Renal Cancers and Infections – Flashcards
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From which cells does renal cell carcinoma arise?
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Proximal tubules cells
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How does renal cell carcinoma clasiaclly present?
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classic triad: hematuria - most common sx palpable mass flank pain (all three rarely occur together) also present sometimes: wt loss, fever, paraneoplastic syndrome (EPO (polycyhemia), renin, PTHrP, ACTH) rarely: left-sided varicocele
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What does a left-sided varicocele in renal cell carcinoma cause?
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involvement of L renal vein --> blocks drainage of L spermatic vein --> varicocele
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Why aren't R sided varicoceles seen in RCC?
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since the right renal veins drain directly into IVC, right varicoceles are not seen
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RCC is most common in which demographic?
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men 50-70 years of age
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What are RF for RCC/
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smoking, obesity
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How does RCC spread?
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Renal vein --> IVC --> hematogogenous spread to lugn, bone
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What is the most common renal malignancy?
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RCC
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What are the genetics of RCC?
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Associated with a gene deletion on chromosome 3 - can be inherited or spontaneous (inherited = VHL) Loss of VHL (3p) tumor suppressor --> increased IGF-1 and increased HIF (increases PDGF, VEGF)
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Trt for RCC?
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Resect if localized Chemotherapy/radiation doesn't work, usually resistant
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Grossly and microscopically, how does RCC appear?
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gross: yellow mass histo: clear cell mass
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What are other cancers for those with an inherited VHL gene mutation?
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increased risk of hemanbioblastoma of cerebellum renal cell carcinoma
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How is RCC staged?
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T - based on size, involvement of renal vein N - spread of RETROPERITONEAL lymph nodes
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What is the most common renal malignancy of early childhood (avg age 3 yr)?
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Wilm's tumor
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What is Wilm's tumor comprised of?
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blastema (immature kidney mesenchyme) primitive glomeruli, tubules, stromal cells
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How does Wilm's tumor present?
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Huge, palpable flank mass, hematuria
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What causes Wilm's tumor
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WT1 gene on chromosome 11 mutation, especially in syndromic cases
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With which syndromes is Wilms' tumor associated?
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Beckwith Wiedemann syndrome - Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy, organomegaly (including tongue) WAGR syndrome - Wilms, Aniridia (no iris), Genital abnormalities, Retardation (mental, motor)
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What are the findings in Beckmann-Wiedmann syndrome?
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Wilms tumor neonatal hypoglycemia Organomegaly (including tongue) muscle hemihypertrophy
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What are the findings in WAGR syndrome?
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Wilms tumor Aniridia genital abnormalities retardation - mental and motor
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What is the most common tumor of the urinary tract system?
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Transitional cell (urothelial) carcinoma
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Where does urothelial cell carcinoma arise?
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Urothelial lining of renal pelvis, ureter, bladder, or urethera - most commonly bladder tumors are often multifocal and can recur
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A patient presents with painless hematuria (no casts) - what does this suggest?
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bladder cancer
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What are the major risk factors for transitional cell carcinoma?
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It is associated with problems in your PEE SAC Phenacetin (analgesic) Smoking Aniline dyes (industrial chemicals used in polyurethane production) Cyclophosphamide
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What are the 2 histological types of urothelial carcinoma and how do they arise?
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Flat - a high grade flat tumor that starts out flat and then invades, a/w early p53 muts Papillary - starts out as a low grade papillary tumor that progresses as a high grade papillary tumor that then invades - not a/w p53 muts
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What is acute pyelonephritis usually caused by?
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Ascending infection, increased risk with vesicoureteral reflux
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How does acute pyelonephritis present?
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Fever Flank pain N/V WBC casts Leukocytosis Sx of cystitis
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What are the most common pathogens in acute pyelonephritis?
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E. coli Klebsiella Enterococcus faecalis
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How does acute Pyelo appear on histo?
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affects cortex w/ relative sparing of glomeruli /vessels neutrophilic infiltration into renal interstitium
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How does chronic pyelo result?
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It is the result of recurrent episodes of acute pyelonephritis, typically requiring some predisposition to infection: vesicoureteral reflux chronic kidney stones)
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How does chronic pyelo appear on histology?
