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CPR II Exam 3 > Chapter 20: Renal Pathology Part 2 > Flashcards

Chapter 20: Renal Pathology Part 2 Flashcards

1
Q

Acute Tubular Injury/Necrosis (ATI)

What is it, what is it the most common form of, and what are its two types?

What is its pathogenesis?

A
  • damage to tubular epithelial cells with acutely diminished renal function; most common form of ACUTE kidney injury/renal failure and is REVERSIBLE
  • either Ischemic ATI (trauma, sepsis, shock) or Nephrotoxic ATI (exogenous: gentamycin, contrast, heavy metals)

P: begins with tubular injury leading to persistent and severe disturbances in blood flow

  • loss of cell polarity = inc. distal Na delivery
  • causes vasoconstriction
  • ischemic cells detach and cause luminal obstruct.
  • inc. Hydrostatic pressure = decr. GFR
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2
Q

Acute Tubular Injury/Necrosis (ATI)

What is the difference in morphology between Ischemic and Toxic ATI, and what protein are casts commonly made from?

A

Ischemic: focal tubular epithelial cell necrosis and BM eruption with large skip areas (unaffected)

Toxic: focal, nonspecific necrosis, especially at STRAIGHT portion of Proximal Tubule and Thick Ascending Limb

  • distal tubule/collecting duct casts contain mostly Tamm-Horsfall protein (urinary glycoprotein secreted by cells of ascending thick limb and distal tubules)
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3
Q

Acute Tubular Injury/Necrosis (ATI)

What is this disease NOT clinically associated with and why?

What are its 3 phases of development (I/M/R)?

A
  • not associated with HEMATURIA due to patchiness of disease and tendency to maintain basement membrane
    • repair and resolution is very common

Stages:

  1. Initiation: first 36 hrs in which insult has not yet caused renal failure (slight inc. BUN/dec. urine output)
  2. Maintenance: sustained dec. urine output, HYPERKALEMIA, rising BUN concentration
  3. Recovery: renal function begins to improve rapidly with resolution in a few weeks
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4
Q

Acute Tubular Injury/Necrosis (ATI)

How does a pt. recovering from ATI typically present and what histological finding is diagnostic for ATI?

A

Pt: initial polyuria due to release of excess fluid that was backed up; beware of HYPOkalemia and inc. risk of infection

Dx: Dirty Brown Granular Casts = “renal failure casts”

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5
Q

What is Tubulointerstitial Nephritis and how is it different from glomerular diseases?

A
  • group of renal diseases caused by inflammatory injuries (insidious; manifests with AZOTEMIA)
  • different from glomerular diseases due to ABSCENCE of nephritic/nephrotic syndromes
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6
Q

Pyelonephritis and UTIs

What kind of damage do they cause, what Gram - (4) and Gram + (2) are common causes of disease, and when would viruses causes infection?

A
  • cause Tubulointerstitial Nephritis due to inflammation of tubules, interstitium, and pelvis (MOST COMMON disease of the kidney); mostly spread through ASCENDING INFECTION of lower UT

Gram (-): E. coli, Proteus, Klebsiella, Enterobacter
Gram (+): Strep. faecalis and Staph saprophyticus
- SS –> newly sexually active females

  • *viruses if pt. is IMMUNOCOMPROMISED (typically those with transplanted organ)**
    • polyomavirus, CMV, adenovirus
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7
Q

Pyelonephritis and UTIs

How does an Ascending Infection occur and where does infection most commonly occur once it has reached the kidneys?

What allows bacteria to gain access to the ureters?

A
  • bacteria colonizes urethra, then reaches bladder via catheterization (males) or ascent through small urethra (females); urinary stasis makes it easier to ascend
  • Vesicoureteral Reflux allows access to ureters (no VUR = bacteria stay in bladder)
  • infected bladder can be propelled back into renal parenchyma where it develops in the UPPER and LOWER poles of the kidney
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8
Q

Acute Pyelonephritis

What does it look like morphologically and what are its 3 clinical complications (PN/P/PA)?

