Internal Medicine Board Review: Nephrology

Internal Medicine Board Review:NephrologySteven Wagner M.D.July 16, 2014Purpose of board reviewPass the boardsNot intended as a complete reviewBoards correct real life correctPick the right answer and move onAnd the point isMost questions have a specific teaching pointIf you miss the point, you will probably miss the questionGetting the point will not guarantee that you get the correct answerStill have to understand the rest of the questionInter-nephrologist agreementPut 10 nephrologists in a room with a patient, and you will receive at least 11 diagnosesSome might disagree with question format and/or the answersWith that in mind,

Question 1A 41-year-old female is seen for follow-up of high blood pressure. She follows a healthy, active lifestyle and does not smoke. She is on no medications or birth control.BP 173/112, BMI 23, other vitals WNLLabs are normal, including renal panel, UA, glucose, and lipids

What is the most appropriate NEXT STEP in management of her hypertension?Lisinopril / HydrochlorothiazideDiet and exerciseNorvascSee her back in 2 weeks for a blood pressure recheckKey point: manage hypertensionHypertension is divided into stages

Our patient has stage II hypertensionWill need drug therapy

Why the other choices are wrongLisinopril / HydrochlorothiazideDiet and exerciseNorvascSee her back in 2 weeks for a blood pressure recheckHad a BMI of 23 and a healthy dietNorvasc is unlikely to be effective aloneShe is already following up at the current visit. Time to do something.Question 2A 23-year-old white female is evaluated for 2 months of fatigue, polyarthritis, oral ulcers, and edema. She has no significant medical history and takes no medications.Blood pressure 165/100, other vitals WNL. Ulcers on hard palate and buccal mucose. Erythema and tenderness of the MCP and PIP joints. 2+ LE edema bilaterally.Hb 11, WBC 2.1, PLT 110K, Albumin 3.4, Creat 1.4UA shows 25-50 RBC, 25 WBC, and erythrocyte casts24-hour urine protein is 2.5 grams

Which of the following is the most likely diagnosis?Focal segmental glomerulosclerosisIgA nephropathyPost-infectious glomeulonephritisProliferative lupus nephritisKey point: diagnose lupus nephritisLupus nephritis is characterized by hematuria and proteinuria in the setting of clinical findings of lupusDiagnosed with:>500 mg protein in 24 hour sample>10 RBC per HPFRBC or WBC casts in sterile urine (active sediment)OR by kidney biopsyRemember that lupus is a syndromeRBC casts indicate GLOMERULAR hematuriaWhy the other choices are wrongFSGS generally presents with more proteinuria (nephrotic syndrome)IgA nephropathy is unlikely in the setting of clinical findings of lupusThe answer cant be post-infectious without evidence of recent infection (at least on the boards) NONE of the incorrect answers explain her cytopenias etcFocal segmental glomerulosclerosisIgA nephropathyPost-infectious glomeulonephritisProliferative lupus nephritisQuestion 3A 75-year-old man with known alcoholic cirrhosis has 3 weeks of worsening ascites. He still drinks and is not a transplant candidate. Dont even ask. His only medication is propranolol.He is alert and oriented. BP 109/68, pulse 58, other vitals WNLNo neurologic findings, no asterixesAbdominal exam nontender with significant ascites. 1+ LE edemaLabs: Albumin 2, BUN 8, Creat 1.6, Na 119, K 3.6, OSM 250Urine: OSM 156, Na 6 in the setting of hypokalemic acidosis, Sjogrens, and nephrocalcinosis is HIGHLY SUGGESTIVE of distal RTAThis one is not subtleWhy the other choices are wrongGitelman syndrome would be hypotensive and lytes would look like HCTZ useLaxative abuse would have a negative urine anion gapCompensatory increase in ammonium excretionProximal RTA would be expected to have a normal urine pHDistal acidification still intactProximal also often associated with glucosuria, Fanconi syndromeGitelman syndromeDistal (type I) renal tubular acidosisLaxative abuseProximal (type II) renal tubular acidosisQuestion 7A 45-year-old female with a history of frequent UTIs presents with foul smelling urine, dysuria, and urgency. Her last UTI was Morganella morganii. She has a known history of kidney stones.Vitals are WNLExam is benignLabs: Creat 1.2, Albumin 4.2, Calcium 9.3, PTH 12UA: pH 7.2, WBC 2+, leukocyte esterase, no hematuria, no proteinDue to frequent infections in the setting of kidney stones, a CT scan is performed, which confirms the presence of bilateral staghorn calculi. She proceeds to Urology.What is the most likely composition of her kidney stones?Calcium oxalateUric acidAmmonium magnesium phosphateCystineKey point: Diagnose struvite stones in the setting of Urease-splitting bacteriaCommon urease splitting bacteria are Proteus and MorganellaThe boards will not always give you Proteus in these questionsUrine pH is key:High pH with mention of infection is almost always struvite stones

