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What is human but an ingenious
 machine designed to turn, with
 “infinite artfulness, the red
 wine of Shiraz into urine”?

      Storyteller in Isak Dinesen’s   Seven Gothic Tales
ACUTE GLOMERULONEPHRITIS
    Deposition of immune complexes
     formed in conjunction with group A
     Streptococcus infection

    Macroscopic hematuria, proteinuria rbc
     and granular casts

    Antistreptolysin O titer and Anti-group A
     streptococcal enzymes
RAPIDLY PROGRESSIVE (CRESCENTRIC)
      GLOMERULONEPHRITIS
    Deposition of immune complexes from
     systemic immune disorders on the
     glomerular membrane (i.e. Systemic Lupus
     Erythematosus)

    Macroscopic hematuria, proteinuria and
     rbc casts

    BUN, Creatinine and Creatinine clearance

    Possible progression of ESRF
This immunofluorescence micrograph of a glomerulus demonstrates positivity
with antibody to fibrinogen. With a rapidly progressive GN, the glomerular
damage is so severe that fibrinogen leaks into Bowman's space, leading to
proliferation of the epithelial cells and formation of the bright crescent.
GOODPASTURE’S SYNDROME
   Cytotoxic antibody formed during viral
    respiratory infection attach to glomerular
    and alveolar basement membrane

   Hemoptysis and dyspnea followed by
    hematuria, proteinuria and rbc casts

   Antiglomerular basement membrane
    antibody
This immunofluorescence pattern shows positivity with antibody to IgG
and has a smooth, diffuse, linear pattern that is characteristic for
deposition of antiglomerular basement membrane antibody with
Goodpasture syndrome.
WEGENER’S GRANULOMATOSIS
   Antineutrophilic cytoplasmic antibody
    binds to neutrophils
    in vascular walls

 Pulmonary symptoms (hemoptysis)
  followed by hematuria, protenuria and
  rbc casts
 ANCA test
 Progress to ESRF
HENOCH-SCHONLEIN PURPURA
    Occurs in children after
     viral respiratory infection



  Initial appearance of purpura followed by
   blood in stool and sputum then renal
   involvement
  Stool occult blood
IgA NEPHROPATHY/
        Berger’s Disease
   Deposition of IgA on glomerular
    membrane resulting from increased
    levels of serum IgA

   Recurrent macroscopic hematuria
    following mucosal infection or strenuous
    exercise

   Slow progression to CGN
MEMBRANOUS
    GLOMERULONEPHRITIS
 Most common cause of Nephrotic
  Syndrome in Adult
 Thickening of glomerular basement
  membrane from deposition of IgG
  immune complexes
 Associated with SLE, Sjogrens
  syndrome, secondary syphilis, Hep B
  and malignancy
 ANA, HbS Ag and FTA-ABS
MEMBRANOPROLIFERATIVE
 GLOMEROLUNEPHRITIS
 Cellular proliferation affecting the capillary
  walls or glomerular basement membrane
 Double contour or “tram-track” appearance
 Subendothelial deposits of C3, IgG, C1, C4

   Hematuria and proteinuria
   Slow progression to nephrotic syndrome or
    possible remission

   Serum complement level
Membranoproliferative
glomerulonephritis (MPGN).
-glomerulus has increased
overall cellularity
- Silver stain “tram-tracking”
characteristic
CHRONIC
    GLOMERULONEPHRITIS
 Marked decreased in renal function due
  to glomerular damage precipitated by
  other renal disorders
 Hematuria, proteinuria, glucosuria, urin
  e casts (cellular, granular, waxy and
  broad)
 BUN, Creatinine, Creatinine
  clearance, Electrolytes
NEPHROTIC SYNDROME
 Acute onset following systemic shock
 Gradual progression from other gromerular
  disorder to renal failure
 Massive proteinuria
  (>3.5), hypoalbuminemia, generalized
  edema, hyperlipidemia & lipidosis

 Microscopic hematuria, renal tubular
  cells, oval fat bodies and fat droplets, fatty
  and waxy casts
 Serum albumin, cholesterol and
  triglycerides
MINIMAL CHANGE DISEASE
    (Lipid Nephrosis)
 NS in children after allergic reactions
  and immunizations
 Heavy proteinuria, transient hematuria
  and fat droplets
 Complete remission following
  corticosteroid treatment

   Serum albumin, cholesterol and
    triglycerides
Thickened Basement Membrane                        Effaced foot processes




Minimal change disease (MCD) characterized by effacement of the epithelial cell
(podocyte) foot processes and loss of the normal charge barrier
FOCAL SEGMENTAL
        GLOMERULONEPHRITIS
   Disruption of podocytes in some areas
    of glomeruli associated with
    heroin, analgesic abuse and HIV