A

M: patchy interstitial suppurative inflammation (focal abscesses) w/intratubular WBC aggregates and tubular necrosis (WBC casts in urine) –> HALLMARK

  1. Papillary Necrosis - diabetics, sickle cell disease
    • distal grey-white to yellow necrosis
    • preservation of tubule outlines
  2. Pyonephrosis - PUS in the renal pelvis/calyces
    • seen with total/near complete obstruction
  3. Perinephric Abscess - inflamm. into perinephric tissue through renal capsule

irregular scars with PATCHY JIGSAW pattern replace inflammation

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9
Q

Acute Pyelonephritis

What are reasons for development in males < 1 yo and > 40 yo, and when is it more likely to develop in females?

A

Males:

  • < 1 yo: due to congenital defects
  • > 40 yo: catheter and prostate obstruction

Females: more common in adult age

  • due to shorter urethra
  • can sometimes occur during PREGNANCY
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10
Q

Acute Pyelonephritis

How does it present clinically, where is pain typically located, and what is Polyomavirus Nephropathy?

A

C: dysuria with frequency and sudden onset pain at the COSTOVERTEBRAL ANGLE (“FLANK PAIN”)

  • see fever, malaise, pyuria (leukocytes in urine)
  • WBC casts indicate renal involvement

PN: seen in post-transplant pts. who are immunocomp.

  • reactivation of latent virus
  • infects tubular epithelial cell nuclei
  • nuclear enlargement w/crystalline-like lattices
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11
Q

What are the only two pathological manifestations that show damage to the Pelvis AND Calyces?

A
  1. Chronic Pyelonephritis

2. Analgesic Nephropathy

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12
Q

What is the difference between Reflux Nephropathy and Chronic Obstructive Pyelonephritis?

What does Chronic Pyelonephritis look like morphologically?

A

RN: most common pyelonephritic scarring
- occurs early in childhood due to congenital VUR

COP: obstructions predisposed to infections
Unilaterally: calculi/other unilateral obstructions
Bilaterally: defective post. urethral valves

M: coarse, discrete corticomedullary scars over dilated/blunted calyces with flattened papillae

  • more common in UPPER and LOWER poles
  • dilated/flattened epi with THYROID COLLOID
  • can see hyaline arteriosclerosis with HTN
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13
Q

How does Chronic Pyelonephritis present clinically?

What rare form of Chronic Pyelonephritis can mimic Renal Cell Carcinoma (XP) and what organism is it caused by?

A

Sx: back/flank pain, fever, pyuria, bacteremia

major cause of kidney destruction in kids with severe lower urinary tract abnormalities

  • also see dilated renal CALYCES and PELVISES
  • Xanthogranulomatous Pyelonephritis can mimic Renal Cell Carcinoma (rare form with FOAM CELLS mixed with plasma and giant cells; associated with PROTEUS inf.)
    • large, yellow-orange nodules
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14
Q

Acute (DRUG-INDUCED) Tubulointerstitial Nephritis

What is it, how does it develop, what does it look like morphologically, and how does it present clinically?

A
  • immune-mediated reaction to drugs = tubulitis/acute renal failure (2nd MCC of AKI after pyelonephritis)
    • NOT dose related; drugs act as HAPTEN
    • activates IgE and T/B/plasma cells in localized area

M: interstitial edema, medullary inflammation, inc. eosinophils and neutrophils; normal glomeruli

C: fever, rash, eosinophilia, acute renal failure usually 15 DAYS after exposure to offending agent
- sometimes see papillary necrosis w/gross hematuria

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15
Q

What is Analgesic Nephropathy and what are pts. more likely to develop due to it?

A
  • chronic tubulointerstital nephritis caused by PHENACETIN-containing analgesics
    • incidence down due to withdrawal from most countries
  • pts. at inc. risk of developing UROTHELIAL CARCINOMA of RENAL PELVIS
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16
Q

What is seen in these Tubulointerstitial Diseases:

  1. Urate Nephropathy
  2. Hypercalcemia/Nephrocalcinosis
  3. Acute Phosphate Nephropathy
  4. Light Chain Cast Nephropathy
  5. Bile Cast Nephropathy
A
  1. hyperuricemic disorder pts. (GOUT)
    • acute: crystals in tubules (leukemia pts)
    • chronic: birefringent needle-like crystals in tubules
  2. calcium stones/calcium deposits in kidney
    • inability to concentrate urine
  3. phosphate accumulation in COLONOSCOPY pts.
    • due to oral phosphate solutions
    • pts. NOT HYPERCALCEMIC
  4. mostly caused by MULTIPLE MYELOMA
    • Bence-Jones proteinuria and cast nephropathy
    • kappa light chains in GBMs and mesangium
    • casts = pink-blue amorphous masses
  5. in pts. with acute/chronic liver disease
    • inc. serum bilirubin lvls = bile cast formation
    • direct toxicity and obstruction of nephron
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17
Q

Benign Nephrosclerosis

What is it, what does it look like morphologically, and how does it present clinically?

What is the appearance of kidneys affected by this disease?

A
  • sclerosis of renal arteries due to AGING and HTN; have thickened walls/narrow lumens = focal ischemia

M: hyalinized arterioles; “grain leather” kidneys; patchy ischemic atrophy with tubular atrophy and interstitial fibrosis

C: usually asymptomatic (inc. in AA, diabetics, older pts) but can have proteinuria, dec. GFR, and inc. risk towards chronic renal failure

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18
Q

Malignant Nephrosclerosis

What is it and what is it caused by, what are 3 distinct morphological features (PH/FN/OS), and how does it present clinically?

A
  • arterial disease associated with malignant/accelerated HTN, usually due to EXTREME blood pressure; activates RAAS due to ischemia (exacerbates HTN)

M: Petechial Hemorrhage (“flea bitten” appearance), Fibrinoid Necrosis (smudgy eosinophilia due to fibrin deposition), “Onion Skinning” concentric BM duplication

C: seen in pts. BP > 200/120; papilledema, retinal hemorrhage, encephalopathy

  • early Sx due to inc. intracranial pressure
  • occurs more often in BLACK MEN
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19
Q

Unilateral Renal Artery Stenosis

What is it, what does it look like morphologically (BS), and how does it present clinically (B)?

A
  • atherosclerotic plaque (old DM men) or fibromuscular dysplasia (20-30 yo F) that leads to HTN due to inc. Renin production

M: plaque formation in renal artery, potential thrombus, renal artery has “Beads on a String” appearance

C: pts. look like they have essential HTN; auscultation reveals BRUIT over affected kidney; elevated plasma renin (pts. due well on ACEi/ARBs)

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20
Q

Thrombotic Microangiopathies

What are they, what are the two main types and how do they respond to plasmapheresis, and what is each types pathogenesis?

A
  • insults that lead to excessive PLATELET activation that deposit in small vessels (THROMBOCYTOPENIA –> microangiopathic hemolytic anemia = schistocytes)

Types:

  1. Thrombotic Thrombocytopenic Purpura (TTP)
    • DO plasmapheresis
    • due to large amounts of vWF (ADAMTS13 deficient)
  2. Hemolytic-Uremia Syndrome (HUS)
    • do NOT do plasmapheresis
    • usually caused by SHIGA-like TOXIN (EHEC)
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21
Q

What is the difference between Typical and Atypical Hemolytic-Uremia Syndrome?

A

Typical - seen in childhood/elderly; diarrhea (+)

  • E. coli hamburgers (OO157:H7) shiga-like toxin
  • sudden hematemesis and melena, flu-like prodrome
  • fibrinoid necrosis, intimal hyperplasia/thrombosis

Atypical - seen in adults; diarrhea (-); BAD prognosis

  • excessive complement activation (Factor H mut)
  • normal levels of ADAMTS13 (vs TTP)
22
Q

What 3 vascular diseases and what 3 chemotherapeutic agents can lead to Hemolytic-Uremia Syndrome (C/B/C)?

A

Vascular
- Wegner’s, Scleroderma, HTN

Chemotherapeutic
- cyclosporine, bleomycin, cisplatin

23
Q

Thrombotic Thrombocytopenic Purpura (TTP)

What is its pentad (F/RF/N/T/MHA), what is it caused by, who does it commonly affect, and how can it be treated?

