MKSAP Nephrology Flashcards

1
Q

How do you calculate urine anion gap? When is it negative vs. positive?

A

(Urine Na + Urine K) - (Urine Cl)
In response to met acidosis kidney increases acid excretion -> increased urine ammonium and urine Cl (to balance the + charge of ammonium)
In GI losses of acid, and type 2 RTA urine anion gap is negative
RTA type 1 and type 4 results in positive urine anion gap

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2
Q

What bone pathology is seen in patients w/ CKD? Are PTH and ALP low/normal/high? How is it treated?

A
  1. Adynamic bone disease - lack of bone cell activity and reduced rate of bone turnover; typically associated with vascular calcifications
  2. Normal
  3. Allow PTH to rise - avoid calcium based binders, conservatively use vitamin D, decrease dialysate calcium concentration
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3
Q

What are 3 medications that can be used in SIADH? What are their main side effects?

A

Demeclocycline - photosensitivity and GI sx
Tolvaptan - liver toxicity
Urea - unpalatable taste

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4
Q

In hypernatremia what is the urine osmolality in non-renal losses vs. osmotic diuresis?

A

> 600 mOsm/kg H2O

300-600 mOsm/kg H2O

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5
Q

What levels suggest renal wasting of potassium, phosphate, and magnesium?

A

> 15 mEq/24 hours
100 mg/24 hours of phosphate or FEPO4 >5%
10 mg/24 hours of magnesium or FEMg >2%

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6
Q

What are some medications that can cause low Mg? Name 5.

A

Diuretics, cisplatin, aminoglycosides, amphotericin B, calcineurin inhibitors, VEGF inhibitors

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7
Q

What are some signs/symptoms of high Mg? Name 5. What is the treatment?

A
  1. Somnolence, loss of deep tendon reflexes, bradycardia, hypotension, and hypocalcemia; flaccid paralysis, respiratory failure, complete heart block at levels >12
  2. Discontinue Mg products, saline diuresis, IV calcium
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8
Q

What conditions are associated w/ eosinophils in the urine? Name 5.

A

AIN, post-infectious GN, atheroembolic disease of the kidney, septic emboli, small vessel vasculitis, parasitic disease, prostatic infections

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9
Q

Comparing Bartter and Gitelman syndrome - where do they act? Which has elevated renin and aldosterone? Which causes low Mg? Which causes low urine Ca?

A

Bartter - thick ascending loop of Henle; has elevated renin and aldosterone levels
Gitelman - distal convoluted tubule; causes low Mg and low urine Ca

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10
Q

In whom can acquired hypokalemic periodic paralysis occur?

A

Patients w/ thyrotoxicosis, typically of Asian or Mexican descent

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11
Q

What are some findings in severe hypophosphatemia? Name 4.

A

Muscle weakness, HF, rhabdomyolysis, hemolytic anemia, and metabolic encephalopathy

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12
Q

What is the diagnostic criteria for pre-eclampsia? Name 5 criteria besides proteinuria. What can be used to reduce risk in high risk women?

A
  1. HTN and proteinuria >300 mg/24 hr or UPC >300 mg/g
    OR in absence of proteinuria, HTN + platelets <100, Cr >1.1, elevated LFTs (2x ULN), pulmonary edema, or cerebral/visual sx
  2. ASA 81 mg after 12 weeks of pregnancy
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13
Q

How does atherosclerotic renovascular disease present? Name 4.

A

Severe HTN after age 55, recurrent flash pulmonary edema, refractory HF, AKI after starting ACEi/ARB, asymmetry in kidney sizes of >1.5 cm, or presence of unilateral small kidney <9 cm

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14
Q

What are the guidelines per ACP and AFP for HTN in patients age >60?

A

Goal <150/90 mmHg for all patients unless they have history of stroke or TIA, then goal is <140 mmHg

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15
Q

What BP med can cause myopathy when used with high dose statin?

A

Calcium channel blockers (especially non-DHP)

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16
Q

What is the most common cause of infection-related GN? What is the time course w/ staph vs. strep GN?

A
  1. Staph aureus
  2. Staph-mediated IRGN occurs at the same time as the infection; strep mediated occurs 7-10 days after an oropharyngeal infection, 2-4 weeks after skin infection
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17
Q

What is the HCO3 compensation for acute vs. chronic respiratory acidosis? Acute vs. chronic respiratory alkalosis? What is the pCO2 compensation for metabolic alkalosis?

