Lecture 14 (Renal)-Exam 5 Flashcards

Question

Role of ACE-Is and ARBs * However, it has not been proven that what? * When BP is controlled, what is more effective?

Answer 1

* However, it has not been proven that combination therapy improves renal outcomes and adverse effects may be more common * When BP is controlled, renin-angiotensin system (RAS) inhibitors such as ACE-I and ARBs are more effective than other antihypertensive drugs in reducing proteinuria, regardless of the etiology of CKD

Answer 2

* Restrict protein to 0.6 – 0.8 g/kg/day * Restrict sodium to 2 g/day * Restrict Potassium once GFR falls below 10-20 mL/min/1.73m2 * Restrict Phosphorus to 800-1000mg/day – educate patients regarding level of phosphorus in processed food/colas, eggs, dairy, nuts, beans, meat

Answer 3

* Adjust doses of meds excreted by kidney * Restrict laxatives and antacids * **Restrict NSAIDS** * Watch morphine – metabolites can accumulate * Watch IV contrast

Answer 4

* GFR <15; in actuality 5-10 mL/min/1.73m2 * Requires hemodialysis, peritoneal dialysis or kidney transplant to sustain life

Answer 5

Refer patients to Nephrology in late stage 3 or if GFR declining rapidly Dialysis Indications: * Refractory Hyperkalemia * Metabolic Acidosis * Volume Overload * Mental Status Changes

Answer 6

MUST still ask if patients make urine while on dialysis * Will affect your decision-making regarding IV contrast or Medications in fluid overload (Lasix) * Cup of urine= some drugs that will work but NOT contrast * No urine= use contrast because kidneys are already dead

Answer 7

* Need vascular access – arteriovenous fistula or prosthetic graft * Indwelling (Quinton) catheter may be used short-term – high risk of infection * Dialysis happens three times a week and lasts 3-5 hours * Result is a state of low dose heparinization (for each session) ## Footnote Overall lower risk of clotting due to heparinization at each session, so less likely to develop PE

Answer 8

* Fistula Infection rate 1/10 that of a shunt * Survival time 3 times that of a shunt->44% at 10 years * 250-300 mL/min can be as high as 600 mL/min * Thrombosis (common problem in fistula)

Answer 9

* Dialysate instilled into the peritoneal cavity through an indwelling catheter * Water and solutes move across the capillary bed that lies between visceral and parietal layers of the membrane into the dialysate

Answer 10

* Continuous ambulatory peritoneal dialysis (CAPD) – patient exchanges the dialysate a few times per day manually * Continuous cyclic peritoneal dialysis (CCPD) – utilizes a cycler machine to automatically perform exchanges at night * Risk of **peritonitis** but can be done at home * Culture all cloudy dialysate fluid + Intraperitoneal ABX ## Footnote peritonitis: abdominal pain+ dialysis

Answer 11

* 2/3 come from deceased donors * Avg wait is 2-3 years * 5-year survival rate of 80% for living donor transplants, 66% for deceased donor transplants * **Offers the best potential for complete rehabilitation** ## Footnote >100,000 on the waiting list in US

Answer 12

* initiation of dialysis if patient not stable enough for outpatient * Patient with worsening acid-base status, electrolyte abnormalities and volume overload

Answer 13

* Common with missed dialysis sessions * Frequently presents with HTN emergency

Answer 14

* IV Nitroglycerin 20-500 micrograms/minute * IV Lasix 3-5 mg/kg (must make at least a cupful of urine per 24hrs) * Hemodialysis (Definitive Tx)

Answer 15

* Renal failure is patient with severely compromised liver function in the absence of other known causes of renal failure (decreased effective circulating volume) * Resembles prerenal failure (marked renal vasoconstriction) but does not respond to conventional volume replacement * Precipitated by worsening liver failure, sepsis, antibiotics or NSAIDs, diuretics, diarrhea and GI bleeding

Answer 16

Laboratory hallmarks: * High urine osmolality * Low urine sodium < 10 mEq/L Physical Exam: * Refractory ascites, evidence of portal hypertension

Answer 17

* No specific treatment, prognosis poor; mortality as high as 95% with established hepatorenal syndrome, usually due to worsening liver failure, infection or hemorrhage. * Some have advocated peritoneovenous shunts (LeVeen or Denver); repeated large-volume paracentesis with IV albumin replacement

Answer 18

* Acute Kidney Injury (AKI) – worsening of kidney function over hours to days – waste product retention – measured by Blood Urea Nitrogen (BUN) and Creatinine * Retention of these substances is called azotemia. * Chronic Kidney Disease (CKD) – abnormal loss of kidney function over months to years * Management of most kidney related issues depend on 1 big factor: is patient WET-DRY-or NORMAL?

