Pathology of the Kidney

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Pathology of the Kidney and Its Collecting System
Dr. Francisco G. La RosaFrancisco.LaRosa_at_UCHSC.ed
u
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Embriology of the Kidney and Collecting System
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Anatomy of the Kidney
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KIDNEY FunctionsExcretion of waste
productsRegulation of water and saltMaintenance
of acid balanceSecretion of hormones and
by-products Structures and DiseasesGlomeruli
(immune damage)Tubuli (toxic or
infections)Interstitium (toxic or
infections)Blood vessels (metabolic)
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CLINICAL MANIFESTATIONSOF RENAL
DISEASE Syndromes Acute Nephritic
syndromeNephrotic syndromeAsymptomatic
hematuria Asymptomatic proteinuriaAcute renal
failureChronic renal failureUrinary tract
infection (UTI)NephrolitiasisTumors
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GLOMERULAR DISEASES Primary GlomerulonephritisAc
ute diffuse proliferative GNRapidly progressive
GNMembranous GNLipoid nephrosis (minimal change
disease)Focal segmental glomerulosclerosisMembra
noproliferative GNIgA NephropathyChronic
GNSecondary (Systemic) DiseasesSystemic lupus
erythematosusDiabetes mellitusAmyloidosisGoodpa
stures syndromePolyarteritis nodosaWageners
granulomatosisHenoch-Scholein purpuraBacterial
endocarditis Hereditary DisordersAlports
syndromeFabrys disease
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Ischemia / Toxins
Tubular Injury
Intrarenal Vasoconstriction (Increased
Endothelin decreased NO)
Tubule Obstruction
Back- Leakage
Reduced Glomerular Plasma Flow
Reduced O2 delivery to Outer Medulla
Increased Intratubular Pressure
? Direct Glomerular Effect
Reduced GFR ?
Oliguria
Acute Renal Failure
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Schematic Representation of a Glomerular Lobe
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Low-power electron micrograph of rat glomerulus
CL, capillary lumen End, endothelium Mes,
mesangium B, basement membrane Ep, visceral
epithelial cells with foot processes US,
urinary space.
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Antibody-mediated glomerular injury (A)
Circulating Ag-Ab complexes, (B) Anti-basement
membrane, (C) In situ Ag-Ab complexes.
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Albumin
Epithelial cell injury and destruction of the
basement membraneas a result of immune complex
in the glomerulus.Normally, the basement cell
membrane does not filter large molecules such
asalbumin (70,000 kD), which is present in urine
if the membrane is damaged.
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• NEPHROTIC SYNDROME
• Proteinuria (3.5 g/day)
• General edema
• Hypoalbuminemia (
• Hyperlipidemia
• Lipiduria

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Lipoid Nephrosis (A and C) and Membranous
Glomerulonephritis (B and D).
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Nephrotic syndrome
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IgA Nephropathy Focal mesangialproliferativeglom
erulonephritis
Immunofluorescence in the glomeruliIgG , IgA
(shown here), IgM Negative,and C3 .
IgA
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IgA Nephropathy
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Acute Nephritic Syndrome
C3
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Acute Nephritic Syndrome
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Cast
Proliferation, glomerular crescents, necrosis
IgG linear pattern
Fibrinogen
Acute nephritic syndrome Goodpasture's syndrome
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• Membranoproliferative Glomerulonephritis (MGN)
  Mesangial proliferation, basement membrane
• thickening, leukocyte infiltration and
  accentuation of lobular architecture.
• (B) Type I and Type II MGN .

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IgG
Proliferative Glomerulonephritis Systemic Lupus
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Tubular and InterstitialDiseases Tubulointerstit
ial NephritisAcute pyelonephritisChronic
pyelonephritis Drug-Induced interstitial
nephritis Acute tubular necrosis
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Pathways of Renal Infection
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Acute Cystitis
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Hydronephrosis andchronic obstructive
pyelonephritis
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Chronic pyelonephritis
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Vascular Diseases Benign nephrosclerosis Malignan
t hypertension/Malignant nephrosclerosis Thrombot
ic microangiopathies
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Malignant hypertension leads tofibrinoid
necrosis of small arteries.The damage to the
arteries leads toformation of pink fibrin--
hence the term "fibrinoid".
Thickening of the arterial wallwith malignant
hypertension produces a hyperplastic
arteriolitis.The arteriole has an "onion skin"
appearance
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CONTINUE IN LECTURE 2
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