CHAPTER 8: RENAL DISEASE Flashcards
Deposition of immune complexes, in conjunction with streptococcal Infection, on the glomerular membrane
Acute or Post-streptococcal
Glomerulonephritis
Deposition of immune complexes from systemic immune disorders on the glomerular membrane
Rapidly Progressive Glomerulonephritis
Attachment of a cytotoxic antibody formed during viral respiratory infections to glomerular and alveolar
basement membranes
Goodpasture’s Syndrome
Binding of antineutrophilic cytoplasmic antibody to neutrophils in vessel walls
Wegener’s Granulomatosis
Disruption of vascular integrity
following viral respiratory infections
Henoch-Schonlein Purpura
Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA
IgA Nephropathy
Thickening of the glomerular membrane following IgG immune complex deposition associated with systemic disorders
Membranous Glomerulonephritis (MGN)
Type of MPGN that displays increased cellularity in the subendothelial cells of the mesangium (interstitial area of Bowman capsule), causing thickening of the capillary walls
Type 1 Membranoproliferative glomerulonephritis (MPGN)
Type of MPGN that displays extremely dense deposits in the glomerular basement membrane, tubules, and Bowman capsule
Type 2 Membranoproliferative glomerulonephritis (MPGN)
Type of MPGN that is characterized by both subepithelial and subendothelial deposits
Type 3 Membranoproliferative glomerulonephritis (MPGN)
Refers to a sterile, inflammatory process that affects the glomerulus and is associated with the finding of blood, protein, and casts in the urine
Glomerulonephritis
Marked by the sudden onset of symptoms consistent with damage to the glomerular membrane
Acute glomerulonephritis (AGN)
Symptoms usually occur in children and young adults after respiratory infections caused by certain strains of group A β-hemolytic streptococci that contain M protein in the cell wall
Acute glomerulonephritis (AGN)
Primary urinalysis findings include marked hematuria, proteinuria, and oliguria, accompanied by red blood cell (RBC) casts, dysmorphic RBCs, hyaline and granular casts, and white blood cells (WBCs)
Acute glomerulonephritis (AGN)
These are a hallmark characteristic of acute glomerulonephritis
RBC casts
Formerly called Wegener granulomatosis
Granulomatosis with polyangiitis (GPA)
This autoantibody can be detected in a patient’s serum
Antiglomerular basement membrane antibody
Initial laboratory results are similar to AGN but become
more abnormal as the disease progresses, including protein levels that are markedly elevated and glomerular filtration rates
that are very low
Rapidly Progressive (or crescentic) Glomerulonephritis (RPGN)
Key to the diagnosis of GPA is the
demonstration of?
Antineutrophilic cytoplasmic antibody (ANCA) in the patient’s serum
If the neutrophils are fixed in ethanol, the antibodies form a perinuclear pattern which is called?
p-ANCA
This includes incubating the patient’s serum with either ethanol or formalin/formaldehyde-fixed neutrophils and examining the preparation using indirect immunofixation to detect the serum antibodies attached to the neutrophils
ANCA for GPA
This disease occurs primarily in children after upper respiratory infections.
Henoch-Schönlein Purpura
When the neutrophils are fixed with formalin/formaldehyde, the pattern is granular
throughout the cytoplasm and is referred to as
c-ANCA
Cellular proliferation affecting the capillary walls or the glomerular basement membrane
Membranoproliferative Glomerulonephritis
A marked decrease in renal function resulting from glomerular damage precipitated by other renal disorders
Chronic Glomerulonephritis
Disruption of the electrical charges that produce the tightly fitting podocyte barrier resulting in a massive loss of protein and lipids
Nephrotic Syndrome
Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic abuse and with HIV and hepatitis viruses
Focal Segmental Glomerulosclerosis
Disruption of the podocytes that occurs primarily in children after allergic reactions and immunizations; dysfunction of T-cell immunity
Minimal Change Disease (MCD)
Ascending bacterial infection of the bladder
Cystitis
Complete recovery with normal renal function is seen in more than 50% of patients.
In other patients, progression to a more serious form of glomerulonephritis and renal failure may occur
Henoch-Schönlein Purpura
Its predominant characteristic is a pronounced thickening of the glomerular basement membrane resulting from the deposition of immunoglobulin G immune complexes
Membranous Glomerulonephritis
Their presence is often seen in chronic glomerulonephritis that progresses to ESRD
Broad casts
Also known as Berger disease
IgA nephropathy
The most common cause of glomerulonephritis.
IgA nephropathy
Marked by massive proteinuria (greater than 3.5 g/day), low levels of serum albumin, high levels of serum lipids, and pronounced edema
Nephrotic syndrome
Genetic disorder showing lamellated and thinning glomerular basement membrane
Alport syndrome
Acute onset after systemic shock
Gradual progression from other glomerular disorders and then to renal failure
Nephrotic syndrome (NS)
Frequent complete remission after corticosteroid treatment
Minimal change disease (MCD)
It may resemble nephrotic syndrome (NS) or minimal change disease (MCD)
Focal segmental glomerulosclerosis (FSGS)
Slow progression to nephrotic syndrome (NS) and end-stage renal disease
Alport syndrome
Hemoptysis and dyspnea followed by hematuria
Goodpasture syndrome
Their presence in the urine sediment is characteristic
for ATN
RTE cell casts and RTE cells
Demonstration of positive results of these tests provides evidence that the disease is of streptococcal origin (2pts)
Anti–group A streptococcal enzyme tests (antistreptolysin O [ASO] and
Antideoxyribonuclease-B antibody [anti-DNase B])
These are under the Acute Poststreptococcal Glomerulonephritis