Answer 19

* Oliguria only observed in AKI * May have normal to large kidneys

Answer 20

* Anemia suggests CKD * Small kidney size on US * May have normal to large kidneys in early disease

Answer 21

* An increase in serum creatinine by 0.3 mg/dL or more in 48 hours Or an increase of 1.5 x the known (or assumed) baseline * Inability to maintain acid-base, fluid and electrolyte imbalance * May be oliguric * “Oliguric” – urine production less than 400-500ml per day or less than 20 ml per hour

Answer 22

* Stage 1 – 1.0 to 1.5 fold increase in creatinine or a decline in urinary output to less than 0.5 ml/kg/h over 6-12 hours * Stage 2 – 2.0 to 2.9 fold increase in serum creatinine or decline in urinary output to less than 0.5 mL/kg/h over 12 hours or longer

Answer 23

Stage 3 – 3 fold increase or greater in serum creatinine, an increase in serum creatinine to greater than 4 or decline in urinary output to less than 0.3 mL/kg/h for 24 hours or longer, anuria for 12 hours or longer or initiation of renal replacement therapy

Answer 24

* Most will not display symptoms or signs * “Uremia” is a clinical presentation of azotemia due to build-up of waster products, is a constellation of nonspecific signs and symptoms – nausea, vomiting, malaise, altered sensorium (uremic encephalopathy) * HTN may be present

Answer 25

* Pericardial effusion and a pericardial friction rub may be present * Arrhythmias can occur especially with hyperkalemia * May have rales, diffuse abd pain, bleeding disorders * Severe – may have asterixis, confusion, seizures

Answer 26

* **Elevated creatinine levels present** * BUN may be elevated * KEEP in mind – both of these may be true for CKD as well * Hyperkalemia may be present – if so, ECG may show peaked T waves, PR prolongation and QRS widening.

Answer 27

* Hypocalcemia may occur = long QT segment * Hyperphosphatemia may occur * Anemia due to erythropoietin production * Platelet dysfunction

Answer 28

* Pre-renal – it’s all about loss of flow to kidneys (perfusion problem) * Intrinsic/Intrarenal – there’s an issue in the kidney * Post- renal – something is blocking urine * For ALL serum creatinine is up from baseline more than 50%; BUN is up as well * In pre-renal – BUN is up first

Answer 29

* This may lead to Intrinsic if allowed to persist (acute tubular necrosis) * The most common type of AKI * Hypovolemia primary cause – diuretics, GI loss, dehydration, sepsis * Hemorrhage, shock, burns, CHF, low Cardiac output

Answer 30

– NSAIDS, IV dye – causing afferent arteriole vasoconstriction, ACE inhibitors (esp in setting of bilateral RAS), ARBs causing efferent arteriole dilation, Hypotension due to CHF, anything causing heart to pump inefficiently

Answer 31

* If GFR falls acutely – determine if it’s due to prerenal or intrinsic causes * **In pre-renal AKI – BUN:creatinine ratio often exceeds 20:1 (Azotemia)** * Fractional excretion of sodium (FENa) – less than 1%. * Oliguric patients with intrinsic kidney dysfunction typically have a high fractional excretion of sodium – greater than 1-2% * Lower FENa reliable as predictor of pre-renal AKI, higher not reliable as predictor of intrinsic cause due to variability associated with diuretic use. And – use is limited in nonoliguric pts.

Answer 32

* Urine sodium <20 * High specific gravity of urine > 1.030 * Increased urine osmolality > 400-500 mOsm/kg * TX – replace volume

Answer 33

* May be anuric or polyuric (partial obstruction) * Obstruction may be constant or intermittent * Causes – BPH, tumors, bladder outlet obstruction, b/l ureteral stones or strictures

Answer 34

* Clues – usually asymptomatic – may notice change in urinary output, may be hypertensive * Some have back or lower abd pain * On exam – may have enlarged prostate, distended bladder, mass in pelvis

Answer 35

* There is something obstructing the passage of urine * **ALWAYS caused by obstruction-> Hydronephrosis** * DX – Creatinine is usually ONLY elevated with bilateral kidney involvement ## Footnote This is actually quite rare

