Renal Pathology Flashcards
Horseshoe kidney
congential pathology conjoined kidney (usually lower pole) gets caught on inferior mesenteric artery --> abnormally located in lower abdomen
Renal Agenesis
Congenital pathology
Bilateral –> leads to oligohydraminos –> lung hypoplasia, flat face, low ears, extremity defects –> incompatible with life
Unilateral –> hypertrophy of existing kidney –> increased risk for renal failure later in life
Dysplastic Kidney
Noninherited congenital pathology
Unilateral or bilateral (if bilateral, distinguish from polycystic)
congential malformation of renal parenchyma with cysts and cartilage tissue
Polycystic Kidney Disease (PKD)
inherited defect leading to bilateral enlarged kidneys with cysts in renal cortex and medulla
- Autosomal recessive - infants with Potter sequence and hepatic fibrosis
- Autosomal dominant - young adults with HTN, hematuria, renal failure (cysts develop over time)
- associated with berry aneurysm, hepatic cysts, mitral valve prolapse
Medullary Cystic Kidney Disease
inherited defect leading to cysts in medullary collecting duct
Acute Renal Failure
Acute, severe decrease in renal function
Azotemia with oliguria
3 Types
Prerenal Azotemia
due to decreased blood flow (CHF, hemorrhage)
decreased GFR, azotemia, oliguria
increased BUN/Cr ratio
tubular function normal = FENa <1%
Postrenal Azotemia
due to obstruction in urinary tract
decreased GFR, azotemia, oliguria
EARLY - increased BUN/Cr ratio, FENa 2% because of tubular damage
Acute Tubular Necrosis
Injury and necrosis of tubular epithelial cells
Necrotic cells plug up tubule –> obstruction
decreased GFR, azotemia, oliguria, brown casts in urine
decreased BUN/Cr ratio, FENa >2%
Can be ischemic or nephrotoxic etiology
Acute Interstitial Nephritis
Drug-induced hypersensitivity involving interstitium and tubules
NSAIDs, penicillin, diuretics
Oliguria, fever, rash, eosinophilia
Renal Papillary Necrosis
Necrosis of renal papilla
Gross hematuria and flank pain
Causes:
- chronic analgesic use, DM, sickle cell, acute pyelonephritis
Nephrotic Syndrome
glomerular disorder with proteinuria (>3.5 g/day)
- hypoalbuminemia, hypogammaglobulinemia, hypercoaguable (AT III), hyperlipidemia
Minimal Change Disease
Idiopathic, some association with Hodgkin lymphoma (massive overproduction of cytokines)
Normal glomeruli on H&E
Effacement of foot processes on EM (HALLMARK)
No immune complex deposition
Selective proteinuria (albumin)
Excellent response to steroids
Focal Segmental Glomerulosclerosis
Idiopathic, some association with HIV, heroin, sickle cell Focal, segmental sclerosis on H&E Effacement of foot processes on EM No immune complex Poor response to steroids
Membranous Nephropathy
Idiopathic, some association with Hep B/C, SLE, drugs
Thick glomerular BM on H&E
Immune complex deposition (subepithelial) –> spike and dome appearance
Poor response to steroids
Membranoproliferative glomerulonephritis
Thick glomerular BM on H&E, ‘tram-track’ appearance
Immune complex deposition
Type 1 - subendothelial (Hep B, C)
Type 2 - intramembranous –> C3 nephritic factor (stabilizes C3 convertase)
Poor response to steroids
Diabetes Mellitus
high serum glucose –> nonenzymatic glycosylation of vascular BM –> leaky –> hyaline arteriolosclerosis
Stenosis of efferent arteriole –> high glomerular filtration pressure
Sclerosis of mesangium
ACE inhibitors slow progression
Systemic Amyloidosis
Kidney is most commonly involved organ of systemic amyloidosis
Deposits in mesangium –> Congo Red stain
Nephritic Sydnrome
Glomerular disease with glomerular inflammation and bleeding
