Pathology Flashcards
Immunofluorescence findings in membranoproliferative glomerulonephritis
- Granular pattern of C3
- Deposition of IgG, C1q, C4
- Tram-track appearance on PAS stain
Mutated gene in Alport syndrome
*COL4A5, leads to a defective type 4 collagen production
Signs and symptoms of Alport syndrome
- Hereditary nephritis in childhood (X-linked)
- Sensorineural hearing loss
- Ocular abnormalities of the lens and cornea
Light microscopy findings in membranous glomerulonephritis
- Glomerular capillary wall thickening
* Basement membrane projections (silver staining)
Most common cause of nephrotic syndrome in children
Minimal change disease
Affected chromosome in Wilms tumor
Chromosome 11
Light microscopy findings in Wilms tumor
- Metanephric blastema
- Epithelial elements (immature glomeruli and tubules)
- Stromal elements
Type of diuretics that can help decrease levels of calcium in hypercalcemia
Loop diuretics
Loop diuretic that can be used in patients with sulfa allergy
Ethacrynic acid
Urine calcium levels seen in Bartter and Gitelman synrome
- Bartter: high
* Gitelman: low
Enzyme deficiency seen in syndrome of apparent mineralocorticoid excess (SAME)
Deficiency of 11beta-hyroxysteroid dehydrogenase
*Normally converts cortisol (active at mineralocorticoid receptors) to cortisone (inactive at mineralocorticoid receptors)
Dietary substance that can cause blockage of 11beta-hydroxysteroid dehydrogenase activity, leading to syndrome of apparent mineralocorticoid excess (SAME)
Glycyrrhetinic acid (present in licorice)
Syndrome of apparent mineralocorticoid excess (SAME) treatment
Corticosteroids
Pathophysiology of renal tubular acidosis (RTA) type 1
Defect in ability of alpha intercalated cells to secrete H leads to no new generation of HCO3 and metabolic acidosis
Urine pH seen in renal tubular acidosis (RTA) type 1
Greater than 5.5
*Leads to increase risk for calcium phosphate kidney stones
Pathophysiology of renal tubular acidosis (RTA) type 2
Defect in proximal convoluted tubule HCO3 reabsorption leads to increased excretion of HCOR in urine and subsequent metabolic acidosis
Urine pH seen in renal tubular acidosis (RTA) type 2
Lower than 5.5
Acid-base disturbance seen at high altitude
Respiratory alkalosis, then kidneys decrease H secretion and HCO3 reabsorption in order to create a compensatory metabolic acidosis
Biopsy findings in acute poststreptococcal glomerulonephritis (ASPGN)
- Infiltrate of neutrophils in the glomeruli
- All glomeruli are affected
- Granular deposits of IgG and C3 throughout the glomerulus
- Subepithelial immune complexes (humps)
Electrolyte imbalances seen in chronic kidney failure
- Hyperkalemia
- Hyperphosphatemia
- Hypocalcemia
- Hypomagnesemia
Pathologies associated with focal segmental glomerulosclerosis
- Obesity
- HIV
- Heroin use
- Sickle cell
- Interferon treatment
- CKD
Waxy casts are associated with which pathologies
End-stage renal disease/chronic renal failure
Glomerular diseases that can lead to nephritic syndrome
“MARIA”
- Membranoproliferative glomerulonephritis
- Alport syndrome
- Rapidly progressive glomerulonephritis
- IgA nephropathy (Berger disease)
- Acute poststreptococcal glomerulonephritis (APSGN)
Glomerular pathologies that lead to the development of rapidly progressive (crescentic) glomerulonephritis
- Goodpasture syndrome
- APSGN or diffuse proliferative glomerulonephritis
- Granulomatosis with polyangiitis (Wegener’s), microscopic polyangiitis, and Churg-Strauss syndrome
Pathologies that can lead to the development of diffuse proliferative glomerulonephritis
- SLE
* Membranoproliferative glomerulonephritis
Biopsy findings in diffuse proliferative glomerulonephritis
- Wire looping of capillaries