Answer 36

* **BUN: Creatinine ratio <10:1 ONLY if decreased urea, usually initially >15:1 (mimics pre-renal) then later FeNa >2 and decreased BUN/Cr ratio** * Use US or CT (± contrast depending on cause and renal function) to look for stones, hydronephrosis, mass etc. * TX – remove obstruction

Answer 37

BUN greater than 21 mg/dL

Answer 38

* BUN: Cr ratio greater than 20:1 * FeNa less than 1, FeUr less than 35% * Ur Osmo 500 mOsm/kg * UA can show hyaline casts

Answer 39

* BUN: Cr ratio less than 20:1 * FeNa greater than 2, FeUr greater than 50% * Ur Osmo less than 300 mOsm/kg * UA: Cellular debris, muddy brown casts red cell casts, eosinophils, + proteinuria

Answer 40

* BUN: Cr ratio less than 20:1 * FeNa greater than 2 * Ur Osmo less than 300 mOsm/kg * UA: WBC casts * Imaging findings: pyelonephritis, nephrolithiasis, bladder mass

Answer 41

* May initially reveal high urine osmolality, low urine sodium, high BUN:creatinine ratio and low FENa * This looks like pre-renal azotemia because extensive intrinsic renal damage has not yet occurred * After few days - urine sodium increases, **isosthenuria** present

Answer 42

* Isosthenuria – excreted urine with specific gravity that is equal to that of protein free plasma (~1.008-1.012) * Kidneys have lost ability to concentrate urine

Answer 43

* Bladder cath and ultrasonography to assess for hydroureter, hydronephrosis, large bladder volume despite inability or lack of sensation to void. * If cause not determined by US – CT or MRI (don’t use gadolinium with a eGFR less than 30mL/min/1.73m2). * TX – treat obstruction – caths, stents, surgical

Answer 44

* Pt with signs of AKI not reversed over 1-2 weeks without uremia – refer to nephrologist * Pt with signs of persistent urinary tract obstruction – refer to Urologist * Admit all patients with sudden loss of kidney function that cannot be handled quickly in outpatient setting (hyperkalemia, volume overload, uremia) and those who need dialysis or emergent urologic procedures

Answer 45

* Acute Interstitial Nephritis * Acute Tubular Necrosis * Acute Glomerulonephritis * **Normal BUN/CR ratio: 10-15:1**

Answer 46

* Inflammatory or allergic response in the interstitium * Spares the glomeruli * Most common cause – Drug Hypersensitivity ~70%

Answer 47

* Drug culprits – PCN, Sulfa, Cipro, Cephalosporins, Rifampin, Allopurinol, NSAIDs, APAP * Other causes – infection, autoimmune, and in almost 10% of cases – we never know (idiopathic) ## Footnote * NSAIDs do shunting of blood from cortex to medulla and interfere with urine output * Phenacetin/APAP – phenacetin no longer on market

Answer 48

* Fever, arthralgias, maculopapular rash, eosinophilia * Urinalysis will show WBC Casts and eosinophils with proteinuria * TX – remove offending agent * Typically a spontaneous recovery * Normal kidney function typically returns within a year

Answer 49

* Acute destruction and necrosis of the renal tubules of the nephron * 2 ways it happens – exogenous and/or endogenous nephrotoxins or prolonged prerenal azotemia * If due to prerenal azotemia – often present hypotensive and/or hypovolemic

Answer 50

* Exogenous nephrotoxins – IV dye (immediate), Vancomycin , aminoglycosides, cyclosporine, NSAIDS, Cocaine/PCP intoxication * Endogenous – tumor lysis syndrome, myoglobinuria (rhabdomyolysis), lymphoma, Bence-Jones proteins of Multiple Myeloma, leukemia. ## Footnote Aminoglycosed cause ARF in 5-25% of patients, drug is not metabolized but excreted by kidney, damaging tubules causing ATN after 8-10 days of therapy

Answer 51

* Urinalysis - **”Muddy Brown Casts”**, epithelial cell casts * Sodium and water reabsorption is lost * Low specific gravity * Low urine osmolarity <500 mOsm/kg ## Footnote Isostheuria: cannot cont. urine

Answer 52

* Increased FENA > 2% * Increased urine sodium >40 meq/L * BUN: creatinine ration < 15:1

Answer 53

TX – first – IV fluids and remove offending agent(s)

