHOPHYSIOLOGY CHECK
• Most forms of AGN are mediated by an immunologic process. For
  PSAGN, the evidence suggests that immune complexes, preformed
  by the combination of specific antibodies against streptococcal
  antigens, localize on the glomerular capillary wall and activate the
  complement system. The immunologic system also may be
  activated by streptococcal antigens that adhere to the glomerular
  structures and act as "planted antigens" or by alterations in
  endogenous antigens. The activation of the complement cascade
  then generates chemotactic plasma-activated complement 5 (C5a)
  and platelet-derived inflammatory mediators. Various cytokines and
  other cellular immunity factors initiate an inflammatory response
  manifested by cellular proliferation and edema of the glomerular tuft.
  At least 2 antigens isolated from nephritogenic streptococci,
  zymogen (a precursor of exotoxin B) and glyceraldehyde phosphate
  dehydrogenase (GAPDH), have been identified and are believed to
  be capable of initiating the immunologic response.
•   Although streptococcal infections are associated intimately with PSAGN, the
    mechanism of renal injury still is defined incompletely. Current evidence
    suggests that the inflammatory lesion in the glomerulus is associated with
    the fixation of soluble streptococcal antigen-antibody complexes.
•   Several investigators have detected streptococcal antigen in renal biopsy
    material obtained early in the course of infection; however, the major
    evidence supporting an immune complex type of nephritis has been the
    finding of nodular deposits of immunoglobulin G (IgG) and the third
    component of complement (C3) on the capillary basement membrane. The
    finding of C3 in the renal glomerulus usually is associated with decreased
    serum concentrations of C3 and total hemolytic complement.
•   Decreased concentration of properdin and C3 proactivator and inconsistent
    decreases in the early components of complement indicate that
    complement activation occurs primarily by the alternate pathway. Reduced
    serum concentrations of C3 have been demonstrated in 80-92% of children
    with PSAGN. Values return to normal in most children within 6-8 weeks.
    The fourth component of complement (C4) value also may be depressed;
    however, this is an inconsistent finding.
•   PSAGN can occur in epidemics, or, more commonly, it can be sporadic. The sporadic form is seasonal; the winter-
    spring peak is associated with respiratory infection, and the summer-fall peak most often is associated with
    pyoderma. The most common serotype of group A beta hemolytic streptococci associated with nephritis from
    nasopharyngeal infections is type 12, whereas type 49 most often is recovered during outbreaks of pyoderma-
    related PSAGN. In individuals with pharyngitis-related AGN, the latent period is approximately 10 days, and more
    than 80% of patients exhibit a significant rise in serum titer of antistreptolysin-O (ASO).
•   Conversely, a latent period is difficult to define in persons with impetigo-related AGN, and a rise in the titer of ASO
    is observed in only 50% of patients. Serum concentrations of other streptococcal indicators (eg, antihyaluronidase
    [AH] titer, antideoxyribonuclease B titer [anti-DNase B]) usually are elevated in individuals with PSAGN secondary
    to either pharyngeal or skin infections. When a variety of antibody titers is used, almost 95% of patients with
    PSAGN demonstrate evidence of a prior streptococcal infection.
•   Although renal biopsies now are indicated rarely in children with typical PSAGN, they have contributed
    substantially to the understanding of this disease. Irrespective of the degree of severity of the initial inflammatory
    response, the histologic picture is consistent and specific. As observed by light microscopy, glomerular changes
    are generalized and diffuse. The glomerular tufts usually appear enlarged and swollen, and a moderate-to-marked
    increase in proliferation of mesangial and epithelial cells is present.
•   Polymorphonuclear leukocytes also are observed often as part of the inflammatory process. In persons with the
    most severe disease, the glomeruli appear bloodless due to the associated edema of the capillary walls, which
    impedes glomerular perfusion. A direct correlation exists between the severity of the histologic process and the
    clinical manifestations of the disease during the acute phase, and possibly the prognosis.
•   Granular deposits of IgG and C3 typically are found when the specimen is studied by immunofluorescent
    microscopy; other immunoglobulins (Igs) and fibrinogen often are observed. Electron microscopy of renal tissue
    from patients with PSAGN usually reveals subepithelial electron-dense deposits (humps).
