Unit 8 Flashcards
1
Q
Glomeruler, Tubular, and Interstitial are examples of what kind of disease?
A
Renal Disease
2
Q
deposited in the
glomerular membranes
A
Circulating IgA molecules
3
Q
deposited in this site can
cause damage
A
Inflammatory cells
4
Q
Components of the immune system (neutrophils, cytokines, etc.) are attracted to the deposit area, producing changes and damage to the membranes.
A
GLOMERULAR DISEASES
5
Q
Non-immunologic components
- Exposure to chemicals/toxins
- Disruption of electrical membrane charges in
nephrotic syndrome
- Deposition of amyloid material
- Basement membrane thickening
A
GLOMERULAR DISEASES
6
Q
- An inflammatory process that affects the glomerulus
- finding of blood, protein and casts in the urine
A
GLOMERULONEPHRITIS
7
Q
Clinical Findings:
- Sudden onset of symptoms consistent with damage to the glomerular membrane
- fever, edema, fatigue, nausea, hypertension, oliguria, proteinuria and hematuria
- Occurs usually after respiratory infections caused by Group A Beta-hemolytic streptococci that
contain M protein in the cell wall.
A
ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (APSGN)
8
Q
low urine volume
A
Oliguria
9
Q
positivity of protein in
the chemical examination of urine
A
Proteinuria
10
Q
positive blood pads,
and intact RBCs
A
Hematuria
11
Q
are the ones
commonly affected by APSGN
A
Children and young adults
12
Q
Pathophysiology:
- Nephrogenic forms of the streptococci form immune complexes with their circulating antibodies and become deposited in the
glomerular membranes.
A
ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (APSGN)
13
Q
Urinalysis Findings:
- Marked hematuria
- Proteinuria
- Red Blood Cell (RBC) Casts
- Dysmorphic RBCs
- Hyaline and Granular Casts
- White Blood Cells (WBC)
- Positive ASO and anti-DNase B
- Elevated BUN
A
ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (APSGN)
14
Q
RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS (RPGN) is also called as
A
Cresenteric Glomerulonephritis
15
Q
Pathophysiology:
- Deposition of immune complexes in the
glomerulus
- Damage by macrophages to the capillary walls
releases cells into the plasma into Bowmanʼs
Space = leads to the formation of “crescentsˮ
A
RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS (RPGN)
16
Q
Laboratory Results
- Similar urine picture like in AGN
Clinical Manifestations
- Almost the same with AGN but with a more rapid
progression
A
RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS (RPGN)
17
Q
One of the methods in renal pathology are
A
immunofluorscence
18
Q
Morphological changes to the glomeruli like in RPGN in
conjunction with the autoimmune disorder termed
A
Goodpasture Syndrome
19
Q
- Due to anti-glomerular basement membrane antibodies.
- An autoimmune disease
- Usually caused by viral infections
- Deposition of these antibodies trigger complement activation thus destruction of the membranes
- Progression to End-Stage Renal Failure is common
A
GOODPASTURE SYNDROME
20
Q
Clinical:
- Hemoptysis
■ Pag spit ng dugo
■ Hematemesis = vomiting of blood
- Dyspnea
- Hematuria
A
GOODPASTURE SYNDROME
21
Q
Urinalysis Results:
- Proteinuria
- Hematuria
- RBC Casts
A
GOODPASTURE SYNDROME
22
Q
GRANULOMATOUS WITH POLYANGIITIS (GPA) formerly called
