|
Hint
|
Answer
|
|
Deposition of immune complexes, formed in conjunction with beta-hemolytic group A Streptococcus infection, on the glomerular membranes
|
Acute Poststreptococcal 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 syndrome
|
|
Antineutrophilic cytoplasmic autoantibody (ANCA) binds to neutrophils in vascular walls, producing damage to small vessels in the lungs and glomerulus
|
Wegener’s granulomatosis
|
|
Occurs primarily in children after viral respiratory infections; a decrease in platelets disrupts vascular integrity
|
Henoch-Schonlein Purpura
|
|
Thickening of the glomerular membrane after IgG immune complex deposition associated with systemic disorders
|
Membranous Glomerulonephritis
|
|
Cellular proliferation affecting the capillary walls or the glomerular basement membrane, possibly immune mediated
|
Membranoproliferative Glomerulonephritis
|
|
Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA
|
IgA Nephropathy
|
|
Marked decrease in renal function resulting from glomerular damage precipitated by other renal disorders
|
Chronic Glomerulonephritis
|
|
Disruption of the podocytes occurring primarily in children after allergic reactions and immunizations; dysfunction of T-cell immunity
|
Minimal change disease
|
|
Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic abuse and with HIV and hepatitis viruses
|
Focal segmental glomerulosclerosis
|
|
Genetic disorder showing lamellated and thinning glomerular basement membrane
|
Alport syndrome
|
|
Most common cause of End Stage Renal Disease
|
Diabetic Nephropathy
|
|
Damage to the glomerular membrane occurs as a result of glomerular membrane thickening and increased deposition of cellular and noncellular material within the glomerular matrix.
|
Diabetic Nephropathy
|
|
Damage to renal tubular cells caused by ischemia or toxic agents
|
Acute tubular necrosis
|
|
Inherited in association with cystinosis and Hartnup disease or acquired through exposure to toxic agents
|
Fanconi syndrome
|
|
Inherited defect in the production of normal uromodulin by the renal tubules and increased uric acid causing gout
|
Uromodulin-associated kidney disease
|
|
Inherited defect of tubular response to ADH or acquired from medications
|
Nephrogenic diabetes insipidus (DI)
|
|
Inherited autosomal recessive trait
|
Renal glucosuria
|
|
Infection of the renal tubules and interstitium related to interference of urine flow to the bladder, reflux of urine from the bladder, and untreated cystitis
|
Acute pyelonephritis
|
|
Recurrent infection of the renal tubules and interstitium caused by structural abnormalities affecting the flow of urine
|
Chronic pyelonephritis
|
|
Allergic inflammation of the renal interstitium in response to certain medications
|
Acute interstitial nephritis
|
|
Ascending bacterial infection of the bladder
|
Cystitis
|
|
enzyme deficient in phenylketonuria
|
Phenylalanine hydroxylase
|
|
FeCl3 tube test color in PKU
|
blue-green
|
|
Confirmatory test for PKU
|
Ion exchange HPLC
|
|
Enzyme deficient in Type 1 Tyrosinemia/Tyrosyluria
|
Fumarylacetoacetate hydrolase
|
|
Enzyme deficient in Type 2 Tyrosinemia/Tyrosyluria
|
Tyrosine aminotransferase
|
|
Enzyme deficient in Type 3 Tyrosyluria/Tyrosinemia
|
p-hydroxyphenylpyruvic acid dioxygenase
|
