Renal Pathology Flashcards
ADPKD: describe
autosomal dominant polycystic kidney disease, it’s adult onset, CLINICALLY: hematuria, flank pain, UTI, renal stones, HTN, chronic renal failure beginning at 40-60 y/o, cysts are spherical and uniformly distributed, chromosome 16, PKD1 mutations
ARPKD
autosomal recessive polycystic kidney disease, manifests in children and is often fatal, enlarged, cystic kidneys at birth, cysts are from collecting ducts and form a sunburst pattern, chromosome 6, PKHD1 mutations
Distinguish the clinicopathologic features between acute and chronic renal failure
Acute is rapid onset of oliguria or anuria with azotemia while chronic is the end stage of all chronic renal diseases and results in uremia—fatigue, neuropathy, anorexia, Vit D deficiency, nausea, and more.
Discriminate between the clinicopathologic features and pathogenesis of nephrotic and nephritic syndrome
Nephritic syndrome is damage to the glomeruli resulting in mild proteinuria and hematuria. Nephrotic syndrome is also glomerular damage but is more severe, with a proteinuria of 3.5 g/day or more and systemic edema, hypoalbuminemia, and hyperlipidemia. The main difference between the two is the amount of proteinemia; the rest of the symptoms can be equally bad.
Outline the generalities of Primary glomerulonephritis
is when the kidney is the primary organ involved, whereas secondary is when systemic disease causes the damage. Primary is usually caused by hypersensitivity reactions. Antigen can be from the GBM itself (glomerular basement membrane) or circulate from blood and get trapped in glomerulus.
What are the two types of glomerulonephritis (GN) progression?
once GFR reaches 30-50% the kidney will steadily approach end-stage renal failure (ESRF). There’s 2 types of progression: focal segmental glomerulosclerosis and tubulointerstital fibrosis. In the former, undamaged glomeruli undergo compensatory hypertrophy, but this hypertrophy eventually leads to sclerosis and their failure. This causes a cycle as other glomeruli then repeat this trend. Tubulointerstitial fibrosis is the progression of ischemia causing interstitial inflammation and fibrosis.
Post infectious, aka acute, nephritis
common in children, usually post-streptococcal (Group A, strains 1, 4, 12, B hemolytic) 1-4 weeks post infection, Ig-mediated, histo: diffuse GN and proliferation and leukocytic infiltrate
Rapidly progressive glomerulonephritis (RPGN)
has 3 types. Type 1 is mediated by anti-GBM Ig’s, linear IgG deposit on immune staining, idiopathic, may be a part of Goodpasture syndrome. Type 2 is immune complex mediated, and Type 3 is pauci-immune (not immune mediated) and caused by ANCAs (anti-neutrophil cytoplasmic antibodies), histo: proliferation, crescents
Membranous glomerulopathy
common cause of adult nephrotic syndrome, insidious onset, usually idiopathic, in situ Ig mediated, histo: diffuse capillary wall thickening, GBM granular staining (vice linear) on immunochemical stain
Minimal change disease
most often cause of nephrotic syndrome in children, beteween 2-6 y.o, idiopathic/maybe podocyte injury, responds very well to corticosteroids, good prognosis, histo: looks pretty normal except for lipid in tubules
Focal segmental glomerulosclerosis
nephrotic, can be idiopathic primary disease or secondary to a bunch of stuff like drug abuse, caused by visceral epithelial damage, can also be caused by HIV, Histo: focal and segmental sclerosis and hyalination
Membranoproliferative nephritis
nephrotic, immune-complex mediated, usually adolescence or young adulthood, Histo: GBM thickening of both capillary loops and mesangial cells, mesangial proliferation
IgA nephropathy
most common type of GN worldwide, recurrent proteinuria and/or hematuria often following an infection, idiopathic, Histo: pretty normal except for a bit of focal proliferative GN, mesangial cell widening
what titer can you do for acute nephritis?
anti-streptolysin O titer (ASOT)
bid difference between nephritic and nephrotic syndrome?
Nephritic has hematuria, nephrotic doesn’t. Also, nephrotic leaks more protein (>3.5 g/day)
What’s anasarca?
diffuse, systemic edema with swelling of almost or all skin. It happens with nephrotic syndrome
What systemic diseases can cause secondary GN?
diabetes, amyloidosis, myeloma, lupus, Goodpasture syndrome, Wegener’s granulomatosis
Myeloma associates with Bence Jones proteins
acute tubular necrosis
aka “acute kidney injury”, most common cause of ESRF, characterized by damage to renal tubules, often by ischemia (MI, shock, HTN, dehydration), toxic injury, or in response to urinary obstruction, HISTO: necrosis, usually in the proximal tubule, but not always evident. It is often characterized by 3 phases: the causative stress, following oliguria, and eventually a return to normal renal function.
Tubulointerstitial Nephritis
characterized by polyuria (excessive urine amounts of low concentration), salt wasting, and metabolic acidosis. Can be caused by a urinary tract infection (UTI), specifically cystitis (infection of bladder), of the urethra or ureters, or of the kidney (pyelonephritis). Usually G(–) bacteria. Can be caused by long-term catheterization, vesicoureteral reflux, pregnancy, diabetes, benign prostatic hypertrophy, and more. Can manifest as Acute Pyelonephritis, Chronic Pyelonephritis (CPN) which is characterized by tubulointerstitial fibrosis and broad kidney scars.
causes of urinary tract obstruction
causes of urinary tract obstruction
malignant tumors involving the kidney
clear cell, papillary, and chromophobe renal cell carcinoma. usually 50-70 y/o, men more often than women, ↑ chance with tobacco
CLINICAL: flank pain, hematuria, palpable mass, hypercalcemia, weight loss, fevers, malaise
Clear cell
VHL mutation, HISTO: clear cells full of glycogen, and alveolar-wall looking capillary septae
Papillary cell
MET oncogene mutation. GROSSLY can be multifocal and bilateral, HISTO cuboidal cells in papillary arragenments separated by foam cells.
Chromophobe renal cell carcinoma
HISTO pale, eosinophilic cells
Hematuria
presence of RBC’s in urine
• BUN
blood urea nitrogen
• Azotemia
elevated BUN and creatinine levels which resulted from decreased GFR. Prerenal azotemia is renal hypoperfusion—decreased blood flow to kidneys from shock, CHF, hypovolemia. Postrenal azotemia is an obstruction to urinary outflow occurring post-kidney.
• Uremia
systemic effects of azotemia
• Oliguria
low urine output, below 300-500 mL/day
• Goodpasture syndrome
a hypersensitivity reaction in which autoantibodies attack both the GBM (Glomerular basement membrane), causing rapidly progressive glomerulophritis, and also attack pulmonary alveolar basement membranes to cause pulmonary hemorrhage