A
Wegener granulomatosis
23
Q
- Due to antineutrophilic cytoplasmic antibodies (ANCA)
- Deposition of these antibodies in the vessel walls can initiate the immune response and induce granuloma
formation
A
GRANULOMATOUS WITH POLYANGIITIS (GPA)
24
Q
Clinical Manifestations:
- Pulmonary symptoms then renal involvement
- Urinalysis: Proteinuria, hematuria, RBC Casts,
elevated creatinine and BUN
A
GRANULOMATOUS WITH POLYANGIITIS (GPA)
25
Method wherein we attach the antibody/antigen in the slide is
indirect immunofixation
26
Result of indirect immunofixation
Perinuclear Pattern = P-ANCA,
Cytoplasmic Pattern(granular) = C-ANCA
27
green fluorescence in the
periphery of the nucleus
perinuclear
28
dots within the cytoplasm
C-ANCA
29
Occurs primarily in children
Clinical Manifestations:
- Red, raised patches in the ski
- Respiratory and gastrointestinal symptoms
- Blood in the sputum and stools
- Renal disease manifestation is a serious complication of this disease
HENOCH-SCHONLEIN PURPURA
30
- Thickening of the glomerular basement membrane
- Due to immune complex deposition (IgG)
MEMBRANOUS GLOMERULONEPHRITIS (MGN)
31
Associated with other diseases:
- Systemic Lupus Erythematosus (SLE)
- Sjogren Syndrome
- Secondary Syphilis
- Hepatitis B
- Au (gold) and Hg (mercury) treatments
- Malignancy
MEMBRANOUS GLOMERULONEPHRITIS (MGN)
32
Lab Findings:
- Microscopic hematuria
- Proteinuria
- RBC Casts may be seen
MEMBRANOUS GLOMERULONEPHRITIS (MGN)
33
- Marked by different alterations in the cellularity of the glomerulus and peripheral capillaries
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS (MGN)
34
- Increased cellularity in the subendothelial cells of the mesangium (interstitial area of Bowman Capsule) causing thickening of the capillary walls
- Progress to nephrotic syndrome
Type 1 MGN
35
- Dense deposits in the glomerular basement
membrane, tubules and Bowman Capsule.
- Experience symptoms of chronic glomerulonephritis
Type 2 MGN
36
Children are most commonly affected
Clinical Findings:
- Hematuria
- Proteinuria
- Decreased serum complement levels
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS (MGN)
37
Both subendothelial and subepithelial deposits are present
Type 3 MGN
38
- When the damage to the glomerulus does not resolve or repeatedly happens
- Leads to end-stage renal disease
CHRONIC GLOMERULONEPHRITIS
39
Symptoms:
- Fatigue, anemia, hypertension, edema, and oliguria
CHRONIC GLOMERULONEPHRITIS
40
Lab findings:
- Broad Waxy Casts
- Hematuria
- Proteinuria
- Glucosuria
CHRONIC GLOMERULONEPHRITIS
41
IMMUNOGLOBULIN A NEPHROPATHY (IgA) is also known as
Berger disease
42
- Common in children
- Immune complexes of IgA deposits in the glomerular
membrane
- Considered the most common cause of glomerulonephritis
IMMUNOGLOBULIN A NEPHROPATHY (IgA)
43
Lab Findings:
- Macroscopic Hematuria after infection or strenuous
exercise
IMMUNOGLOBULIN A NEPHROPATHY (IgA)
44
- Massive Proteinuria
- Low Levels of Albumin in Plasma
- High Levels of Serum Lipids
- Low plasma level in urine = kidney damage
NEPHROTIC SYNDROME
45
- The “shield of negativityˮ is compromised which results in the passage of high molecular weight particles like albumin and lipids.
- can progress into chronic renal failure.