Answer 54

* ATN is a common complication of contrast administration, occurring 1-2 days after admin * High-risk patients should be kept well hydrated by administration of half-normal saline for 8-12 hours prior to and after procedure * Risk is 40% for patient with diabetes * Oliguria and other symptoms develop in 24 hrs

Answer 55

N-acetylcystine 600 mg po bid x 2d (1 before and day of) * Half-life 5.6-18 hours depending on race * This is same drug used in Tylenol overdoses

Answer 56

* Several etiologies – **post-infection (think strep) and AUTOIMMUNE (Lupus)** * IgA nephropathy called Berger’s Disease - **most common cause of Chronic GN in adults. Younger males a day or two post URI or GI illness**

Answer 57

* Membranoproliferative/Mesangiocapillary – SLE, hepatitis – this one has a mixed nephrotic/nephritic presentation * Only 2 present, always, as rapid/progressive - Goodpasture’s disease (anti-GBM disease) and vasculitis * Rapid/progressive – poor prognosis, ESRD in months

Answer 58

* Acute nephritic syndrome is a group of symptoms that occur with some disorders that cause swelling and inflammation of the glomeruli in the kidney, or glomerulonephritis. * Glomerulonephritis refers to a number of kidney problems that involve inflammation in the glomeruli, which are the kidney's filtration units. Acute glomerulonephritis can cause nephritic syndrome.

Answer 59

* Hematuria – classic sign “tea colored” or “coca cola colored” urine * Edema (peripheral and periorbital) -> HTN is common * Fever, abdominal pain, flank pain, malaise, oliguria (remember this is AKI) * Lupus rash and other characteristics (ANA; anti-dsDNA)

Answer 60

* Hematuria, RBC casts, proteinuria, high specific gravity greater than 1.020 osm. * Increased BUN and creatinine * Renal biopsy (IgA deposits in mesangium for IgA nephropathy)

Answer 61

* All forms except the rapidly progressive forms are typically self-limiting * IgA nephropathy – ACE inhibitors, maybe corticosteroids * Only transplant shown to be effective therapy, but IgA redeposits ~ 30% in 20yrs

Answer 62

* Edema, HTN, hypervolemia – Loop diuretics, beta-blockers, CCBs * Post strep AGN- maybe antibiotics * Rapid/progressive or severe disease – Corticosteroids plus Cyclophosphamide

Answer 63

* Glomerular damage leads to protein loss * Dx – proteinuria, hypoalbuminemia, edema (think osmosis or decreases intravascular oncotic pressure), hyperlipidemia * Clinical – peripheral EDEMA, dyspnea due to pleural effusion, fatty casts in urine, **Proteinuria > 3.5g/DAY**

Answer 64

* Minimal Change disease or Nil disease * DM * Focal segment glomeruosclerosis * Membranous nephropathy

Answer 65

* “Minimal Change Disease” or “Nil Disease” – **MCD in children** – viral illness, allergies, Hodgkin disease – loss of negative charge of basement membrane causes proteinuria * ”Membranous nephropathy” – most common in Caucasian males over 40 * 75% primary, 25% secondary to SLE, hep B, tumors

Answer 66

HIV, heroin, HTN * Most common form of nephrotic syndrome in African American patients * Stems from abnormalities in the podocyte * Hallmark of Histology =Podocyte detachment and death lead to the segmental sclerosis

Answer 67

* Minimal change disease – cannot see under regular microscope, need electron microscope to visualize microscopic damage to base membrane of glomeruli. * Podocytes are specialized epithelial cells that cover the outer surfaces of glomerular capillaries. * Oval fat body casts exhibit "Maltese cross" configuration by polarized light microscopy

Answer 68

* Urine protein > 3500 mg/24hr OR proteinuria >3500 mg (or 4+)-> cause urine to be frothy * HYPOalbuminemia (usually <3.0 g/dL [30g/L]) * Hypercholesterolemia * EDEMA (anasarca, ascites) * Hypercoagulable state (loss of anticoagulant proteins) ## Footnote **NO HTN (unless pre-existing)**

Answer 69

* DX: H&P, 24 hr urine, renal bx * UA – “foamy” urine, lipids in urine * Need to measure protein via 24 hour urine which should show > 3.5 g/day * Hyperlipidemia, hypoalbuminemia

Answer 70

* Diagnostic clue to membranous nephropathy – thick basement membrane on biopsy showing Subepithelial immune deposits of IgG * TX – glucocorticoids (SLE or MCD), loop or thiazide diuretics, ACE or ARB, statin, immunosuppressives * 90% respond to steroids, 70% relapse and may eventually need cytotoxics

