Professional Documents
Culture Documents
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A Little Higher Please The Details
Immunological injury
Glomerulus
Interstitial tissue
Vascular injury or compromise
Diabetes
Hypertension
Infections
Upper urinary tract
Lower urinary tract
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Nephritic Syndrome
Clinical Syndromes
Acute injury, multiple
possible causes
Nephritic syndrome Major, acute injury to
the glomerular
Nephrotic syndrome basement membrane.
Basic clinical pattern
Chronic renal failure
RBCs in the urine
Localized pain RBC casts in urine
Decreased urine output
Increased protein
Increased B/P
Urinary Casts
Clinical Syndromes
Material cleared or shed
by a sick glomerulus.
Congeals within the
Convoluted tubules or Nephritic syndrome
Collecting ducts
Nephrotic syndrome
Creates a ‘cast’ of the
interior of the duct it Chronic renal failure
formed in. Localized pain
Is Cleared in urine.
Observed
microscopically
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Glomerulonephritis General Features
Mesangial cell
proliferation
Leukocyte
infiltration
BM thickening
Regular
(linear)
Irregular
(lumpy)
Follows Streptoccocal
infection
Antigen-
Antigen-antibody
complexes lodge
beneath the foot
processes.
Elicit a flaming
inflammatory reaction
Complement deposited
Huge holes in BM
Nephritic syndrome
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Membranous Glomerulonephritis
Acute Glomerulonephritis
Slow accumulation of Ag-
Ag-Ab complexes
Anti- Small holes, but numerous
Anti-human IgG
Anti-
Anti-human IgG Antibodies specifically
against BM
labeled with
Different from immune
fluorescence.
complex disease.
Identifies the Starts as a pulmonary
immune complexes infection (virus).
Linear pattern Make antibodies against
Smooth contours pulmonary BM
Smaller holes Cross reacts with
glomerular BM
Protein loss
No RBC loss
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Minimal Change Glomerulonephritis
Non-
Non-Enzymatic Glycosylation IgA Nephropathy
Glucose sticks to, and
alters, all sorts of proteins.
No way of getting rid of the Mesangial deposits of
modified protein. IgA antibodies.
BMs especially Mid 20’s
Small vessels narrow Multiple episodes of
Glomerular BM hematuria.
Thickens
Becomes inefficient More common than
Loss of protein once thought
Renal failure Transplant
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Tubular and Interstitial Disease
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Chronic Pyelonephritis Renal Papillary Necrosis
Vascular
insufficiency. Death of the papillae
Arteriolar problem
Slough and obstruct
Chronic ureter
inflammation
Round cells Inflammatory and/or
Tissue destruction vascular causes
Fibrosis Diabetes
Diabetes Analgesic nephropathy
Hypertension Chronic pyelonephritis
Repeat infections
‘Thyroidization’
Arteriolar changes
Onion skinning
Loss of luminal size
Reduced blood flow
Release of renin
Higher blood pressure
Chronic pyelonephritis
In time renal failure
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Cystic Disease Tumors of the kidney
Polycystic renal disease
Growth of tubular
Benign vs. malignant
epithelium causes cyst
formation. Primary vs. metastatic
Cysts accumulate fluid
and squeeze the rest of
the kidney out of
existence.
Adult and juvenile forms
Infections
Stones
Cancer
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Bladder Infections Kidney Stones
Large calculus
Transition cell
Hydronephrotic kidney origin
Tobacco
Industrial
chemicals
Hematuria
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