Why the other choices are wrongCalcium oxalate stones are the most common stone (90%) but not with a high pHUric acid stones are almost never seen with alkaline urine. Alkalinization is a TREATMENT for uric acid stonesCystine stones are seen in Cystinuria, a genetic disorder. Think 6-sided crystalsCalcium oxalateUric acidAmmonium magnesium phosphateCystine

Question 8A 47-year-old female is seen for diabetes followup. She has CKD, HTN, retinopathy, and neuropathy. She is active and follows a diabetic diet. She is on glyburide, amlodipine, and gabapentin.Vitals: BP 124/80, otherwise WNLExam: Trace edema, otherwise WNLLabs: Creat 3.1, HCO3 17, BUN 88, K 4.8

Which of the following is the most appropriate addition to her current medical regimen?AllopurinolPhosphate binderSodium bicarbonateSodium polystyreneKey point: Treat metabolic acidosis in CKD with bicarbonateNon-gap acidosis with chronic kidney diseaseCan have a gap with severe renal failureTreatment with bicarbonate may reduce bone loss and possibly CV morbidity, and seems to slow CKD progressionWhy the other choices are wrongHigh uric acid is associated with renal disease progression, but multiple studies have failed to show benefit from allopurinolPhosphate binder is not needed in the setting of normal phosphorusSodium polystyrene is not needed in this patient with a normal serum phosphorus, and has a role ONLY in acute hyperkalemia (if even then)AllopurinolPhosphate binderSodium bicarbonateSodium polystyreneQuestion 9A 54-year-old female is seen for followup of diabetes and hypertension. She is overweight and noncompliant with all lifestyle interventions. She is on metformin, glipizide, irbesartan, HCTA, and simvastatin.BP 154/82, BMI 38, other vitals WNLExam: No LE edemaLabs: creat 1.2, K 5.1, Phos 3.8, 24-hour urine protein 200 mg

In addition to lifestyle modification, which of the following is the most appropriate next step in management?DiltiazemFurosemideLisinoprilSpironolactone

Key point: Manage hypertension in a diabetic patientDiltiazem is the best choice in this patientShe is well above the guideline of 130 systolic in a diabetic patientWhy the other choices are wrongFurosemide is not needed as she has no evidence of volume overloadLisinopril is not indicated. Studies show no benefit with dual RAS blockade, and there is an increased risk of hyperkalemiaSpironolactone might be effective, but is relatively contraindicated in the setting of borderline hyperkalemiaDiltiazemFurosemideLisinoprilSpironolactoneQuestion 10A 54-year-old male is seen for a history of frequent nephrolithiasis. At least 2 of his stones were analyzed and found to be uric acid. After his third stone, potassium citrate was initiated. He also has diabetes, HTN, and hyperlipidemia. No known history of gout. His diet consists of red meat with most meals, and he has inconsistent fluid intake. He is on metformin, metoprolol, atorvastatin, and aspirin.Vitals and exam WNL. BMI 32.Labs: BUN 15, creat 1.1, Uric acid 7.824-hour urine (mg): Ca 220, Citrate 400, Oxalate 26, uric acid 710Urine volume: 1600 mg in 24 hours. Urine pH 6.2Which of the following is the most appropriate treatment?AcetazolamideAllopurinolCalcium carbonateChlorthalidone