A

P: fever, renal failure, neuro symptoms, thrombocytopenia, microangiopathic hemolytic anemia

  • caused by deficiency in ADAMTS13 due to auto-antibodies and typically presents in adults < 40 yos

Tx: plasmapheresis (do in the MIDDLE OF THE NIGHT) to remove auto-antibodies

24
Q

How doe these other renal vascular disorders present:

  1. Atherosclerotic Ischemic Renal Disease
  2. Atheroembolic Renal Disease
  3. Sickle Cell Nephropathy
  4. Diffuse Cortical Necrosis
  5. Infarcts
A
  1. bilateral renal artery stenosis = renal ischemia in adults
    • inc. angiotensin II –> NO ACEi/ARBs
    • dec. ANGII = dilated arterioles = dec. GFR
  2. emboli from atheromatous plaques (cholesterol crystals appear as rhomboid clefts)
  3. vasa recta sickling = dec. concentrating ability
    • DILUTE URINE with hematuria
  4. follows obstetric emergencies, septic shock = abrupt hypoperfusion
  5. most due to EMBOLI; white and wedge-shaped
    • fibrose = depressed, pale, gray-white scars (V-shape)
25
Q

Congenital Kidney Anomalies

  1. Agenesis of Kidneys
  2. Hypoplasia
  3. Ectopic Kidneys
  4. Horseshoe Kidney
A
  1. bilateral = no survival; unilateral can survive
    • no amniotic fluid production = POTTERs sequence
    • pulmonary hypoplasia
  2. failure to kidney to develop to normal size (low birth weight)
  3. metanephros develops at ectopic foci (pelvic brim or within pelvis) –> small and asymptomatic
    • can cause torsion or obstruction (INFECTION)
  4. usually fusion of kidneys at LOWER pole
    • gets caught by INFERIOR MESENTERIC ARTERY
26
Q

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

What is it, what two mutations lead to its development, what does it look like morphologically, and what are 3 clinical presentations it has (NE/ECA/IBA)?

A
  • multiple expanding cysts in BOTH kidneys (4 kg/kidney) that destroy renal parenchyma and cause renal failure in 30-40 yos
    • histology shows functional parenchyma
  1. PKD1 (16p13.3) - tubular epithelial cells (distal neph.)
    • 85% of cases; WORSE prognosis
  2. PKD2 (4q13-p23) - membrane protein for Ca permeable cation channel

C: most common in Northern Europeans/Black males; flank pain due to hemorrhage; Extrarenal Congenital Abnormalities (polycystic LIVER disease); Intracranial Berry Aneurysm
- isolated, basilar SAH in young pts.

27
Q

Autosomal Recessive Polycystic Kidney Disease

How does it develop and what pts is it seen in, what does it look like morphologically, and how does it present clinically?

A
  • due to PKHD1 (Chromosome 6) mutation = fibrocystin change (disrupt collecting tubule); usually seen in CHILDREN

M: enlarged, smooth, tiny elongated cysts along INTERIOR replace cortex/medulla (looks like SPONGE when CUT)
- cysts lined by CUBOIDAL CELLS (from collecting ducts)

C: smaller cysts at right angles to cortical surface; perinatal and neonatal MOST COMMON
- survivors develop CONGENITAL HEPATIC FIBROSIS

28
Q

Autosomal Recessive Polycystic Kidney Disease

What are the 4 clinical subtypes of this disease (P/N/I/J)?

A 
Perinatal - 90% of CD cystic
   - minimal hepatic fibrosis
Neonatal - 60% of CD cystic
   - mild hepatic fibrosis
Infantile - 20% of CD cystic
   - hepatic fibrosis and failure
Juvenile - 10% of CD cystic
   - HEPATIC FIBROSIS progressive
   - esophageal varices, HTN, splenomegaly
29
Q

What is Medullary Sponge Kidney?

A
  • medullary cystic disease occurring in adults with unknown pathogenesis (scarring typically absent)
  • multiple cystic dilations consisting of cuboidal or transitional epithelium from collecting ducts
30
Q

Nephronophthsis

What is it, which variant is most common, and what is its pathogenesis?