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interstitial fibrosis and atrophy of tubules cortical scarring with blunted calyces
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What predisposes to chronic pyelo?
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vesicoureteral reflux (children) obstruction - BP, cervical carcinoma (adults)
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What is scarring at the upper and lower poles characteristic of?
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vesicoureteral reflex
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What do the tubules contain in chronic pyelonephritis?
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Eosinophilic proteinaceous material resembling thyroid follicles
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What may be seen in the urine of chronic pyelo pts?
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waxy casts
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What is lower urinary tract squamous cell carcinoma?
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Malignant proliferation of squamous cells usually involving bladder
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In what setting does squamous cell carcinoma arise?
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squamous metaplasia first since the bladder is not lined with squamous epithelium
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What are risk factors for squamous cell carcinoma of the bladder?
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chronic cystitis in an older woman Schistosoma hematobium (egyptian man) long standing nephrolithiasis
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What is adenocarcinoma of the lower urinary tract?
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malignant proliferation of glands, usually in bladder
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From what does adenocarcinoma of the bladder arise?
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Urachal remnant, cystitis landularis, or exstrophy (congenital failure to form the caudal part of the anterior abdominal/bladder walls)
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What is acute interstitial nephritis caused by?
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It is a drug-induced hypersensitivity reaction which involves the interstitium and the tubules and results in acute renal failure (intrarenal azotemia)
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What is azotemia?
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acute, severe deccrease in renal fx marker - increased BUN and Cr, often with oliguria Prerenal ass w/ BUN:CR>20 Postrenal ass w/ BUN:CR>15 Interrenal ass w/ BUN:CR<15
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What are causes of prerenal azotemia?
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Decreased blood flow to kidneys This leads to decreased GFR, azotemia, oliguria Resorption of fluid, BUN ensues (hence the BUN:Cr ratio >15) and tubular function remains intact (FENa 500 mOsm)
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What does FENa tell you?
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Whether the acute kidney injury is is due to prerenal or acute tubular necrosis
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Drug-induced interstitial nephritis typically occurs when and how?
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1-2 weeks after certain drugs (diuretics, penicillin derivatives, sulfonamides, rifampin) months after NSAIDs
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What is the mechanism of drug-induced interstitial nephritis?
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the drugs act as haptens and induce hypersensitivity
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What are the signs and symptoms of drug-induced tubulointerstitial nephritis
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fever, rash, hematuria, CVAT can also be asx EOSINOPHILS IN URINE
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What is the course of drug-induced tublointerstitial nephritis
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can resolve with cessation of drug, or present to renal papillary necrosis
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What is diffuse cortical necrosis caused by?
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combination of vasospasm and DIC
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What is diffuse cortical necrosis?
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vasospasm, DIC
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With what is diffuse cortical necrosis a/w?
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obstetric catastrophes (abruptio placenta), septic shock
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What is the most common cause of intrinsic renal failure?
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Acute tubular necrosis (ATN)
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What is the clinical course for ATN?
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can be reversible, but also fatal if untreated death is most common in the initial oliguric phase
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What are the stages of ATN?
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1) Some inciting event 2) maintenance phase - oliguric, 1-3 weeks (risk of hyperkalemia) 3) recovery phase; BUN and creatinine fall, risk of hypokalemia
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What is the risk during the oliguric phase of ATN?
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hyperkalemia
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What is the risk during the recovery phase of ATN?
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hypokalemia
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What happens in ATN?
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some injury causes necrosis and necrotic cells plug the tubules, which decreases GFR
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What are the lab findings of ATN?
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Dysfunctional tubular epithelium results in decreased reabsorption of BUN (serum BUN:Cr 2%) and inability to concentrate urine (urine osm <500)
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What is the key finding associated with ATN?
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granular "muddy brown" casts
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Which parts of the nephron are particularly susceptible to damage
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proximal tubule and medullary segment of the thick ascending limb
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What causes ATN?
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ischemia, nephrotoxocity from drugs (aminoglycosides), chemicals (lead, ethylene glycol - a/w oxalate crystals in urine), or crush injury (myoglobinuria - mm injury) also a/w radiocontrast die and urate (e.g., tumor lysis syndrome)
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What is used prior to the initiation of chemotherapy to decreased the risk of urate-induced ATN?