Answer 71

* Immune-mediated – increased urinary protein and RBC loss * Clues – proteinuria, HTN, azotemia, oliguria, hematuria ->**RBC casts** * Clinical – HTN, hematuria, less than 400ml per day of urine, fever, abd/flank pain – might have edema

Answer 72

* Proteinuria <3.5 g/day, hematuria, RBC casts * termed rapidly progressive glomerulonephritis

Answer 73

* Mild edema * Moderate proteinuria * HTN: Always causes HTN * Hematuria (brown or “smoky”) & RBC casts

Answer 74

* Small-vessel vasculitis associated with necrotizing granulomatous inflammation affecting the upper and lower respiratory tracts and kidneys * Renal pathology not specific for WG->**ANCAs positive** in 65-90% * Definitive: biopsy-> large necrotizing granulomas

Answer 75

Clinical features: fever, malaise, purpuric rash, pulmonary hemorrhage, sinusitis (septal perforation, saddle nose deformity) & Thrombocytosis-> Triad of URI (nose MC), LRI (lung) and glomerulonephritis Prognosis poor without treatment (90% mortality 2 years) * Steroids and cytotoxic agents can produce remission in about 75% * 11% progress to ESRD

Answer 76

* Falls within “Rapidly Progressive Glomerulonephritis” * Autoimmune response ( UgG against type IV collagen) and antibody generated directly against glomerular membrane and alveoli * ANCA + in 80%, Anti-glomerular basement membrane antibodies

Answer 77

Sxs: * Pulmonary hemorrhage (cough, **hemoptysis**, dyspnea) 70% * CXR: patchy or diffuse alveolar infiltrates * Renal failure: rapid, oliguric, **hematuric** with modest proteinuria Treatment: aimed at reducing circulating preformed anti-GBM antibodies by daily plasma exchange for 14 days, steroids, cytotoxics

Answer 78

* A form of thrombotic microangiopathy: systemic platelet consumption with formation of intraluminal platelet thrombi * Classic childhood HUS is preceded by an acute diarrheal illness caused by an E. coli strain * Clinical features: renal failure (uremia), mental status changes preceded by 1 week of diarrheal illness

Answer 79

* Lab: hemolytic anemia with abnormal RBCs (schistocytes – scarred RBC) on peripheral blood smear, low platelet count, increased LDH, increased bilirubin, decreased haptoglobin * Thrombocytopenia with normal coagulation studies * Treatment is supportive (dialysis if necessary)

Answer 80

* IgA nephropathy associated with systemic vasculitis * Small vessel vasculitis most often seen in children. * Higher incidence in winter and spring * Clincally but coagulation labs are normal, kidney biopsy shows IgA depostis and leujocytoclastic vasculitis

Answer 81

* **Palpable purpuric** lesions over buttocks, hematuria, synovial arthritis, abdominal pain (HSP-> Affects IGA so HSPA) * IgA + C3 deposits seen on biopsy of skin lesions * Hematuria, proteinuria, RBC casts, normal C3 levels * Self-limited course normally (supportive Tx), but 10% progress to end-stage renal disease ## Footnote Henoch-Schönlein Purpura

Answer 82

* M>F(sex linked) * Renal failure usually develops by age 30 * Biopsy **shows thinned and thickened capillary loops with splitting of GBM**

Answer 83

* Usually presents in childhood with recurrent gross hematuria, mild proteinuria, nephrotic syndrome is rare * No effective treatment available * Common in East Tennessee * **High association with deafness**

Answer 84

* Know there are both microvascular and macrovascular etiologies * Know that anything that impacts systemic vascular system can also impact renal function * Renal artery dissection, renal vein thrombosis occurs, as does embolic disease

Answer 85

* Renal vasculature is unusually complex with a rich arteriolar flow – basically a filter organ. * Large-vessel atherosclerosis, fibromuscular diseases, and embolic disorders commonly threaten the blood supply of the kidney * The glomerular capillary endothelium shares susceptibility to oxidative stress, pressure injury and inflammation with other vascular territories. * Changes in blood supply are followed by tubulointerstitial fibrosis and loss of kidney function

Answer 86

* HTN onset before age 20 or after age 50 * HTN resistant to 3 or more drugs * You detect epigastric or renal artery bruits * There is atherosclerotic disease of the aorta or peripheral arteries * There is an abrupt increase of more than 25-30% in level of serum creatinine after admin of ACE inhibitors * There are episodes of pulmonary edema associated with abrupt surges in blood pressure