Key point: Manage uric acid stones with AllopurinolPatient has uric acid stones in spite of urinary alkalinizationSerum uric acid is elevatedOther risk factors:High meat intakeLow urine volumeDietary modification and increased fluid intake would be helpful as wellWhy the other choices are wrongAcetazolamide would alkalinize the urine but would cause metabolic acidosisCalcium carbonate is used for oxalate stonesChlorthalidone is a thiazide diuretic, which will increase serum uric acid levels and might lead to the development of goutAcetazolamideAllopurinolCalcium carbonateChlorthalidoneQuestion 11A 75-year-old female is seen for escalating hypertension. She quit smoking 5 years ago after a TIA. She takes metoprolol, amlodipine, and HCTZ. Six months ago her BP was 148/82, three months ago it was 158/90. Today it is 174/96.Vitals: BP 174/96, pulse 61, otherwise WNLExam: Carotid bruits, epigastric bruits, s4 gallop, 1+ LE edemaLab: Creat 1.7, Na 14, UA normal

Which of the following is the most appropriate next step in management?Add an ACE inhibitorIncrease the metoprolol doseObtain doppler ultrasound of the renal arteriesObtain renal angiographyKey point: Manage revovascular hypertensionThis patient has accelerating hypertensionSevere PVD on exam, including epigastric bruitsTreat renal artery stenosis medically unless there is a hemodynamically significant lesion on imagingCurrently much debate on stent vs medical managementWhy the other choices are wrongAn ACE inhibitor might cause significant acute renal failure, especially if she has bilateral diseaseMetoprolol would slow her pulse furtherRenal angiogram is relatively contraindicated with her GFR of about 30Add an ACE inhibitorIncrease the metoprolol doseObtain doppler ultrasound of the renal arteriesObtain renal angiographyQuestion 12A 25-year-old male has dark urine and oliguria. He has 5 days of a URI with rhinitis, sore throat, and fever. Has mild myalgia and bilateral flank pain but no dysuria. He is taking ibuprofen for painVitals: BP 135/88, remainder WNLExam: Erythematous pharynx without exudate, neck lymphadenopathy, 1+ LE edemaLabs: Hb 9.8, WBC 9.9, PLT 258K, C3+C4 WNL, CK 95, Creat 2.3, ASO negativeUA: >100 RBC, 2-5 WBC, no bacteriaRenal US: Essentially normalWhich of the following is the most likely cause of acute renal failure?Analgesic nephropathyIgA nephropathyPost-infectious glomerulonephritisRhabdomyolysisKey point: IgA nephropathy causes renal failure concurrent with URIGross hematuria with URI can be the first presentation of IgA nephropathyMucosal infection causes production of IgA, with abnormally formed IgA antibodies causing nephropathyMacroscopic hematuria is a favorable prognostic findingWorrisome findings include severe AKI, age > 50, crescents or fibrosis on renal biopsyWhy the other choices are wrongHematuria is not a feature of analgesic nephropathyPost-infectious is similar but generally presents after a latency periodRhabdomyolysis may lead to AKI, but CK was normal and there was no myoglobin on UA.Analgesic nephropathyIgA nephropathyPost-infectious glomerulonephritisRhabdomyolysisQuestion 13A 54-year-old female has a 4-week history of LE edema and 5 kg weight gain. No hematuria or dysuria. She has a 14-year history of well controlled HTM and DM. She is on lisinopril, metformin, and simvastatin.Vitals: BP 135/85. Otherwise WNL.Exam: Retinal exam WNL. Bilateral 3+ LE edemaLabs: Albumin 2.3, BUN 21, Creat 0.7. The following are normal: Complement, cryoglobulin, SPEP, PF, ANA, Hepatitis panelUrine: 24-hour protein 12 gramsKidney biopsy shows subepithelial deposits with foot process effacement.Which of the following is the most likely diagnosis?Diabetic nephropathyMembranous lupus nephritisMinimal change glomerulopathyPrimary membranous glomerulopathyKey point: Patients are allowed to have 2 diseasesShe has a long history of well-controlled diabetes and suddenly presents with nephrotic syndromeUnusual progression for diabetic nephropathyMembranous nephropathy is common in this age groupSecondary membranous associated with medications, malignancies, and infections.Why the other choices are wrongThis is an unusual progression for diabetic nephropathy, which generally progresses much slowerMembranous lupus is generally seen in the setting of systemic lupusMinimal change disease might present similarly but would not have deposits on biopsyDiabetic nephropathyMembranous lupus nephritisMinimal change glomerulopathyPrimary membranous glomerulopathyQuestion 14A 65-year-old male is hospitalized following emergent surgery for perforated bowel. He has stage 4 CKD at baseline. He has HTN treated with amlodipine.Vitals: Temp 38.1, BP 150/95, pulse 102Exam: Bowel sounds present, colostomy well perfusedSerum K increases from 4.8 to 6.9, creatinine increases from 5.4 to 6.4. Bicarbonate is 17. Urine output has fallen to 50 mL over 8 hours and does not improve with fluids.ECG reveals peaked T-wavesIn addition to calcium and insulin-dextrose, which of the following is the most appropriate treatment?FurosemideHemodialysisSodium bicarbonateSodium polystyrene sulfonateKey point: Manage hyperkalemiaPatient has hyperkalemia due to tissue necrosisWill need to have potassium removed from his bodyOptions are limited without urine output.After stabilization, hemodialysis is the best option to quickly remove large amounts of potassiumWhy the other choices are wrongLasix is unlikely to be effective in the setting of oligo-anuria unresponsive to fluidsSodium bicarbonate is seldom effective in acidosis of chronic kidney disease for lowering potassiumSodium polystyrene sulfonate is contraindicated in the setting of recent bowel surgery. The risk is increased with solutions containing sorbitol. Never give a kayexelate enema.FurosemideHemodialysisSodium bicarbonateSodium polystyrene sulfonateQuestion 15A 27-year-old female is evaluated for 4 months of hypertension. She feels well. History is otherwise unremarkable.BP 166/108, other vitals WNLExam: Bruit in the right epigastric region. Otherwise WNLLabs: Renal panel and UA are unremarkableRenal angiogram shown at right

