Strasinger AUBF - Renal Diseases
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Glomerular disease
cellular infiltration damage
proliferation damage
Glomerulonephritis
Glomerulonephritis
Acute glomerulonephritis
Rapidly progressive glomerulonephritis
Goodpasture syndrome
Wegener granulomatosis
Henoch-Schonlein purpura
Membranous glomerulonephritis
Membranoproliferative glomerulonephritis
Chronic glomerulonephritis
IgA nephropathy
Nephrotic syndrome
Minimal change disease
Focal segmental glomerulosclerosis
Alport syndrome
Acute glomerulonephritis
Rapidly progressive glomerulonephritis
Goodpasture syndrome
Wegener granulomatosis
Henoch-Schonlein purpura
Membranous glomerulonephritis
Membranoproliferative glomerulonephritis
Chronic glomerulonephritis
IgA nephropathy
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Immune complexes formed are deposited on the glomerular
membranes
Complement-mediated damage to the capillaries and basement
membrane
Thickening of the glomerular basement membrane
Sterile, inflammatory process that affects the glomerulus
Associated with the finding of blood, protein, and casts in the urine
Deposition of immune complexes, formed in conjunction with
group A streptococci infection, on the glomerular membranes
deposition of immune complexes from systemic immune disorders
on the glomerular membrane
Attachment of a cytotoxic antibody formed during viral respiratory
infections to glomerular and alveolar basement membrane
Antineutrophilic cytoplasmic autoantibody binds to neutrophils in
vascular walls producing damage to small vessels in the lungs and
glomerulus
Occurs primarily in children following viral respiratory infections; a
decrease in platelets disrupts vascular integrity
Thickening of the glomerular membrane following IgG immune
complex deposition associated with systemic disorders
Cellular proliferation affecting the capillary walls or the glomerular
basement membrane, possibly immune-mediated
Marked decrease in renal function resulting from glomerular dam-
age precipitated by other renal disorders
Deposition of IgA on the glomerular membrane resulting from
increased levels of serum IgA
Disruption of the shield of negativity and damage to the tightly
fitting podocyte barrier resulting in massive loss of protein and
lipids
Disruption of the podocytes occurring primarily in children follow-
ing allergic reactions and immunizations
Disruption of podocytes in certain areas of glomeruli associated
with heroin and analgesic abuse and AIDS
Genetic disorder showing lamellated and thinning glomerular
basement membrane
Rapid onset of hematuria and edema, permanent renal damage
seldom occurs
Rapid onset with glomerular damage and possible progression to
end-stage renal failure
Hemoptysis and dyspnea followed by hematuria with possible
progression to end-stage renal failure
Pulmonaary symptoms including hemoptysis develop first fol-
lowed by renal involvement and possible progression to end-stage
renal failure
Initial appearance of purpura followed by blood in sputum and
stools and eventual renal involvement
Slow progression to the nephrotic syndrome or possible remission
Slow progression to chronic glomerulonephritis or nephrotic syn-
drome
Noticeable decrease in renal function progressing to renal failure
Strasinger AUBF - Renal Diseases
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Nephrotic syndrome
Minimal change disease
Focal segmental glomerulosclerosis
Alport syndrome
p-ANCA
c-ANCA
Immunoglobulin A Nephropathy
Acute tubular necrosis
Acute tubular necrosis
Fanconi Syndrome
Fanconi Syndrome
Uromodulin-associated kidney disease
Uromodulin-associated kidney disease
Nephrogenic diabetes insipidus
Nephrogenic diabetes insipidus
Renal glucosuria
Renal glucosuria
Tubulointerstitial disease
Urinary tract infection
Cystitis
Cystitis
Acute pyelonephritis
Acute pyelonephritis
Chronic pyelonephritis
Chronic pyelonephritis
Acute interstitial nephritis
Acute interstitial nephritis
Acute renal failure
End-stage renal disease
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Recurrent macroscopic hematuria following exercise with slow
progression to chronic glomerulonephritis
Acute onset following systemic shock
Frequent complete remission following corticosteroid treatment
May resemble nephrotic syndrome or minimal change disease
Slow progression to nephrotic syndrome and end-stage renal
disease
Perinuclear pattern formed by the antibodies, formed when neu-
trophils are ethanol fixed
Granular pattern throughout the cytoplasm when neutrophils are
formalin fixed
Also known as Berger disease
Damage to renal tubular cells caused by ischemia or toxic agents
Acute onset of renal dysfunction usually resolved when underlying
cause is corrected
Inherited in association with cystinosis and Hartnup disease or
acquired through exposure to toxic agents
Generalized defect in renal tubular reabsorption requiring sup-
portive therapy
Inherited defect in the production of normal uromodulin by the
renal tubules and increased uric acid causing gout
Continual monitoring of renal function for progression to renal
failure and possible kidney transplantation
Inherited defect of tubular response to ADH or acquired from
medications
Requires supportive therapy to prevent dehydration
Inherited autosomal recessive trait
Benign disorder
Condition caused by disorders affecting the interstitium that also
affects the tubules
Most common renal disease
Ascending bacterial infection of the bladder
Acute onset of urinary frequency and burning resolved with antibi-
otics
Infection of the renal tubules and interstitium related to interfer-
ence of urine flow to the bladder, and untreated cystitis
Acute onset of urinary frequency, burning, and lower back pain
resolved with antibiotics
Recurrent infection of the renal tubules and interstitium caused by
structural abnormalities affecting the flow of urine
Frequently diagnosed in children; requires correction of the un-
derlying structural defect
Allergic inflammation of the renal interstitium in response to cer-
tain medications
Acute onset of renal dysfunction often accompanied by a skin rash
but resolves following discontinuation of medication and treatment
with corticosteroids
exhibit sudden loss of renal function and is reversible
characterized by a marked decrease in glomerular filtration rate
(<25 mL/min)
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Prerenal causes of Acute Renal Failure
Renal causes of Acute Renal Failure
Postrenal causes of Acute Renal Failure
Renal lithiasis
Lithotripsy
Calcium calculi
Magnesium ammonium phosphate calculi
Uric acid calculi
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Decreased blood pressure / cardiac output, Hemorrhage, Burns,
Surgery, Septicemia
Acute glomerulonephritis, Acute tubular necrosis, Acute
pyelonephritis, Acute interstitial nephritis
Renal calculi, tumors
kidney stones
procedure using high-energy shock waves, used to break stones
located in the upper urinary tract into pieces that can then be
passed in the urine
Frequently associated with metabolic calcium and phosphate dis-
orders and occasionally diet
Frequently accompanied by urinary infections involving urea-split-
ting bacteria
Associated with increased intake of foods with high purine content
and with uromodulin-associated kidney disease