A
  • progressive diseases characterized by variable #’s of cysts in the medulla, usually in corticomedullary junction
    • MOST COMMON genetic cause of ERSD in kids
  • familial juvenile nephronophthisis is most common (inherited autosomal RECESSIVE)

P: begins at distal tubules with tubular BM disruption –> progressive atrophy of medulla/cortex (FIBROSIS)
Juvenile - NPG genes
Adult - AD MCKD1/2 mutations in adults (ERSD)

31
Q

Nephronophthsis

What is its morphology and how does it present clinically?

A

M: small kidneys with contracted granular surfaces; LARGE cysts at cortico-medullary junction and SMALL cysts in the cortex

C: polyuria and polydipsia reflecting inability to concentrate urine
- suspected in unexplained renal failure w/Family History

32
Q

What is Multicystic Renal Dysplasia?

What is its main characteristic histological feature?

A
  • sporadic disorder that is either unilateral/bilateral
    • U: dysplasia mimics neoplasm (good prognosis)
    • B: renal failure (bad prognosis)
  • kidneys are enlarged, extremely irregular, and multi-cystic
  • cysts are lined by flattened epithelium and kidney shows presence of islands of undifferentiated mesenchyme with cartilage and immature collecting ducts (CHARACTERISTIC FEATURE)
33
Q

What is Acquired (Dialysis) Cystic Disease?

What is contained within the walls of the cysts and what cancer is this disease associated with?

A
  • caused by end-stage kidney disease with prolonged dialysis; cysts are lined by hyperplastic/flattened tubular epithelium and contain CALCIUM OXALATE CRYSTALS
    • calcium phosphate is more common in gen. pop
    • calcium oxalate in pts. getting dialysis
  • associated with Renal Cell Carcinoma (cyst walls); seen in patients on dialysis for a long period of time
34
Q

What are Simple Renal Cysts and how can they be differentiated from tumors?

A
  • translucent, gray, glistening, lined by a single layered membrane (cuboidal or flattened)
    • usually small and cortical
  • cysts have smooth contours, avascular, and give fluid signals on US (how to differentiate from tumors)
35
Q

Hydronephrosis

What is it, what is its morphology, and how do Acute, Bilateral Partial, and Bilateral Complete obstructions differ?

A
  • dilation of renal pelvis/calyces associated with progressive ATROPHY of kidney due to obstruction of urine outflow
    • high pressure transmitted from collecting ducts to cortex (compresses renal vasculature)

Acute: pain from distension; can remain silent for long time
Bilateral Partial: inability to concentrate urine (polyuria/nocturia), HTN common
Bilateral Complete: oliguria/anuria; incompatible with survival unless obstruction is removed
- removal = inc. NaCl in urine for awhile

36
Q

Calcium Oxalate Stones

What are they made out of, what are they associated with, and what is the cause of formation if hypercalcemia is present?

A
  • made of calcium and oxalate; is the MOST COMMON type of kidney stone (75% incidence)
  • associated with HYPERCALCIURIA, with or without hypercalcemia
    • due to renal impairment of reabsorption or hyper-absorptive intestinal tract
    • if both are present = HYPERPARATHYROIDISM
37
Q

Struvite Stones

What are they made out of, what are they caused by, and what do they look like?

A
  • made of magnesium ammonium phosphate and are caused by urea-splitting PROTEUS species and Staph
  • inc. ammonia from urea degeneration in tubules causes an alkylation of the urine
  • forms the LARGEST kidney stones and appear as STAGHORN CALCULI occupying the renal pelvis
38
Q

Uric Acid Stones and Cystine Stones

A

UAS: common in pts. with gout or leukemias, forming at acidic urinary pH

  • inc. pH helps degrade stones - give BICARBONATE
  • RADIOLUCENT (no calcium present)

CS: formed with genetic diseases that prevent reabsorption of proteins from lumen (Cystinuria)
- form at acidic urinary pH

39
Q

Kidney Stones

How do they present clinically?

A
  • usually affect males between 20-30 yo
  • cause RENAL COLIC: intermittent, sharp flank pain that radiates to the groin, as well as HEMATURIA as stone is passed (shreds ureter)
  • large stones do not pass and stay in pelvis, causing obstruction and leading to HYDRONEPHROSIS; can also become INFECTED
40
Q

What are 3 types of benign Renal Neoplasms? (RPA/A/O)

A
  1. Renal Papillary Adenoma
  2. Angiomyolipoma
  3. Oncocytoma
41
Q

What is a Renal Papillary Adenoma?