Which of the following is the mostappropriate next step?ACE inhibitorCalcium channel blockerPTCASurgical revascularization

Key point: PTCA is effective for fibromuscular dysplasiaMedial fibroplasia of the renal arteryGenerally in young patients with sudden onset of hypertensionAngiography is the best way to diagnose FMD

Why the other choices are wrongDrug therapy should not be attempted until after the results of PTCA are apparent.Surgical revascularization is not first-line therapy but might be needed for difficult anatomy or those who do not respond to PTCAACE inhibitorCalcium channel blockerPTCASurgical revascularizationQuestion 16A 59-year old man is evaluated for worsening kidney function. He was hospitalized since yesterday with a diabetic foot ulcer, which has been progressing for 4 weeks. He has CKD, HTN, and diabetes. He is on metformin, insulin glargine, lisinopril, and cefipime.Vitals: BP 160/100, otherwise WNL. BP 3 months ago was 130/78Exam: Erythematous foot ulcer, 2+ LE edemaLabs: Albumin 2.3, C3 and C4 decreased, creatinine 4.1 (BL=1.4)Urine: 25 RBC, erythrocyte casts. 24-hour protein 1.5 grams

Which of the following is the most likely cause of AKI?Diabetic nephropathyIgA nephropathyPost-infectious glomerulonephritisPrimary membranous glomerulopathyKey point: Diagnose post-infectious GNQuestion stem notes a chronic infectionLow complementSkin flora are common causes of post-infectious GNCan manifest as a rapidly progressive glomerulonephritis (RPGN) or a more indolent courseOften progresses to advanced CKD, especially in adultsWhy the other choices are wrongDiabetic nephropathy progresses slower and is not associated with hematuriaIgA nephropathy is generally seen in association with a mucosal infectionMembranous nephropathy generally presents with more than 1.5 grams of protein and generally has minimal hematuriaDiabetic nephropathyIgA nephropathyPost-infectious glomerulonephritisPrimary membranous glomerulopathyQuestion 17A 51-year-old male is evaluated for 1 year of uncontrolled hypertension. There is no family history of HTN. He never smoked and has no other medical problems. He is on max doses of chlorthalidone, lisinopril, and amlodipine.Vitals: BP 160/94, pulse 76, remainder WNLExam: Unremarkable.Lab: Creat 1.1, K 4.1, urianlysis WNL

Which of the following is the most appropriate next step in management?Switch chlorthalidone to furosemideSwitch lisinopril to aliskirenObtain renal ultrasound with dopplersObtain a plasma renin aldosterone activity ratio