Answer 87

* most common cause of secondary HTN * HTN due to renal artery stenosis (RAS) * Pathophysiology – decreased renal blood flow leading to activation of the renin-angiotensin-aldosterone system * Causes – atherosclerosis (elderly), fibromuscular dysplasia (women, typically under 50) ## Footnote Beta blockers reduce renin

Answer 88

* Suspect it in pts with headache + HTN + less than 20 y/o or over 50 y/o with severe HTN. * If you are unable to get HTN controlled via several drugs. * If AKI occurs after initiation of ACE-I * Exam – Abdominal bruit (rare)

Answer 89

Ultrasound – typical test done outpatient to r/o RAS in resistant HTN Gold standard – revascularization via renal catheter arteriography both diagnoses and treats * You only order diagnostic imaging if the plan includes treatment intervention (only in severe disease)

Answer 90

* Medical management – ACE-I or ARBs. BUT – both are contraindicated if bilateral stenosis present or if the patient has only 1 kidney! * May require adding a thiazide diuretic, long-acting CCB or mineralocorticoid receptor antagonist (Aldactone).

Answer 91

* Ultrasonography of the kidneys and bladder should be obtained for suspected urinary tract obstruction or when the underlying cause of AKI is unclear * Kidney size may help distinguish between AKI and CKD because diminished kidney size and cortical thinning suggest CKD * Kidney biopsy should be considered in patients with AKI from no apparent cause, suspected glomerulonephritis, or unexplained systemic disease

Answer 92

* AKI can be divided into prerenal, intrinsic, and postrenal causes * Tx may require short-term dialysis (known as RRT – renal replacement therapy) * Find the cause quickly: the kidneys may recover!!!

Answer 93

* Risks – bladder cancer, Balkan nephropathy, Lynch syndrome, **smoking**, exposure to radioactive thorium (‘60’s) and who have a long history of analgesic abuse. * Majority are urothelial cell cancers. * **Hematuria** – gross or microscopic usually present

Answer 94

* CT will show intraluminal filling defect or nonvisual of collecting system and hydronephrosis * Most are excised, chemo prior to surgery thought to improve outcomes

Answer 95

* Tumor of the proximal convoluted renal tubule cells * These cells are high metabolically active which increases risk of dysplasia * Renal Cell tumors are by far the most common tumor originating in the kidney (~95%) * Difficult to diagnose due to typically being asymptomatic. * Once diagnosed – difficult to treat – resistant to chemo and radiation

Answer 96

* Male to Female ratio is 2:1 * Uncommon diagnosis in patients under 45 * Peak incidence 65-74 years * **Cigarette smoking, obesity and hypertension** thought to be risk factors * There are some rare genetic familial forms * MC form – Clear cell RCC

Answer 97

* Hematuria (May be microscopic and asymptomatic otherwise) * Flank or Abdominal pain * Flank or palpable Abdominal mass * Fever, weight loss, anemia and varicocele (sudden, elderly)

Answer 98

* Typically found as an incidental finding on x-ray * Hypercalcemia is common

Answer 99

* Urinalysis * Urine cytology * CT scan of abdomen and pelvis * Chest radiograph – get a CT if anything suspicious on CXR

Answer 100

* Transitional cell carcinoma of the renal pelvis * Sarcoma * Lymphoma * Wilms’ tumor

Answer 101

* Surgical if no metastasis * Individualized plan if metastasis present * 5 year survival rate ~74% across all stages, goes down of course with later stages (8% in stage IV)

Answer 102

* Most common in children under 5 years old * Most common cause of abdominal mass in children * May be accompanied by GU abnormalities

Answer 103

* Clinical – palpable abdominal mass does NOT cross midline, hematuria, nausea, vomiting, HTN, anorexia – may be present. Mass may be only clinically apparent finding * DX – **US first**, CT with contrast or MRI * Do a CXR – lungs most common site for metastasis. * ~10% will have metastasis at time of diagnosis

Answer 104

* Treatment **begins with surgical exploration of the abdomen** via an anterior surgical approach – allows for inspection and palpation of contralateral kidney * En bloc resection of the tumor. * Therapy is tailored to staging during surgery – need experienced surgeon. * TX – total nephrectomy plus chemotherapy/radiation ## Footnote En bloc resection involves the surgical removal of the entirety of a tumor without violating its capsule, and requires resection of the lesion encased by a continuous margin of healthy tissue.