•   In most patients with moderate-to-severe AGN
               CLINICAL FEATURES
•   THEY INCLUDE ;
•   FACIAL PUFFINESS; The edema first collects in those sites where tissue resistance is low, such
    as the periorbital area. Later, it becomes more generalized, and, in those few patients in whom
    loss of albumin is exaggerated with resultant hypoalbuminemia, the edema even may simulate
    that of the nephrotic syndrome
•   REDUCTION IN URINE VOLUME; Glomerular inflammation (ie, cellular proliferation, edema)
    reduces glomerular filtration without a coexistent decrease in total renal blood flow.The reduced
    volume of GF and the normal tubular function lead to an increase in the reabsorption of salt and
    water, with resulting oliguria and edema
•   APATHYHypertensive encephalopathy has been reported in approximately 5% of hospitalized
    children and is the most serious early complication of this disease.
•   In these patients, hypertension usually is severe and is accompanied by signs of central nervous
    system dysfunction such as headache, vomiting, depressed sensorium, confusion, visual
    disturbances, aphasia, memory loss, coma, and convulsions. SEIZURES 2 TO UREAMIA
•   Hypertensive encephalopathy has been reported in the occasional individual with minimal or no
    edema and with minimal urinary abnormalities.
•   DIFFICULTY IN BREATHING;. Circulatory congestion is apparent in most children admitted to the
    hospital but is responsible only rarely for significant early symptoms.
     –   Dyspnea, orthopnea, and cough may be present.
     –   Pulmonary rales often are audible.
     –   At times, the only evidence of congestion is detected on chest radiograph.
     –   In the patient with an otherwise normal cardiovascular system, cardiac failure is unusual
     •
• HYPERTENSION; Hypertension is the third cardinal
  feature of PSAGN and is reported in 50-90% of children
  who are hospitalized with AGN.
   – The pathogenesis of the hypertension is unknown; however,
     pathogenesis probably is multifactorial and related only in part to
     ECF volume expansion.
   – The magnitude of the increase in BP is highly variable; however,
     systolic pressures greater than 200 mm Hg and diastolic
     pressures greater than 120 mm Hg are not unusual
   – ALTERED URINE COLOURATION; Gross hematuria occurs at
     onset in 30-50% of children with PSAGN who require
     hospitalization.
   – The urine usually is described as being smoky, cola colored, tea
     colored, or rusTY
   • SMOKY DARK BROWN FRANKLY BLOODY
• CONSISTUTIONAL SYMPTOMS LIKE malaise,
  lethargy, anorexia, fever, abdominal pain, and headache.
  Observant parents also may note oliguria.
• HISTORY OF the siblings and/or household contacts of
  children affected with PSAGN IS IMPORTANT
    – An insidious onset of edema is more indicative of other forms of
      renal disease.
    – An occasional child may have a scarlatiniform rash or evidence
      of a viral exanthema, but petechial or purpuric rashes suggest
      other conditions.
    – Almost characteristic by their absence are arthralgia, arthritis,
      carditis, hepatic involvement, and GI bleeding
•
                           INVESTIGATIONS
•   URINALYSIS;RED CELL CAST OBSERVERED IN FRESH URINE SAMPLES/HEAM GRANULAR CAST
•   PROTEINURIA EVIDENCEND BY DIP STICK OF +1/+2 corresponding to less than 2 g/m2/d when assessed quantitatively
•   S.G;ELEVATED
•   FBC/PLATELET; RBC/PLATELET IS DECREASED [ANEMIA]
•   UREA/CR –ELEVATED
•   SERUM PROTEIN LOW
•   FRACTIONATING NA IS <1%IN AGN NEPHROTIC SYNDROME DEHYDRATION/ UNLIKE AKI WC IS >1%
•   RENAL USS Renal ultrasonography generally demonstrates normal to slightly enlarged kidneys bilaterally with some evidence of
    increased echogenicity.
•   ASOTITRE SHLD BE DOCUMENTEDLook for evidence of streptococcal infection in all patients.
•   Cultures from either the pharynx or skin may be positive; however, high streptococcal antibody titers are more compelling.
•   A number of laboratory tests can be used to measure antibodies to a variety of streptococcal antigens (eg, ASO, AH, anti-DNase B) or to
    combinations of antigens (eg, streptozyme test).
•   Whatever test is used, a rise in the titer of the antibody, measured at an interval of 2-3 weeks, is more meaningful than a single
    measurement.

