Unit 8 Flashcards
Glomeruler, Tubular, and Interstitial are examples of what kind of disease?
Renal Disease
deposited in the
glomerular membranes
Circulating IgA molecules
deposited in this site can
cause damage
Inflammatory cells
Components of the immune system (neutrophils, cytokines, etc.) are attracted to the deposit area, producing changes and damage to the membranes.
GLOMERULAR DISEASES
Non-immunologic components
- Exposure to chemicals/toxins
- Disruption of electrical membrane charges in
nephrotic syndrome
- Deposition of amyloid material
- Basement membrane thickening
GLOMERULAR DISEASES
- An inflammatory process that affects the glomerulus
- finding of blood, protein and casts in the urine
GLOMERULONEPHRITIS
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.
ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (APSGN)
low urine volume
Oliguria
positivity of protein in
the chemical examination of urine
Proteinuria
positive blood pads,
and intact RBCs
Hematuria
are the ones
commonly affected by APSGN
Children and young adults
Pathophysiology:
- Nephrogenic forms of the streptococci form immune complexes with their circulating antibodies and become deposited in the
glomerular membranes.
ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (APSGN)
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
ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (APSGN)
RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS (RPGN) is also called as
Cresenteric Glomerulonephritis
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
RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS (RPGN)
Laboratory Results
- Similar urine picture like in AGN
Clinical Manifestations
- Almost the same with AGN but with a more rapid
progression
RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS (RPGN)
One of the methods in renal pathology are
immunofluorscence
Morphological changes to the glomeruli like in RPGN in
conjunction with the autoimmune disorder termed
Goodpasture Syndrome
- 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
GOODPASTURE SYNDROME
Clinical:
- Hemoptysis
■ Pag spit ng dugo
■ Hematemesis = vomiting of blood
- Dyspnea
- Hematuria
GOODPASTURE SYNDROME
Urinalysis Results:
- Proteinuria
- Hematuria
- RBC Casts
GOODPASTURE SYNDROME
GRANULOMATOUS WITH POLYANGIITIS (GPA) formerly called
Wegener granulomatosis
- Due to antineutrophilic cytoplasmic antibodies (ANCA)
- Deposition of these antibodies in the vessel walls can initiate the immune response and induce granuloma
formation
GRANULOMATOUS WITH POLYANGIITIS (GPA)
Clinical Manifestations:
- Pulmonary symptoms then renal involvement
- Urinalysis: Proteinuria, hematuria, RBC Casts,
elevated creatinine and BUN
GRANULOMATOUS WITH POLYANGIITIS (GPA)
Method wherein we attach the antibody/antigen in the slide is
indirect immunofixation
Result of indirect immunofixation
Perinuclear Pattern = P-ANCA,
Cytoplasmic Pattern(granular) = C-ANCA
green fluorescence in the
periphery of the nucleus
perinuclear
dots within the cytoplasm
C-ANCA
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
- Thickening of the glomerular basement membrane
- Due to immune complex deposition (IgG)
MEMBRANOUS GLOMERULONEPHRITIS (MGN)
Associated with other diseases:
- Systemic Lupus Erythematosus (SLE)
- Sjogren Syndrome
- Secondary Syphilis
- Hepatitis B
- Au (gold) and Hg (mercury) treatments
- Malignancy
MEMBRANOUS GLOMERULONEPHRITIS (MGN)
Lab Findings:
- Microscopic hematuria
- Proteinuria
- RBC Casts may be seen
MEMBRANOUS GLOMERULONEPHRITIS (MGN)
- Marked by different alterations in the cellularity of the glomerulus and peripheral capillaries
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS (MGN)
- 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
- Dense deposits in the glomerular basement
membrane, tubules and Bowman Capsule. - Experience symptoms of chronic glomerulonephritis
Type 2 MGN
Children are most commonly affected
Clinical Findings:
- Hematuria
- Proteinuria
- Decreased serum complement levels
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS (MGN)
Both subendothelial and subepithelial deposits are present
Type 3 MGN
- When the damage to the glomerulus does not resolve or repeatedly happens
- Leads to end-stage renal disease
CHRONIC GLOMERULONEPHRITIS
Symptoms:
- Fatigue, anemia, hypertension, edema, and oliguria
CHRONIC GLOMERULONEPHRITIS
Lab findings:
- Broad Waxy Casts
- Hematuria
- Proteinuria
- Glucosuria
CHRONIC GLOMERULONEPHRITIS
IMMUNOGLOBULIN A NEPHROPATHY (IgA) is also known as
Berger disease
- Common in children
- Immune complexes of IgA deposits in the glomerular
membrane - Considered the most common cause of glomerulonephritis
IMMUNOGLOBULIN A NEPHROPATHY (IgA)
Lab Findings:
- Macroscopic Hematuria after infection or strenuous
exercise
IMMUNOGLOBULIN A NEPHROPATHY (IgA)
- Massive Proteinuria
- Low Levels of Albumin in Plasma
- High Levels of Serum Lipids