NEPHROTIC SYNDROME
46
Urinalysis Findings:
- Marked proteinuria
- Urinary Fat Droplets
- Oval Fat Bodies
- Renal Tubular Epithelium
- Fatty and Waxy Casts
- Microscopic hematuria
NEPHROTIC SYNDROME
47
- Little changes in the glomerulus are seen but there is damage in the podocytes and the shield of negativity
- Most common cause of nephrotic syndrome in children
MINIMAL CHANGE DISEASE (MCD)
48
Clinical Manifestations -Nephrotic Syndrome
- Edema
- Heavy Proteinuria
- Transient Hematuria
- Normal serum BUN and Creatinine
MINIMAL CHANGE DISEASE (MCD)
49
- Affects only a portion of the glomerulus
- Can be idiopathic
- can also be caused by exogenous substances (drugs)
- Commonly seen in HIV patients, heroin addicts, patients infected with hepatitis viruses
Common laboratory findings:
- Immune deposits – IgM and C3
FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS)
50
- Due to lack of oxygen
- Any condition than can reduce the blood volume
coming into the kidneys
- Toxins
- Certain Drugs
- Some Endogenous Substances (e.g. Ketone bodies, hemoglobin)
ACUTE TUBULAR NECROSIS
51
Urine findings:
- Presence of Renal Tubular Epithelium
- Granular Casts
ACUTE TUBULAR NECROSIS
52
- Conditions that affect or override the tubular reabsorptive maximum
- Failure to inherit a gene or genes that is required for tubular reabsorption
HEREDITARY AND METABOLIC TUBULAR DISORDERS
53
- Generalized failure of reabsorption in the Proximal
Convoluted Tubules
- Inherited
- Associated with cystinosis and Hartnup Disease
FANCONI SYNDROME
54
Urinalysis Findings:
- Glycosuria with normal blood glucose
- Mild Proteinuria
- Very Low Urinary pH
FANCONI SYNDROME
55
- Inherited disorder of collagen production affecting the glomerular basement membrane
- X-linked recessive or autosomal recessive
- Mostly affected are males
ALPORT SYNDROME
56
Clinical Manifestations:
- Macroscopic hematuria
- Hearing and vision abnormalities
- Usually these symptoms appear after respiratory
infections in children
ALPORT SYNDROME
57
glycoprotein and is the only protein produced by the kidney—in the proximal and distal convoluted tubules
Uromodulin
58
- An inherited disorder caused by an autosomal mutation in the gene that produces uromodulin
- decrease in the production of normal uromodulin that is replaced by the abnormal form
- Accumulation of this abnormal form results in the
destruction of the tubular cells
- also results in an increase in serum uric acid
UROMODULIN-ASSOCIATED KIDNEY DISEASE
59
- Currently the most common cause of end-stage renal disease
- deposition of glycosylated proteins resulting from poorly controlled blood
glucose.
DIABETIC NEPHROPATHY
60
Findings:
- Glomerular Basement Membrane Thickening
- Increased proliferation of mesangial cells
- Increased deposition of cellular and non-cellular
material within the glomerular matrix
DIABETIC NEPHROPATHY
61
Urine Findings:
- Microalbuminuria
- Some degree of glycosuria
DIABETIC NEPHROPATHY
62
- Tubules not responding to Anti-Diuretic Hormone
- Inherited as sex-linked recessive
- Can also be acquired (due to drug toxicity) lithium &
amphotericin B
- Can also be a complication of certain diseases such as
sickle-cell disease and polycystic kidney disease
NEPHROGENIC DIABETES INSIPIDUS
63
exhibits a generalized
failure to reabsorb substances from the glomerular filtrate
Fanconi syndrome
64
affects only the reabsorption of glucose
renal glucosuria
65
- Inherited renal glucosuria
- Lack of production of the receptors for glucose in the
tubules thus resulting in faulty reabsorption of glucose in the
tubular fluid
- Results in glucosuria
RENAL GLYCOSURIA
66
most common renal disease
urinary tract
infection (UTI)
67
- involve the lower urinary tract (urethra and bladder)
- upper urinary tract (renal pelvis, tubules, and interstitium)
- infection of the bladder (cystitis)
URINARY TRACT INFECTION
68
Urinalysis:
- presence of numerous WBCs and bacteria
- mild proteinuria
and hematuria and an increased pH
URINARY TRACT INFECTION
69
seen more often in women and children, who present with symptoms of urinary frequency and burning
Cystitis
70
- term used to refer to infection of the upper urinary tract including the tubules and the interstitium
- ascending movement infection of bacteria most of the time from the lower urinary tract into the renal tubules and interstitium
ACUTE PYELONEPHRITIS
71
Symptoms:
- urinary frequency
- burning on urination
- lower back pain.