•   C3/C4 SHLD BE INVESTEGATED;These tests help to differentiate poststreptococcal from other postinfectious forms of AGN
•    Chest radiographs commonly demonstrate central venous congestion in a hilar pattern, the degree of which parallels the increase in ECF
    volume.
          TREATMENT
• THERE
         COMPLICATIONS
•   PULMONARY EDEMA
•   CCF
•   AKI
•   HYPERTENSIVE ENCEPHALOPATY
•   UTI
                                        DD
•   Postinfectious glomerulonephritis
    Poststreptococcal
    After other bacterial infections
    Postviral infectionsthe most common are varicella-zoster virus, cytomegalovirus, and
    the Epstein-Barr virus.
    Postparasitic infections
    IgA-associated glomerulonephritisEvidence of a prior streptococcal illness
    usually is lacking in individuals with HSP nephritis, and complement values (C3
    and/or C4) usually are normal.
    Henoch-Schönlein purpura (HSP) nephritis
    Other IgA nephritis (Berger disease)
    presents as an episode of gross hematuria occurring during the early stages of a
    respiratory illness
    Others (less common)
    Chronic GN (recurrence and/or relapse)
    Shunt nephritis
    Familial nephritis
    Rapidly progressive (crescentic) GN
    SLE nephritis occasionally may be confused with PSAGN when an acute
    exacerbation of the previously present nephropathy is present.
                                                 SELF SLIDE
•   Most patients with acute GN exhibit milder symptoms and/or signs somewhere between the extremes described below.
      –     At one extreme is the asymptomatic child whose disease is discovered only by examination of the urine. Based on
            surveillance studies of the siblings and/or household contacts of children affected with PSAGN, at least 50% of
            persons with laboratory evidence of nephritis (ie, abnormal urinalysis) appear to have no symptoms or signs of clinical
            illness.
      –     At the other extreme is the child who presents with severe disease manifested by oliguria, edema, hypertension, and
            azotemia and with proteinuria, hematuria, and urinary casts (cylindruria).
•   In those patients whose acute GN is the result of a postinfectious cause (ie, PSAGN being the most common), a latent period of 7-21 days between onset of the
    streptococcal infection and development of clinical GN is characteristic.
      –     This latent period, more clearly defined after pharyngeal infections than after pyoderma, averages approximately 10
            days.
      –     The development of clinical nephritis (ie, hematuria and/or edema) either during or within 2-5 days after the onset of a
            respiratory infection is atypical and suggests the possibility of some other form of GN.
•   Gross hematuria and/or edema represent the most common clinical presentation.
      –     One or both findings usually appear abruptly and may be associated with various degrees of malaise, lethargy,
            anorexia, fever, abdominal pain, and headache. Observant parents also may note oliguria.
      –     An insidious onset of edema is more indicative of other forms of renal disease.
      –     An occasional child may have a scarlatiniform rash or evidence of a viral exanthema, but petechial or purpuric rashes
            suggest other conditions.
      –     Almost characteristic by their absence are arthralgia, arthritis, carditis, hepatic involvement, and GI bleeding.
      –     Edema is the most frequent presenting symptom.
                •    According to some investigators, edema is found in approximately 85% of patients.
                •    Edema usually appears abruptly and first involves the periorbital area, but it may be generalized.
                •    The degree of edema varies markedly and depends on a number of factors, including the severity of glomerular involvement, the fluid
                     intake, and the degree of hypoalbuminemia.
      –     Gross hematuria occurs at onset in 30-50% of children with PSAGN who require hospitalization.
                •    The urine usually is described as being smoky, cola colored, tea colored, or rusty.
                •    Observant parents may note oliguria.
                •    Clots are exceedingly rare in persons with AGN.
•   Hypertension is the third cardinal feature of PSAGN and is reported in 50-90% of children who are hospitalized with AGN.
      –     The pathogenesis of the hypertension is unknown; however, pathogenesis probably is multifactorial and related only in
            part to ECF volume expansion.
      –     The magnitude of the increase in BP is highly variable; however, systolic pressures greater than 200 mm Hg and
            diastolic pressures greater than 120 mm Hg are not unusual.
      –     Hypertensive encephalopathy has been reported in approximately 5% of hospitalized children and is the most serious
            early complication of this disease.

				
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