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hydration and allopurinol to decrease risk of urate-induced ATN
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What is renal papillary necrosis?
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Renal papillae slough off causing gross hematuria and proteinuria
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What triggers renal papillary necrosis?
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infection or immune stimulus
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What is renal papillary necrosis a/w?
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DM Acute pyelo Chronic phenacetin use (acetaminophen is a phenacetin derivative) Sickle cell anemia, trait
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In a normal person what happens to BUN and creatinine when they reach the nephron?
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BUN is reabsorbed, creatinine is not
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What is acute renal failure defined as?
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abrupt decline in renal fx with increased creatinine and BUN over a period of several days
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What causes prerenal azotemia?
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decreased RBF (as in hypotension) causes decreased GFR Na/H2O and urea retained by kidney to conserve volume, so BUN/Cr increases
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What causes intrinsic renal failure?
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generally ATN or ischemia/toxins less commonly, acute glomerulonephritis (RPGN)
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What is the pathophysiology of intrinsic renal failure?
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The patchy necrosis causes tubule obstruction and fluid blackflow across the necrotic tubule, which decreases GFR
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What does intrinsic renal failure show on urinalysis?
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epithelial/granular casts
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What is the BUN/Cr ratio in intrinsic renal failre?
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BUN reabsorption is impaired, so BUN/Cr decreases
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What causes postrenal azotemia?
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out flow obstruction (stones, BPH, neoplasms, congenital anomalies) only occurs w/ BILATERAL obstruction
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What is the urine osmolality in prerenal AKI?
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>500
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What is the urine osmolality in postrenal AKI?
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<350
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What is the urine osmolality in intrinsic renal AKI?
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<350
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What is the urine Na in prerenal AKI?
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<20
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What is the urine Na in intrinsic AKI?
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>40
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What is the urine Na in postrenal AKI?
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>40
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What is the FeNa in prerenal AKI?
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<1
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What is the FeNa in intrinsic renal AKI?
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>2
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What is the FeNa in postrenal AKI?
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>2
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What is the serum BUN/Cr in prerenal AKI?
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>20
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What is the serum BUN/Cr in renal AKI?
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<15
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What is the serum BUN/Cr in postrenal AKI?
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>15
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What are consequences of renal failure?
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can't make urine or excrete nitrogenous wastes. this results in: water, salt retention --> CHF, pulm edema, HTN hyperkalemia metabolic acidosis uremia anemia renal osteodystrophy dyslipidemia (esp triglycerdies) growth retardation/developmental delay
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What is uremia?
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clinical syndrome marked by high BUN and creatinine Nausea, anorexia Pericarditis Asterixis Encephalopathy Platelet dysfx
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What is renal osteodystrophy?
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can't hydroxylate vit D = hypocalcemia and hyperpohsphatemia --> 2' hyperpara hyperphosphatemia --> decreases serum Ca2+ further by causing tissue calcifications SUBPERIOSTEAL THINNING OF BONES
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where is subperiosteal thinning of bones seen?
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Renal osteodystrophy
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How does ADPKD present?
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flank pain, hematuria, HTN, urinary infection, progressive renal failure
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What mutations are seen in ADPK?
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PKD1 or 2 - AD!
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How do ADPKD people die?
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chronic kidney disease or HTN (which is caused by high renin production)
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What is ADPKD a/w?
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berry aneurysms mitral valve prolapse benign hepatic cysts
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How does ARPKD present/
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Infantile presentation in the parenchyma Autosomal recessive
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What is ARPKD a/w?
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congenital hepatic fibrosis
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What can those with ARPKD also get in utero?
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significant renal failure, leading to Potter's syndrome
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What are some concerns beyond the neonatal period for those with ARPKD?
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HTN portal HTN progressive renal insufficiency
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What is medullary cystic disease?
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an inherited disease which causes tubulointerstitial fibrosis and progressive renal insufficiency, w/ inability to [] urine
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What does imaging reveal in medullary cystic disease?
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cysts aren't seen, but you do see shrunken kidneys on ultrasound
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What is the prognosis of medullary cystic disease?
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poor
