Pathology - renal Flashcards
RBC casts
glomerulonephritis, malignant hypertension
WBC casts
tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
fatty casts
Nephrotic syndrome
granular casts
acute tubular necrosis
Waxy casts
end-stage renal failure
Nephritic syndrome
sign of GBM disruption
incr. BUN/Cr, oliguria, hematuria, RBC casts
Causes: acute post-streptococcal, rapidly progressive glomerulonephritis, IgA nephropathy, Alport syndrome, membranoproliferative glomerulonephritis
Nephrotic syndrome
podocyte disruption –> charge barrier impaired
Massive proteinuria w/ low serum albumin, incr. lipids, edema, can lead to hyperthrombotic state (loss of antithrombin-3)
primary podocyte damage: PSGS, MCD, membranous nephropathy
secondary podocyte damage: amyloidosis, diabetic glomerulonephropathy
Peripheral/periorbital edema 2 weeks after GABHS infection, cola-colored urine, hypertension
Hypercellular glomeruli
IgG/IgM/C3 deposition along GBM and mesangium
Acute post-streptococcal glomerulonephritis
Subepithelial immune complex humps (Type III reaction!)
Rapidly deteriorating renal function, hematuria
crescents of fibrin and plasma proteins (C3b), with glomerular parietal cells, monocytes, macrophages
RPGN (incl Goodpasture’s, Wegener’s c-ANCA, microscopic polyangiitis p-ANCA)
SLE, presents often as nephrotic and nephritic syndromes concurrently
wire looping of capillaries
immune complex deposition
granular appearance on IF
Diffuse proliferative glomerulonephritis
**most common cause of death in SLE
Renal insufficiency and gasteoenteritis (Henoch-Schonlein Purpura)
Episodic hematuria
mesangial proliferation
IgA nephropathy
mesangial IgA-based IC deposits in mesangium
Eye problems, glomerulonephritis, sensorineural deafness
thinning of GBM
Alport syndrome
Type IV collagen defect
X-linked
Copresentation of nephritic and nephrotic syndrome
Membranoproliferative glomerulonephritis
Type 1: subendothelial IC deposits, tram-track appearance (GBM splitting)
Type 2: intramembranous IC deposits, C3 nephritic factor
Most common cause of nephrotic syndrome in AAs/Hispanics, secondary to sickle cell/HIV/heroin abuse/obesity
FSGS
segmental sclerosis, effacement of podocyte foot processes
inconsistent response to steroids
Most common cause of nephrotic syndrome in children, lots of triggers
MCD
normal glomeruli but podocyte effacement
may be secondary to lymphoma, excellent response to steroids
Most common cause of nephrotic syndrome in Caucasian adults, lots of triggers, assoc w/ SLE and solid tumors (lung, colon)
Diffuse granular capillary and GBM thickening, spike and dome appearance with subepithelial deposits, can have antibodies to podocyte transmembrane proteins
Membranous nephropathy
nephrotic presentation of SLE, poor response to steroids
Congo red stain shows apple green bifringence
Amyloidosis
Nephrotic syndrome
Diabetic glomerulonephropathy
Mesangial expansion, GBM thickening, esoinophilic nodular glomerulosclerosis
Glycosylation of GBM –> incr. permeability and thickening
Glycosylation of efferent arterioles –> incr. GFR –> mesangial expansion
Kidney stones seen in pt w/ hypercalciuria and normocalcemia
Envelope or dumbbell-shaped calcium oxalate stones
Calcium stones
Oxalate: ethylene glycol poisoning, Vit. C abuse, malabsorption, precipitate at low pH
tx: hydration, thiazides, citrate, pyridoxine, low protein diet
Kidney stones seen in pt w/ infection by urease + bugs (proteus, klebsiella, staph sapro)
Coffin lid-shaped stones
Struvite (ammonium magnesium phosphate)
Commonly form staghorn calculi
Kidney stones seen in pt w/ dehydration or incr. cell turnover
Rhomboid-shaped or rosettes
Uric acid
tx: allopurinol, alkalinization of urine, low protein diet
Kidney stones in pt w/ loss of cystine-reabsorbing PCT transporter
Hexagonal shaped
Cystine stones
Hexagonal shaped
Mostly seen in children, with positive sodium cyanide nitroprusside test, and they also have aminoaciduria
tx: alkalinization of urine
Renal cell carcinoma pathology
PCT cells, polygonal clear cells filled with accumulated lipids and carbs/glycogen
invades renal vein then IVC and spreads hematogenously
gene deletion on Ch.3 (sporadic or von Hippel Landau)
assoc. with lots of paraneoplastic syndromes
Renal oncocytoma
Benign epithelial cell tumor
Large eosinophilic cells with abundant mitochondria without perinuclear clearing
Wilms tumor
large, palpable, unilateral flank mass
loss of function of tumor suppressors WT1/WT2
May be part of Beckwith-Wiedemann or WAGR (wilms, aniridia - absence of iris, GU malformation, mental retardation)
SCC of bladder
chronic irritation of bladder (Schistosoma haematobium infection)
presents with painless hematuria
Causes of UTIs
E. coli
Staph sapro
Klebsiella
Proteus - ammonia scent
nitrites in gram negatives (E. coli)
negative cultures suggest urethritis
Pyelonephritis
neutrophils infiltrate renal interstitium
striated parenchymal enhancement on CT
complications: renal papillary necrosis, perinephric abscess, urosepsis
Chronic pyelonephritis
vesicoureteral reflux or chronic kidney stones
asymmetric corticomedullary scarring, blunted calyx
tubular can contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney)
Signs of drug-induced interstitial nephritis
Pyuria and azotemia
Drugs act as haptens, inducing hypersensitivity
Muddy brown granular casts
Acute tubular necrosis
3 stages: inciting phase, maintenance phase, recovery phase
ischemic - decr. renal blood flow (hypovolemia, shock)
nephrotoxic - toxins, crush injury, hemoglobin, most common in PCT
Gross hematuria and proteinuria
Renal papillary necrosis
Seen in SAND…
sickle cell, acute pyelonephritis, NSAIDs, diabetes
incr. Cr and incr. BUN
acute kidney injury
FENa values for AKI
2% = intrinsic renal, postrenal
Low Vit. D, low serum Ca, high serum PO4
renal osteodystrophy
ADPKD
autosomal dominant, mutation in PKD1
assoc. w/ berry aneurysms, mitral valve prolapse, benign hepatic cysts
ARPKD
infantile polycystic kidney disease
congenital hepatic fibrosis, can lead to Potter sequence
Progressive renal insufficiency with inability to concentrate urine
Medullary cystic disease
not visualized, but shrunken kidneys on ultrasound
Anechoic cysts vs. solid components
Simple vs. complex renal cysts
Simple are filled w/ ultrafiltrate
Complex are septated, enhanced or solid, and must be removed due to incr. risk of RCC
Evaluating metabolic alkalosis
First, assess urine chloride (low = vomiting), then volume status
Three most common causes: vomiting/NG suction, thiazide/loop diuretic use, mineralocorticoid use
Hemolytic uremic syndrome (HUS)
s/p E.coli (O157:H7) or Shigella infection
toxins injure endothelium of preglomerular arterioles, leading to platelet aggregation and formation of microthrombi (shear stress –> hemolysis)
Look for thrombocytopenia, anemia and AKI