   May resemble nephrotic syndrome or
    minimal change disease

   Drugs of abuse and HIV test
An area of collagenous sclerosis
                               runs across the middle of this
                               glomerulus




Trichrome stain of a
glomerulus in a patient with
focal segmental
glomerulosclerosis (FSGS)
demonstrates blue collagen
deposition.
ALPORT SYNDROME
   Inherited sex linked or autosomal disorder

   Males before age 6 during a respiratory
    infection may exhibit macroscopic
    hematuria and continue to exhibit
    microscopic hematuria

   Abnormal vision and hearing may be
    present
DIABETIC NEPHROPATHY
   a.k.a. Kimmelstiel-Wilson disease

   Deposition of glycosylated proteins due to
    uncontrolled blood glucose level

   Early monitoring of px with
    microalbuminuria is important

   Most common cause of End Stage Kidney
    Disease.
ACUTE TUBULAR NECROSIS
   Damage to renal tubular cells caused by
    ischemia or toxic agents

 Reversible renal dysfunction
 Microscopic
  hematuria, proteinuria, RTE cells and
  casts (hyaline, granular, broad and
  waxy)

   Hemoglobin, hematocrit and cardiac
    enzymes
HEREDITARY METABOLIC
 TUBULAR DISORDERS
FANCONI’S SYNDROME
 Inherited or acquired through exposure
  to toxic agents, outdated tetracycline or
  complication of Multiple Myeloma.
 Generalized defect in renal tubular
  reabsorption in proximal convoluted
  tubules
 Glucosuria and possible cystine crystals
 Serum and urine electrolytes, amino
  acid chromatography
NEPHROGENIC DIABETES
     INSIPIDUS
   Inherited sex-linked recessive or
    acquired from medication or as
    complication of PCKD or sickle cell
    anemia

   Inability of renal tubules to respond to
    ADH causing polyuria

   Urine is pale yellow, and with low
    specific gravity
RENAL GLYCOSURIA
   Generalized failure to reabsorb
    substances from glomerular
    filtrate, affecting the reabsorption of
    glucose

   Increased urine glucose concentration
    with normal blood glucose.
CYSTITIS
 Ascending bacterial infection of the
  bladder
 Acute onset of urinary frequency and
  burning resolved with antibiotics
 Leukocytoria, bacteruria, microscopic
  hematuria, mild proteinuria and
  increased pH
 Urine culture
ACUTE PYELONEPHRITIS
 Renal tubulointerstitial infection related
  to interference of urine flow to the
  bladder, urine reflux or untreated cystitis
 Acute onset of urinary frequency and
  burning resolved with antibiotics
 Leukocytoria, bacteruria, Casts
  (WBC, bacterial, granular, waxy and
  broad) hematuria and proteinuria
 Urine and blood cultures
CHRONIC
       PYELONEPHRITIS
 Recurrent renal tubulointerstitial infection
  caused by structural abnormalities affecting
  urine flow
 Diagnosed in children and requires
  correction of structural defects
 Leukocytoria, bacteruria, Casts
  (WBC, bacterial, granular, waxy and
  broad) hematuria and proteinuria
 Urine and blood cultures, BUN, Creatinine
  and Creatinine clearance
ACUTE
 INTERSTITIAL NEPHRITIS
 Allergic inflammation of renal interstitium
  in response to certain medications
 Acute onset of renal dysfunction
  accompanied by skin rash
 Resolves with discontinuation of
  medication and treatment with
  corticosteroids
 Hematuria, proteinuria, leukocyturia and
  WBC casts
 Urine eosinophils, BUN, creatinine and
  creatinine clearance
VASCULAR DISORDER
 Renal ischemia and loss of functional
  renal tissue
 Disorders that affect integrity of renal
  blood vessels:
- Autoimmune disorders
- Vaculitis
- Diabetes mellitus
RENAL LITHIASIS
 May form in calyces and pelvis of KUB
 Renal colic or flank pain
 Vary from barely visible to
  staghorn calculi
 75% compose of calcium oxalate
  and phosphates

   Lithotripsy and surgery
RENAL FAILURE
 Exists in both acute and chronic forms
 Gradual progression from the original
  disorder to end-stage renal disease
             Renal insufficiency

            Acute Renal Failure

           Chronic Renal Failure
Acute Renal Failure
Prerenal: decreased blood pressure and
  cardiac
  output, hemorrhage, burns, surgery
  and septicemia
Renal: Acute glomerulonephritis, Acute
  tubular necrosis, Acute
  pyelonephritis, Acute interstitial necrosis
Postrenal: Renal calculi, Tumors and
  Crytallization of ingested substances
            Chronic Renal Failure
Chronic Renal Failure

-   marked decreased in GFR
-   rising BUN and creatinine (AZOTEMIA)
-   electrolyte imbalance
-   Isothenuria, proteinuria, glycosuria
-   Abundance of granular, wax and broad
    casts

        END-STAGE RENAL DISEASE
Thank You!