* Subendothelial and/or intramembranous IgG ICs with C3 deposition (granular)
Glomerular nephritic pathology that is associated with hepatitis B or C infection
Type 1 membranoproliferative glomerulonephritis
Glomerular pathology that is associated with C3 nephritic factor (IgG ab that stabilizes C3 convertase, leading to persisten complement activation)
Type 2 membranoproliferative glomerulonephritis
Most common cause of nephrotic syndrome in African Americans and Hispanics
Focal segmental glomerulosclerosis
Nephrotic presentation of SLE
Membranous glomerulonephritis
Antibodies to phospholipase A2 receptor are associated to which pathology
Membranous glomerulonephritis
Histopathological characteristic of diabetic glomerulonephropathy
Eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)
Shape of urine crystals in calcium oxalate kidney stones
Envelope or dumbbell
Shape of urine crystals in ammonium magnesium phosphate (struvite) stones
Coffin lid
Shape of urine crystals in uric acid kidney stones
Rhomboid or rosettes
Shape of urine crystals in cystine kidney stones
Hexagonal
Cell of origin of renal cell carcinoma
Proximal convoluted tubule cells
Biopsy findings in renal oncocytoma
Large eosinophilic cells with abundant mitochondria without perinuclear clearing
Cell of origin of renal oncocytoma
Collecting ducts
Syndrome that includes Wilms tumor, early-onset nephrotic syndrome, and male pseudohermaphroditism
Denys-Drash (mutation in WT1)
Biopsy findings in Wilms tumor
Embryonic glomerular structures
Risk factors for transitional cell carcinoma
“Pee SAC”
- Phenacetin
- Smoking
- Aniline dyes
- Cyclophosphamide
In patients with UTIs, sterile pyuria and negative urine cultures suggest urethritis by which organisms
- Neisseria gonorrhoeae
* Chlamydia trachomatis
Pathology in which you can see thyroidization of the kidney
Chronic pyelonephritis
Etiology of diffuse cortical necrosis
Acute general cortical infarction of both kidneys, likely due to a combination of vasospam and DIC (obstetric catastrophes, septic shock)
Cells seen in pyuria of acute interstitial nephritis
Eosinophils
Renal papillary necrosis associated risk factors
“SAAD papa”
- Sickle cell disease or trait
- Acute pyelonephritis
- Analgesics (NSAIDs)
- Diabetes mellitus
Dilation of which part of the nephron is seen in autosomal recessive polycystic kidney disease
Collecting ducts
Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine
Medullary cystic disease
Amyloid configuration
Beta-pleated sheet configuration
Type of amyloid deposited in dyalisis-associated amyloidosis
Beta2-microglobulin deposits (in joints)
Type of proteinuria seen in minimal change disease
Selective proteinuria (loss of albumin, not Ig)
Electron microscopy findings in membranous nephropathy
Subepithelial deposits with “spike and dome” appearance
Formulas for expected bicarbonate levels in chronic respiratory acidosis and alkalosis
- 0.4 x (increase in PaCO2)
* 0.4 x (decrease in PaCO2)
Urease producing bacteria that are frequently involved in struvite stone formation
- Proteus mirabilis
- Ureaplasma urealyticum
- Pseudomonas aeruginosa
- Klebsiella pneumoniae
- Enterobacter
Uremia decreases conversion of which hormone to its active form
Decreases conversion of T4 to T3
Most important complications after the recovery phase of acute tubular necrosis (ATN)
- Transient polyuria
* Electrolyte wasting (leading to electrolyte imbalances, particularly hypokalemia)
Molecule that binds to free (ionized) calcium, preventing its precipitation and facilitating its excretion
Citrate
Acid-base imbalance that promotes citrate reabsorption and, therefore, promotes precipitation of calcium and stone formation
Chronic metabolic acidosis