A
  1. Acute - 1 mEq increase for every 10 mmHg increase, Chronic - 4 mEq increase for every 10 mmHg increase
  2. Acute - 2 mEq for each 10 mmHg decrease; Chronic 5 mEq decrease for every 10 mmHg decrease
  3. For each 1 mEq increase in HCO3, pCO2 increases by 0.7 mmHg
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18
Q

Which ingestion presents w/ neurotoxicity, AKI and flank pain, pulmonary edema, and/or hypocalcemic symptoms? In what is this found? How is it treated?

A
  1. Ethylene glycol
  2. Found in antifreeze, solvents, and cosmetics
  3. Treated w/ fomepizole and IV hydration; hemodialysis if CNS depression, AKI, severe acidemia; can use pyridoxine and thiamine in suspected toxicity
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19
Q

Which ingestion presents w/ CNS damage, blindness, abdominal pain, and/or pancreatitis? In what is this found? How is it treated?

A

Methanol - found in windshield washing fluid, commercial solvents, paints, some antifreezes
Treated w/ fomepizole; can give folic acid in suspected toxicity

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20
Q

What type of acidosis can result from chronic acetaminophen ingestion? How is this diagnosed?

A

Pyroglutamic acidosis; most common in critically ill patients, liver disease, CKD, vegetarians, and those w/ poor nutritional status
Diagnose w/ high concentrations of urine pyroglutamate on urine testing for organic anions

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21
Q

What crystals are amorphous, or are like prisms, needles, or star-like clumps? Dumbbell or envelope shaped? Hexagonal shaped? Coffin-lid shaped? Which crystals are associated w/ distal RTA, hyperparathyroid, topiramate, and acetazolamide? Which crystals are rhomboid or needle shaped?

A
  1. Calcium phosphate 2. Calcium oxalate 3. Cystine 4. Struvite 5. Calcium phosphate 6. Uric acid
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22
Q

What is the delta delta ratio and how is it interpreted?

A

(change in anion gap)/(change in bicarbonate)
<1 = concurrent normal anion gap metabolic acidosis
>2 = concurrent metabolic alkalosis

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23
Q

What is the defect in type 1 RTA? What is the urine pH? What are some lab findings? Name 3. What are some common causes? Name 5. What is the treatment?

A
  1. Inability of the distal tubule to excrete H+
  2. urine pH >6 b/c unable to acidify the urine
  3. Hypokalemia, hypercalciuria, hyperphosphatemia, hypocitruria ; kidney stones
  4. Sjogren syndrome, reflux uropathy, obstructive uropathy, amphotericin B, lithium, sickle cell disease, Wilson disease, dysproteinemia
  5. Potassium citrate 1 mEq/kg/d
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24
Q

What is the defect in type 4 RTA? What is the urine pH? What are some causes? Name 5. What is the treatment?

A
  1. Aldosterone deficiency; distal tubule
  2. urine pH <5.5
  3. Primary AI, diabetes, tubulointerstitial disease (sickle cell, medullary cystic kidney disease, urinary obstruction, kidney transplant rejection), ACEi/ARB, heparin, COX-2
  4. Treat underlying cause; can use diuretics if hypertensive and volume up; potassium binder
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25
Q

What is the defect in type 2 RTA? What is the urine pH? What are some lab findings? What are some causes? Name 3. What is the treatment?

A
  1. Failure of proximal tubule to absorb HCO3
  2. Urine pH <5.5 (b/c distal nephron functions fine)
  3. Glycosuria, phosphaturia, hypouricemia, hypokalemia; HCO3 stabilizes 12-14; urine anion gap negative
  4. Fanconi syndrome, monocloncal gammopathies, acetazolamide, Sjogren
  5. Alkali replacement; consider thiazides
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26
Q

What urine Cl in metabolic alkalosis is saline responsive vs. resistant? What are some causes of each if patient has normal ECF & BP?
In patients with increased ECF what are some causes of low urine Na + urine Cl vs. High urine Na + urine Cl?