ACUTE PYELONEPHRITIS
72
- ascending movement of bacteria from the bladder is
enhanced with conditions that interfere with the downward flow of urine from the ureters to the bladder
ACUTE PYELONEPHRITIS
73
Infection may happen due to reflux of urine from the
urinary bladder
vesicoureteral reflux
74
Urinary Findings:
- Numerous leukocytes
- Bacteria
- Mild proteinuria
- Mild hematuria
- WBC casts
acute pyelonephritis can be resolved without permanent damage to the tubules.
ACUTE PYELONEPHRITIS
75
- Due to continuous infection (unresolved/untreated)
- serious disorder that can result in permanent damage to the renal tubules and possible progression to chronic renal failure.
- Some congenital malformations in the urinary tract can
result to this condition.
CHRONIC PYELONEPHRITIS
76
- Manifestations and urinary findings are almost the same in
the acute form, particularly in the early stages.
- WBC Casts, Broad and Waxy casts
CHRONIC PYELONEPHRITIS
77
- Inflammation of the renal interstitium followed by the
inflammation of the renal tubules
- Ultimately results in the kidneys losing the ability to
concentrate the urine
- Differential leukocyte staining for the
presence of increased eosinophils
ACUTE INTERSTITIAL NEPHRITIS (AIN)
78
Clinical Manifestations:
- Oliguria
- Edema
- Decreased renal concentrating ability
- Possible decrease in the GFR
- Fever & skin rash
ACUTE INTERSTITIAL NEPHRITIS (AIN)
79
Primarily associated with an allergic reaction to medications:
- Penicillin
- Methicillin
- Ampicillin
- Cephalosporins
- Sulfonamides
- NSAIDs (Non-steroidal anti-inflammatory drugs like
ibuprofen)
- Thiazide Diuretics
ACUTE INTERSTITIAL NEPHRITIS (AIN)
80
Urinary Findings:
- Hematuria
- Mild to Moderate Proteinuria
- WBC casts without bacteria
- Eosinophils (Special Stains Needed)
ACUTE INTERSTITIAL NEPHRITIS (AIN)
81
- Marked decrease in GFR (less than 25 mL/min)
- Steadily rising serum BUN and Creatinine (azotemia)
- Electrolyte Imbalance
- Lacks concentrating ability
- Proteinuria
- Renal Glycosuria
- Abundance of granular, waxy and broad casts
RENAL FAILURE
82
ACUTE KIDNEY INJURY used to be called
Acute Renal Failure
83
- Constellation of disorders which arises in a short period of time
- exhibits a sudden loss
of renal function and frequently is reversible
- decreased glomerular filtration rate, oliguria, edema, and azotemia.
ACUTE KIDNEY INJURY
84
- caused by lack of blood supply
- sudden decrease in blood flow to the kidney
prerenal
85
- caused by glomerular and tubular disorders
- acute glomerular and tubular disease
renal
86
- caused by obstructive disorders
- renal calculi or tumor obstructions
post renal
87
- presence of RTE cells and casts suggests ATN
of prerenal origin
- RBCs indicate glomerular injury
- WBC casts, with or without bacteria, indicate interstitial infection
ACUTE KIDNEY INJURY
88
Urinary Findings
- Depending on the cause
- Casts are prevalent
ACUTE KIDNEY INJURY
89
- Constellation of disorders due to unresolved injuries in the kidney occurring for a considerable period of time
- Progression of failure (ESRD)
- Common causes are diabetes.
CHRONIC RENAL FAILURE
90
may form in the calyces and pelvis of the kidney, ureters, and bladder.
Renal calculi (kidney stones)
91
the calculi
vary in size from barely visible to large, staghorn calculi resembling the shape of the renal pelvis and smooth, round bladder stones with diameters of 2 or more inches.
renal lithiasis
92
Renal routine test: Stone analysis
RENAL LITHIASIS (KIDNEY STONES)
93
Conditions favoring calculi formation:
- Urinary tract infections (urea splitting bacteria)
- High pH (alkaline fluid)
RENAL LITHIASIS (KIDNEY STONES)
94
Composition of Renal Calculi:
- Calcium Oxalate
- Calcium Phosphate
- Magnesium Ammonium Phosphate
RENAL LITHIASIS (KIDNEY STONES)