Key point: Hyperaldosteronism is a common cause of secondary HTNThis patient has resistant hypertensionBP remains elevated on 3 medications, one of which is a diuretic.Hypokalemia is not consistently seen with hyperaldosteronismHigh aldosteronism in the setting of relatively low renin suggests primary hyperaldosteronismConfirm with a 24-hour aldosterone collectionHigh salt dietWhy the other choices are wrongSwitch to a loop diuretic can be helpful in patients with decreased renal functionAliskerin is not more effective than lisinopril for blood pressure controlWhile RAS could also cause the patients symptoms, he has no other evidence of vascular diseaseSwitch chlorthalidone to furosemideSwitch lisinopril to aliskirenObtain renal ultrasound with dopplersObtain a plasma renal aldosterone activity ratioQuestion 18A 62-year-old male is hospitalized after being found down. He is confused but thinks he was in a fight a few days ago. He has HTN and hyperlipidemia, as well as alcohol abuse.Vitals: BP 165/85, pulse 102, temp 37.3Exam: Multiple bruises, confused, orients to self only, membranes are dry, abdomen soft, no edemaLabs: Hb 9.3, WBC 6.5, PLT 113K, BUN 85, Creat 4.5, K 5.1, HCO3 21, Phos 5.8, CK 15KUrine: FENA 5.7%, 3+ blood, 3-5 RBC, 5-10 WBC, few granular casts

Which of the following is the most likely diagnosis?Acute interstitial nephritisHepatorenal syndromeAbdominal compartment syndromePigment nephropathyKey point: Recognize pigment nephropathy as a cause of AKICommonly presents with a history of muscle traumaFightFound downAlso with myotoxic drugs, exertionStatinsExacerbated by volume depletionUA with positive heme but no RBC on micro

Why the other choices are wrongInterstitial nephritis generally needs to have a history of an offending agentThere is no evidence of liver disease to suspect hepatorenal syndrome, and he is not hypotensiveAbdomen is soft on exam, making compartment syndrome unlikelyAcute interstitial nephritisHepatorenal syndromeAbdominal compartment syndromePigment nephropathyQuestion 19A 30-year-old female has 2 months of edema and weight gain. She has no history and takes no medications. Exam: BP 132/82. 3+ LE edema, otherwise unremarkableLabs: Albumin 3.1, BUN 19, creat 0.7, cholesterol 237, LDL 147, Hepatitis negative, ANA negative, RF negative, HIV negativeUrinalysis: 3+ protein, estimated proteinuria 4 grams/dayKidney biopsy is consistent with membranous glomerulopathy. No evidence of mesangial involvement, glomerulosclerosis, or interstitial changes.Which of the following is the most appropriate treatment?ACE and statinCalcineurin inhibitor such as tacrolimusCorticosteroidsCyclophosphamideMycophenolate mofetilKey point: Treat membranous nephropathyShe has primary membranous nephropathyRisk factors for progression:Age > 50Elevated creatinineHTNGlomerulosclerosis, interstitial changesPersistent proteinuria for 6 monthsACE and statin can control her hypertension and hyperlipidemia of nephrotic syndromeWhy the other choices are wrongShe has a low risk of progression to ESRDImmunosuppressive therapy should be reserved for more aggressive casesShe might need in the future if she worsensRemember to counsel young women regarding fetal risks with ACE and all immune suppressants, esp mycophenolate mofetilACE and statinCalcineurin inhibitor such as tacrolimusCorticosteroidsCyclophosphamideMycophenolate mofetilQuestion 20A 48-year-old female is seen in the ER for fatigue, weakness, and dizziness. She was at an outdoor concert all day. She has a history of lupus without nephritis, as well as HTN. She is on hydroxychloroquine and HCTZ. She took ibuprofen several times today for myalgias.BP 97/52 lying, 90/45 standing. Pulse 108Exam: No rashes or edema. Mucous membranes dryLabs: BUN 32, creat 1.2 (BL=0.7), FENA 1.2%, urinalysis benign

Which of the following is the most likely diagnosis?Acute interstitial nephritisAcute tubular necrosisLupus nephritisPrerenal azotemiaKey point: Recognize the clinical and lab findings of prerenal azotemiaHistory of volume depletionACE and NSAIDs can reduce renal autoregulationIncreased risk for azotemiaFENA is >1.2%, but she is on HCTZ