- Low plasma level in urine = kidney damage
NEPHROTIC SYNDROME
- 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
Urinalysis Findings:
- Marked proteinuria
- Urinary Fat Droplets
- Oval Fat Bodies
- Renal Tubular Epithelium
- Fatty and Waxy Casts
- Microscopic hematuria
NEPHROTIC SYNDROME
- 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)
Clinical Manifestations -Nephrotic Syndrome
- Edema
- Heavy Proteinuria
- Transient Hematuria
- Normal serum BUN and Creatinine
MINIMAL CHANGE DISEASE (MCD)
- 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)
- 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
Urine findings:
- Presence of Renal Tubular Epithelium
- Granular Casts
ACUTE TUBULAR NECROSIS
- 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
- Generalized failure of reabsorption in the Proximal
Convoluted Tubules - Inherited
- Associated with cystinosis and Hartnup Disease
FANCONI SYNDROME
Urinalysis Findings:
- Glycosuria with normal blood glucose
- Mild Proteinuria
- Very Low Urinary pH
FANCONI SYNDROME
- Inherited disorder of collagen production affecting the glomerular basement membrane
- X-linked recessive or autosomal recessive
- Mostly affected are males
ALPORT SYNDROME
Clinical Manifestations:
- Macroscopic hematuria
- Hearing and vision abnormalities
- Usually these symptoms appear after respiratory
infections in children
ALPORT SYNDROME
glycoprotein and is the only protein produced by the kidney—in the proximal and distal convoluted tubules
Uromodulin
- 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
- Currently the most common cause of end-stage renal disease
- deposition of glycosylated proteins resulting from poorly controlled blood
glucose.
DIABETIC NEPHROPATHY
Findings:
- Glomerular Basement Membrane Thickening
- Increased proliferation of mesangial cells
- Increased deposition of cellular and non-cellular
material within the glomerular matrix
DIABETIC NEPHROPATHY
Urine Findings:
- Microalbuminuria
- Some degree of glycosuria
DIABETIC NEPHROPATHY
- 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
exhibits a generalized
failure to reabsorb substances from the glomerular filtrate
Fanconi syndrome
affects only the reabsorption of glucose
renal glucosuria
- 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
most common renal disease
urinary tract
infection (UTI)
- involve the lower urinary tract (urethra and bladder)
- upper urinary tract (renal pelvis, tubules, and interstitium)
- infection of the bladder (cystitis)
URINARY TRACT INFECTION
Urinalysis:
- presence of numerous WBCs and bacteria
- mild proteinuria
and hematuria and an increased pH
URINARY TRACT INFECTION
seen more often in women and children, who present with symptoms of urinary frequency and burning
Cystitis
- 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
Symptoms:
- urinary frequency
- burning on urination
- lower back pain.
ACUTE PYELONEPHRITIS
- 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
Infection may happen due to reflux of urine from the
urinary bladder
vesicoureteral reflux
Urinary Findings:
- Numerous leukocytes
- Bacteria
- Mild proteinuria
- Mild hematuria
- WBC casts
acute pyelonephritis can be resolved without permanent damage to the tubules.
ACUTE PYELONEPHRITIS
- 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
- 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
- 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)
Clinical Manifestations:
- Oliguria
- Edema
- Decreased renal concentrating ability
- Possible decrease in the GFR
- Fever & skin rash
ACUTE INTERSTITIAL NEPHRITIS (AIN)
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)
Urinary Findings:
- Hematuria
- Mild to Moderate Proteinuria
- WBC casts without bacteria
- Eosinophils (Special Stains Needed)
ACUTE INTERSTITIAL NEPHRITIS (AIN)
- 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
ACUTE KIDNEY INJURY used to be called
Acute Renal Failure
- 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
- caused by lack of blood supply
- sudden decrease in blood flow to the kidney
prerenal
- caused by glomerular and tubular disorders
- acute glomerular and tubular disease
renal
- caused by obstructive disorders
- renal calculi or tumor obstructions
post renal
- 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
Urinary Findings
- Depending on the cause
- Casts are prevalent
ACUTE KIDNEY INJURY
- 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
may form in the calyces and pelvis of the kidney, ureters, and bladder.
Renal calculi (kidney stones)
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
Renal routine test: Stone analysis
RENAL LITHIASIS (KIDNEY STONES)
Conditions favoring calculi formation:
- Urinary tract infections (urea splitting bacteria)
- High pH (alkaline fluid)
RENAL LITHIASIS (KIDNEY STONES)
Composition of Renal Calculi:
- Calcium Oxalate
- Calcium Phosphate
- Magnesium Ammonium Phosphate
RENAL LITHIASIS (KIDNEY STONES)