Limited proteinuria
Oliguria and azotemia
Periorbital edema and HTN
Immune complex deposition activates complement –> C5 attracts neutrophils –> damage
Poststreptococcal Glomerulonephritis
Arises after group A strep infection –> M-protein
Hematuria, oliguria, HTN, periorbital edema
Hypercellular, inflamed glomeruli
Immune-complex deposition
Rapidly Progressive Glomerulonephritis
progresses to renal failure in weeks/months
Crescents in Bowmans space on H&E (composed of fibrin and macrophages)
IgA Nephropathy
IgA immune complex deposition in mesangium following mucosal infection (IgA)
Alport Syndrome
Inherited defect in type IV collagen (X-linked)
Results in thinning and splitting of glomerular BM
Presents as isolated hematuria, sensory hearing loss, and ocular disturbances
UTIs
infection of urethra, bladder, kidney
most commonly –> ascending infection
more likely in females (50x)
risk factors: sex, urinary stasis, catheters
Cystitis
bladder infection
presents as dysuria, urinary frequency and urgency, suprapubic pain (systemic symptoms absent)
Positive urine culture (gold standard)
E. Coli (80%)
Staph saprophyticus (young sexually active females)
Klebsiella and proteus (gram + urease -)
Pyelonephritis
kidney infection
ascending infection, increased risk with vesicoureteral reflux
Fever, flank pain and WBC casts (systemic symptoms)
E. Coli (90%)
Enterococcus, Klebsiella
Chronic Pyelonephritis
interstitial fibrosis and atrophy of tubules
vesicoureteral reflux or obstruction
leads to scarring and blunted calyces (thyroidization of kindeys)
Nephrolithiasis
precipitation of urinary solute as stone
Risk factors: urinary stasis, high solute [ ]
presents as colicky flank pain, hematuria
Chornic Renal Failure
Results from glomerlular, tubular, inflammatory or vascular insults
Common causes: DM, HTN, glomerular disease
Features: uremia, salt and water retention –> HTN, Hyperkalemia, anemia, hypocalcemia, renal osteodystrophy
Angiomyolipoma
hamartoma comprised of blood vessels, smooth muscle, and adipose tissue
- increased frequency with tuberous sclerosis
Renal Cell Carcinoma
malignant epithelial tumor from kidney tubules
Classic triad = hematuria, palpable mass, flank pain (rarely see triad)
Sx: fever, weight loss, paraneoplastic syndrome
Left-sided varicocele (right spermatic veins drains directly into IVC so no R)
Pathogenesis: loss of VHL (tumor suppressor gene)
Wilms Tumor
malignant kidney tumor comprised of blastema (common in kids deletion of WT1 gene (Wilms tumor, Aniridia, Genital abnormalities, Retardation)
Beckwith-Wiedemann syndrome –> mutation in WT2 gene
Urothelial Carcinoma
malignant tumor or urothelial lining (transitional epithelium)
involves ureter, renal pelvis, bladder, urethra
Major risk factor = SMOKING, long term cyclophosphamide use
Seen in older adults with painless hematuria
2 distinct pathways
1. Flat - high grade flat tumor that invades
2. Papillary - low grade papillary tumor –> high grade –> invades
Squamous Cell Carcinoma
malignant proliferation of squamous cells (bladder)
Arises from squamous cell metaplasia from chronic inflammation
Risk factors = chronic cystitis, Schistosoma hematobium, long-standing nephrolithiasis
Adenocarcinoma
malignant proliferation of glands (bladder)
Arises from urachal remnany (tumor develops at dome of bladder)
Metaplasia from chronic inflammation
Nomenclature of glomerular disorders
Focal - 50% of glomeruli
Proliferative - hypercellular glomeruli
Membranous - thickening of GBM
Primary glomerular disease - only involves glomeruli
Secondary glomerular disease - involves other organs as well