Why the other choices are wrongThere are no other exposures to suspect AINAlso no WBC or eosinophils on UAATN generally displays muddy casts on UA. She is at risk for ATN if hypovolemia continuesLupus nephritis would have hematuria or some other evidence of lupus activity.Acute interstitial nephritisAcute tubular necrosisLupus nephritisPrerenal azotemiaQuestion 21A 45-year-old female comes to establish care. She is a recent immigrant from Romania. She has CKD and hypertension. Family history includes a cousin with CKD. She has no urinary symptoms, and takes captopril as well as occasional IbuprofenBP 138/67, BMI 22, other vitals WNLExam: Trace ankle edema, otherwise nonfocalLabs: creat 2.8, K 4.9, HCO3 21Urinalysis: Rare granular casts, otherwise normalRenal ultrasound: Small kidneys without hydronephrosis

Which of the following is the most likely diagnosis?Analgesic nephropathyBalkan nephropathyHypertensive nephropathyIgA nephropathyKey point: Recognize Balkan nephropathyThought to be caused by aristolochia spp that grows with wheatResults in regional patternIncreased risk of urothelial cancersSpecific DNA adductsAlso can be caused by chinese herbal remedies

Why the other choices are wrongAnalgesic nephropathy is unlikely without a history of heavy use. Also more likely to present with proteinuriaHypertensive nephropathy unlikely with well-controlled hypertensionIgA nephropathy is unlikely without hematuria or proteinuria, and without a history of hematuria with URIAnalgesic nephropathyBalkan nephropathyHypertensive nephropathyIgA nephropathyQuestion 22A 76-year-old female is seen in the ER with 1 day of nausea, vomiting, weakness, and confusion. She has fallen several times.BP 130/78, pulse 68, BMI 19Exam: Frail appearing, no edema, JVP normalLabs: Albumin 3.6, BUN 10, creat 0.9, Na 120, K 3.6, Cl 83, HCO3 27, glucose 105, OSM 255Urine: OSM 408, urinalysis normal

Which of the following is the most appropriate treatment?0.9% saline infusion3% saline infusionFurosemideTolvaptanKey point: Rapid treatment of symptomatic hyponatremiaThe patient has SIADH with CNS symptoms and is in a state of rapid decline3% saline infusion is indicatedAim to raise serum sodium by 4-6 in the first 24 hoursUse D5W if over-correction occursWhy the other choices are wrong0.9% saline would worsen the situationNa 155 in 0.9% salinePeople are not beakersLasix prevents concentration of urine and forces water excretion, which would help in timeTolvaptan (V2 receptor antagonist) might be helpful but not acutely. Also is difficult to control the rate of correction with vaptan agents0.9% saline infusion3% saline infusionFurosemideTolvaptanQuestion 23A 60-year-old male comes into clinic as a new patient. He was diagnosed with DM 6 months ago at a health fair. No other history. He is on metformin.BP 145/94, BMI 29. Exam normalLabs: HbA1c 6.8%, BUN 10, creat 0.9, glucose 126Urine: No protein on UAEcho: LVH

Which of the following is the most appropriate next step?Add an ACE inhibitorAdd a b-blockerAdd a calcium channel blockerAdd a diureticContinue current regimen

Key point: Prevent diabetic renal diseaseHe has hypertension in the setting of diabetesGoal blood pressure 130/70RAS blockade can help prevent the onset of diabetic renal diseaseIndependent of BP controlGlomerular hyperfiltration in DM?Why the other choices are wrongAll the other agents listed would control the BP but would have no effect on long term renal functionContinuing with current care is not an optionAdd an ACE inhibitorAdd a b-blockerAdd a calcium channel blockerAdd a diureticContinue current regimenQuestion 24A 66 year old female has AKI 4 days after colectomy for perforation. No intra-op hypotension but required 15 L of fluid. Urine output has gradually diminished and she is now oliguric. She received a single dose of tobramycin post-op (just for fun?) and now is on Vancomycin and Imipenem.Intubated and sedated. Temp 37.2, BP 91/52. BMI 35Cardiopulmonary exam as expected, abdominal exam reveals a tense and distended abdomen with abdominal wall and LE edema. BUN 45, creat 2.9 (up from 0.9 post-op), FENA 1.5%Urinalysis with granular casts, no hematuria or pyuriaRenal ultrasound: Normal kidneys without hydronephrosisWhat is the most likely cause of renal failure?Aminoglycoside nephrotoxicityAbdominal compartment syndromePre-renal azotemiaUrinary onstructionKey point: Abdominal compartment syndrome is an important problem in the ICUPatient is intubated and on paralyticsTense abdomen likely from abdominal wall edema as well as bowel edema, fluid resuscitationExact pathophysiology of abdominal compartment syndrome causing renal failure is unknownWhy the other choices are wrongAminoglycoside nephrotoxicity is unlikely with only a single dosePre-renal azotemia should have responded to fluidsUrinary obstruction was effectively ruled out with a normal renal ultrasoundAminoglycoside nephrotoxicityAbdominal compartment syndromePre-renal azotemiaUrinary onstructionQuestion 25A 54-year-old female is seen for recurrent kidney stones. She had gastric bypass 1 year ago and BMI has fallen from 38 to 33. She has passed 3 stones since surgery, none of which was sent for analysis. She also has diabetes and HTN, and is on metoprolol and glyburide.BP 125/78, remainder of exam is unremarkableUrinalysis: Many crystals (see below)Urine calcium and citrate are normalWhich of the following is the most appropriate next step?Calcium carbonate supplementsChlorthalidonePotassium citrateTamsulosin

