Renal Pathology Flashcards by Luke Matzek

Horseshoe kidney

congential pathology
conjoined kidney (usually lower pole)
gets caught on inferior mesenteric artery --> abnormally located in lower abdomen

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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

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Dysplastic Kidney

Noninherited congenital pathology
Unilateral or bilateral (if bilateral, distinguish from polycystic)
congential malformation of renal parenchyma with cysts and cartilage tissue

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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

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Medullary Cystic Kidney Disease

inherited defect leading to cysts in medullary collecting duct

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Acute Renal Failure

Acute, severe decrease in renal function
Azotemia with oliguria
3 Types

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Prerenal Azotemia

due to decreased blood flow (CHF, hemorrhage)
decreased GFR, azotemia, oliguria
increased BUN/Cr ratio
tubular function normal = FENa <1%

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Postrenal Azotemia

due to obstruction in urinary tract
decreased GFR, azotemia, oliguria
EARLY - increased BUN/Cr ratio, FENa 2% because of tubular damage

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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

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Acute Interstitial Nephritis

Drug-induced hypersensitivity involving interstitium and tubules
NSAIDs, penicillin, diuretics
Oliguria, fever, rash, eosinophilia

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Renal Papillary Necrosis

Necrosis of renal papilla
Gross hematuria and flank pain
Causes:
- chronic analgesic use, DM, sickle cell, acute pyelonephritis

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Nephrotic Syndrome

glomerular disorder with proteinuria (>3.5 g/day)

- hypoalbuminemia, hypogammaglobulinemia, hypercoaguable (AT III), hyperlipidemia

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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

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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

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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

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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