A
  • small, yellow-gray, well-circumscribed nodules within the cortex; see branching, papillomatous structures with complex fronds
  • potentially malignant at ANY size, but especially if > 3 cm (consider ALL adenomas as potentially malignant)
42
Q

What is an Angiomyolipoma?

What is it associated with?

A
  • benign neoplasm (Renal Fibroma/Hamartoma) of vessels, smooth muscle, and fat from perivascular epithelioid cells that likes to spontaneously hemorrhage
  • associated with TUBEROUS SCLEROSIS (TSC1/2 LOF)
    • lesions of cerebral cortex that cause epilepsy, mental retardation, skin problems
43
Q

What is an Oncocytoma?

What cells does it originate from?

A
  • epithelial neoplasm composed of large, eosinophilic cells with small, round, benign nuclei with large nucleoli; can get BIG and cause COMPRESSION SYNDROMES
  • massive amounts of mitochondria (oncocyte = eosinophilic cell filled with mitochondria); tumors are TAN-BROWN, well-circumscribed with central scar
  • develop from intercalated cells of COLLECTING DUCT
44
Q

What is Urothelial Carcinoma of the Pelvis?

What two diseases is it associated with and what is the number 1 cause of development?

A
  • primary renal tumor from urothelium of the renal pelvis; SMOKING is #1 risk factor and prognosis is NOT GOOD do to spreading through wall easily
  • found quickly due to PAINLESS hematuria (small cells); can block urine outflow, causing hydronephrosis and flank pain
  • associated with Lynch Syndrome and Analgesic Nephropathy
45
Q

What is the most common type of renal cancer, what is its greatest risk factor, and where does it commonly develop in the kidney?

A
  • Renal Cell Carcinoma is the most common (adenocarcinoma)
  • SMOKING is the greatest risk factor of development
  • can arise in any portion of the kidney, but the POLES are the most common sites for development
46
Q

What is Clear Cell Renal Carcinoma and what mutation is it caused by?

A
  • MOST COMMON type of renal carcinoma; 98% caused by loss on chromosome 3 where VHL is located –> inc. lvls of HIF-1 –> inc. lvls of VEGF and IGF-1 (inc. angiogenesis and cell growth)
47
Q

Renal Cell Carcinoma

What is its morphology and what are they likely to invade?

A
  • causes unilateral tumors (SPORADIC, NONPAPILLARY) that form from proximal tubular epithelium and present with large clear or granular cells
  • masses are YELLOW because of FOAM-LIKE FAT CELLS (shows ‘focal cytoplasmic lipid positivity’)
  • likely to invade the RENAL VEIN and can go all the way to the heart (cause VARICOCELE if located on the LEFT)
48
Q

Papillary Carcinoma

What are the sporadic and familial forms associated with, what disease is it commonly associated with, and what cells are common in the core?

A

Sporadic: trisomies 7 and 17, loss of Y in males
Familial: trisomy 7

  • cancer associated with DIALYSIS-associated CYSTIC DISEASE
  • foam cells are common in the core; usually cuboidal/columnar epithelium arranged in papillary pattern; cells from DISTAL CONVOLUTED TUBULES
49
Q

What is Chromophobe Renal Carcinoma?

A
  • has eosinophilic cytoplasm, perinuclear halo, and is localized to the vasculature in solid sheets
  • grows from intercalated cells of the collecting ducts (like ONCOCYTOMA) and has an EXCELLENT PROGNOSIS
50
Q

Renal Cell Carcinoma

What is its classic triad of symptoms, where does it metastasize to, and what syndromes does it cause?

What is the 5 yr survival of patients with cancer?

A

Triad: hematuria, flank pain, and mass

Metz: 25% prior to discover –> goes to lungs, bones, LNs, liver, adrenal, brain
- usually metastasizes widely before local symptoms occur

  • see Paraneoplastic Syndromes commonly (RCC is a great mimic in medicine)

5 yr survival is HIGH unless: renal vein invasion or extension into perinephric fat (total nephrectomy is curative unless metastasis has occurred)

CPR II Exam 3 (12 decks)

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