Key point: Oxalate stones can be seen after gastric bypassMuch less frequent with newer proceduresFat malabsorbtion leads to decreased intestinal calcium, leaving unbound oxalate to be absorbedTreatment is with supplemental calcium to complex with oxalate and lead to fecal eliminationAlso increase fluid intake and decrease oxalate in dietAlso seen with crohns or any disease that results in small bowel resectionCannot happen after colectomy

Why the other choices are wrongThiazides are useful in other types of calcium stones, by decreasing urine calciumPotassium citrate is helpful in patients with low urine citrateTamsulosin and other a-blockers can help move stones through the ureter but will not help prevent future stonesCalcium carbonate supplementsChlorthalidonePotassium citrateTamsulosinQuestion 26A 71-year-old female is hospitalized for chest pain. She has DM, HTN, hyperlipidemia, and CKD. She is on lisinopril, rosuvastatin, furosemide, carvedilol, insulin, and aspirin.BP 118/50, pulse 70, cardiac exam is normal. Trace edemaLabs: Hb 11, creat 3.1 (baseline), electrolytes normalNuclear study shows reversible ischemia. Patient is scheduled for cardiac cath. Lisinopril is held prior to the procedure.

Which of the following interventions will decrease her risk for contrast-induced nephropathy?Isotonic salineIsotonic saline with mannitol diuresisOral hydrationProphylactic hemodialysis

Key point: Better to prevent contract nephropathyContrast nephropathy incidence increases in those with pre-existing renal diseaseVolume repletion is beneficial for prevention of nephropathyNo clear consensus on whether bicarb is better than normal salineDecreased dye load, low-osmolar dye, etcDont go squirting any dye into the renal arteriesWhy the other choices are wrongMannitol diuresis is used to treat physicians, not patients. Best use of mannitol is in situations where increased osmolality is needed (CNS bleeds, etc)Oral hydration is not more effective, and best to be fasting for a cathProphylactic hemodialysis will lower the creatinine but will not prevent the nephropathy. Contrast dye dialyzes but we cant remove it fast enough to make any differenceIsotonic salineIsotonic saline with mannitol diuresisOral hydrationProphylactic hemodialysisQuestion 27A 32-year-old male is seen for a new diagnosis of autosomal dominant polycystic kidney disease (ADPKD). His mother had ADPKD, HTN, ESRD on dialysis, and died of a stroke. The patient has HTN and takes metoprolol and losartan.BP 132/82, remainder normalExam: Kidneys palpable and not tenderLabs: Creat 1.2, estimated urine protein 150 mg/dayUrinalysis: 5-10 RBCs

Which of the following in the most appropriate next step?24-hour urine collection for proteinCerebral MR angiogramGenotype testing for ADPKDNoncontrast abdominal CT scanKey point: Patients with ADPKD are at risk of cerebral aneurysms8% incidenceMore common in those with a family history of aneurysm ruptureMother had a strokeAlso screen if patient has symptoms such as headache etcRole of screening in patients with no family history of aneurysm is unknownWhy the other choices are wrongRandom UA indicated minimal proteinuria, so a 24-hour collection is not needed. Proteinuria is not usually seen in ADPKD.Genotype testing is not needed. We know he has ADPKD.Abdominal CT would be indicated if he had complaints of cyst rupture or infection24-hour urine collection for proteinCerebral MR angiogramGenotype testing for ADPKDNoncontrast abdominal CT scan