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Kidney Disease Guide

  • 1.
  • 2. What is human but an ingenious machine designed to turn, with “infinite artfulness, the red wine of Shiraz into urine”? Storyteller in Isak Dinesen’s Seven Gothic Tales
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  • 7. ACUTE GLOMERULONEPHRITIS  Deposition of immune complexes formed in conjunction with group A Streptococcus infection  Macroscopic hematuria, proteinuria rbc and granular casts  Antistreptolysin O titer and Anti-group A streptococcal enzymes
  • 8. RAPIDLY PROGRESSIVE (CRESCENTRIC) GLOMERULONEPHRITIS  Deposition of immune complexes from systemic immune disorders on the glomerular membrane (i.e. Systemic Lupus Erythematosus)  Macroscopic hematuria, proteinuria and rbc casts  BUN, Creatinine and Creatinine clearance  Possible progression of ESRF
  • 9. This immunofluorescence micrograph of a glomerulus demonstrates positivity with antibody to fibrinogen. With a rapidly progressive GN, the glomerular damage is so severe that fibrinogen leaks into Bowman's space, leading to proliferation of the epithelial cells and formation of the bright crescent.
  • 10. GOODPASTURE’S SYNDROME  Cytotoxic antibody formed during viral respiratory infection attach to glomerular and alveolar basement membrane  Hemoptysis and dyspnea followed by hematuria, proteinuria and rbc casts  Antiglomerular basement membrane antibody
  • 11. This immunofluorescence pattern shows positivity with antibody to IgG and has a smooth, diffuse, linear pattern that is characteristic for deposition of antiglomerular basement membrane antibody with Goodpasture syndrome.
  • 12. WEGENER’S GRANULOMATOSIS  Antineutrophilic cytoplasmic antibody binds to neutrophils in vascular walls  Pulmonary symptoms (hemoptysis) followed by hematuria, protenuria and rbc casts  ANCA test  Progress to ESRF
  • 13. HENOCH-SCHONLEIN PURPURA  Occurs in children after viral respiratory infection  Initial appearance of purpura followed by blood in stool and sputum then renal involvement  Stool occult blood
  • 14. IgA NEPHROPATHY/ Berger’s Disease  Deposition of IgA on glomerular membrane resulting from increased levels of serum IgA  Recurrent macroscopic hematuria following mucosal infection or strenuous exercise  Slow progression to CGN
  • 15. MEMBRANOUS GLOMERULONEPHRITIS  Most common cause of Nephrotic Syndrome in Adult  Thickening of glomerular basement membrane from deposition of IgG immune complexes  Associated with SLE, Sjogrens syndrome, secondary syphilis, Hep B and malignancy  ANA, HbS Ag and FTA-ABS
  • 16. MEMBRANOPROLIFERATIVE GLOMEROLUNEPHRITIS  Cellular proliferation affecting the capillary walls or glomerular basement membrane  Double contour or “tram-track” appearance  Subendothelial deposits of C3, IgG, C1, C4  Hematuria and proteinuria  Slow progression to nephrotic syndrome or possible remission  Serum complement level
  • 17. Membranoproliferative glomerulonephritis (MPGN). -glomerulus has increased overall cellularity - Silver stain “tram-tracking” characteristic
  • 18. CHRONIC GLOMERULONEPHRITIS  Marked decreased in renal function due to glomerular damage precipitated by other renal disorders  Hematuria, proteinuria, glucosuria, urin e casts (cellular, granular, waxy and broad)  BUN, Creatinine, Creatinine clearance, Electrolytes
  • 19. NEPHROTIC SYNDROME  Acute onset following systemic shock  Gradual progression from other gromerular disorder to renal failure  Massive proteinuria (>3.5), hypoalbuminemia, generalized edema, hyperlipidemia & lipidosis  Microscopic hematuria, renal tubular cells, oval fat bodies and fat droplets, fatty and waxy casts  Serum albumin, cholesterol and triglycerides
  • 20. MINIMAL CHANGE DISEASE (Lipid Nephrosis)  NS in children after allergic reactions and immunizations  Heavy proteinuria, transient hematuria and fat droplets  Complete remission following corticosteroid treatment  Serum albumin, cholesterol and triglycerides
  • 21. Thickened Basement Membrane Effaced foot processes Minimal change disease (MCD) characterized by effacement of the epithelial cell (podocyte) foot processes and loss of the normal charge barrier
  • 22. FOCAL SEGMENTAL GLOMERULONEPHRITIS  Disruption of podocytes in some areas of glomeruli associated with heroin, analgesic abuse and HIV  May resemble nephrotic syndrome or minimal change disease  Drugs of abuse and HIV test
  • 23. An area of collagenous sclerosis runs across the middle of this glomerulus Trichrome stain of a glomerulus in a patient with focal segmental glomerulosclerosis (FSGS) demonstrates blue collagen deposition.
  • 24. ALPORT SYNDROME  Inherited sex linked or autosomal disorder  Males before age 6 during a respiratory infection may exhibit macroscopic hematuria and continue to exhibit microscopic hematuria  Abnormal vision and hearing may be present
  • 25. DIABETIC NEPHROPATHY  a.k.a. Kimmelstiel-Wilson disease  Deposition of glycosylated proteins due to uncontrolled blood glucose level  Early monitoring of px with microalbuminuria is important  Most common cause of End Stage Kidney Disease.
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  • 27. ACUTE TUBULAR NECROSIS  Damage to renal tubular cells caused by ischemia or toxic agents  Reversible renal dysfunction  Microscopic hematuria, proteinuria, RTE cells and casts (hyaline, granular, broad and waxy)  Hemoglobin, hematocrit and cardiac enzymes
  • 29. FANCONI’S SYNDROME  Inherited or acquired through exposure to toxic agents, outdated tetracycline or complication of Multiple Myeloma.  Generalized defect in renal tubular reabsorption in proximal convoluted tubules  Glucosuria and possible cystine crystals  Serum and urine electrolytes, amino acid chromatography
  • 30. NEPHROGENIC DIABETES INSIPIDUS  Inherited sex-linked recessive or acquired from medication or as complication of PCKD or sickle cell anemia  Inability of renal tubules to respond to ADH causing polyuria  Urine is pale yellow, and with low specific gravity
  • 31. RENAL GLYCOSURIA  Generalized failure to reabsorb substances from glomerular filtrate, affecting the reabsorption of glucose  Increased urine glucose concentration with normal blood glucose.
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  • 34. CYSTITIS  Ascending bacterial infection of the bladder  Acute onset of urinary frequency and burning resolved with antibiotics  Leukocytoria, bacteruria, microscopic hematuria, mild proteinuria and increased pH  Urine culture
  • 35. ACUTE PYELONEPHRITIS  Renal tubulointerstitial infection related to interference of urine flow to the bladder, urine reflux or untreated cystitis  Acute onset of urinary frequency and burning resolved with antibiotics  Leukocytoria, bacteruria, Casts (WBC, bacterial, granular, waxy and broad) hematuria and proteinuria  Urine and blood cultures
  • 36. CHRONIC PYELONEPHRITIS  Recurrent renal tubulointerstitial infection caused by structural abnormalities affecting urine flow  Diagnosed in children and requires correction of structural defects  Leukocytoria, bacteruria, Casts (WBC, bacterial, granular, waxy and broad) hematuria and proteinuria  Urine and blood cultures, BUN, Creatinine and Creatinine clearance
  • 37. ACUTE INTERSTITIAL NEPHRITIS  Allergic inflammation of renal interstitium in response to certain medications  Acute onset of renal dysfunction accompanied by skin rash  Resolves with discontinuation of medication and treatment with corticosteroids  Hematuria, proteinuria, leukocyturia and WBC casts  Urine eosinophils, BUN, creatinine and creatinine clearance
  • 38. VASCULAR DISORDER  Renal ischemia and loss of functional renal tissue  Disorders that affect integrity of renal blood vessels: - Autoimmune disorders - Vaculitis - Diabetes mellitus
  • 39. RENAL LITHIASIS  May form in calyces and pelvis of KUB  Renal colic or flank pain  Vary from barely visible to staghorn calculi  75% compose of calcium oxalate and phosphates  Lithotripsy and surgery
  • 40. RENAL FAILURE  Exists in both acute and chronic forms  Gradual progression from the original disorder to end-stage renal disease Renal insufficiency Acute Renal Failure Chronic Renal Failure
  • 41. Acute Renal Failure Prerenal: decreased blood pressure and cardiac output, hemorrhage, burns, surgery and septicemia Renal: Acute glomerulonephritis, Acute tubular necrosis, Acute pyelonephritis, Acute interstitial necrosis Postrenal: Renal calculi, Tumors and Crytallization of ingested substances Chronic Renal Failure
  • 42. Chronic Renal Failure - marked decreased in GFR - rising BUN and creatinine (AZOTEMIA) - electrolyte imbalance - Isothenuria, proteinuria, glycosuria - Abundance of granular, wax and broad casts END-STAGE RENAL DISEASE
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