A
  1. Urine Cl <15 is saline responsive; mostly caused by vomiting and remote diuretic use
  2. Urine Cl >15 is saline resistant; hypoK, hypoMg, Bartter, Gitelman syndrome are causes
  3. Low Na & Cl are due to HF, cirrhosis, and nephrotic syndrome
  4. High Na & Cl are due to renin secreting tumor, malignant HTN, renovascular HTN, primary hyperaldosteronism, exogenous mineralocorticoid
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27
Q

What type of acidosis are patients w/ short bowel syndrome at risk for? How does this present?

A

D-lactic acidosis

Increased anion gap acidosis, intermittent confusion, slurred speech, and ataxia

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28
Q

What interstitial nephritis can be found in patients from Croatia, Bosnia, Serbia, Romania, and Bulgaria? What element increases their risk? What cancer are they at higher risk for?

A
  1. Balkan endemic nephropathy
  2. Aristolochic acid in the diet; can also be found in chinese herbal supplements
  3. Transitional cell carcinoma
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29
Q

What causes a destructive renal mass invading the parenchyma in a patient w/ chronic pyelonephritis?

A

Xanthogranulomatous pyelonephritis

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30
Q

Which medication can cause type 1 RTA, nephrogenic DI, CTIN, and minimal change disease? How does the nephropathy appear on imaging?

A

Lithium

Cystic dilation of distal tubules w/ formation of microcysts

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31
Q

What are the diagnostic criteria for ADPKD (number of cysts)? What are some extrarenal manifestations? Name 3.

A
  1. Age 15-39: 3 or more unilateral or bilateral cysts Age 40-59: 2 or more cysts in each kidney; Age >60: 4 or more cysts in each kidney
  2. Hepatic cysts, MVP, inguinal and umbilical hernias, inracranial aneurysms
32
Q

What disease presents w/ pain/burning sensations in hands and feet, angiokeratomas, decreased perspiration, corneal and lens opacities of the eyes, kidney disease, and/or heart disease?

A

Fabry disease - deficiency of alpha-galactosidase A

33
Q

How does membranous nephropathy look on biopsy? What is the treatment?

A
  1. Subepithelial immune deposits accompanied by intervening spikes of glomerular basement membrane
  2. Observe for 6-12 months w/ conservative therapy b/c 30% achieve spontaneous remission in first 1-2 years; first line agents include steroids + alkylating agents, cyclosporin or tacrolimus, or rituximab
34
Q

What are some causes of minimal change disease? Name 5.

A

Malignancies (Hodgkin, non-Hodgkin, thymoma), NSAIDs, lithium, infections (syphilis, mycoplasma, strongyloides, ehrlichiosis), atopy (pollen, dairy products)

35
Q

What is lead nephropathy associated with?

A

Hyperuricemia, recurrent gout attacks, HTN

Can have exposure from water, soil, paint, food products, or moonshine alcohol

36
Q

How is one exposed to cadmium? How does cadmium nephropathy present?

A
  1. Exposure to plastic, metal, and electrical equipment

2. Hypercalciuria, glucosuria, proteinuria; can develop osteomalacia (present w/ bone pain) and nephrolithiasis

37
Q

What is seen in Class I-V of lupus nephritis? What is treatment and when is it started?

A
I: minimal mesangial II: mesangial proliferative III: focal IV: diffuse V: membranous VI: advanced sclerosing
Treatment is started at class III - pulse IV steroids and IV cyclophosphamide or mycophenolate (preferred); class V can also be treated with cyclosporine or tacrolimus; maintenance is steroids and mycophenolate or azathioprine; class VI has no treatment besides HD
38
Q

What ingestion presents w/ no metabolic acidosis, acetone on breath, ketones, increased osmolal gap, CNS depression? What is the management?

A

Isopropyl alcohol poisoning

Supportive care

39
Q

What is the treatment of nephrogenic diabetes insipidus?

A

Low salt diet, Thiazide

Amiloride if lithium-induced

40
Q

What are 3 ingestions associated w/ calcium oxalate deposition?

A

Ethylene glycol, Orlistat, high doses of Vitamin C

41
Q

What is the treatment for calcium stones?

A

Increase fluids, decrease sodium intake, Thiazides, Potassium citrate or bicarbonate

42
Q

What type of kidney stones is chronic diarrhea, obesity, and DM associated with?

A

Uric acid

* Chronic diarrhea + metabolic acidosis can be associated with calcium oxalate stones - i.e. Crohns

43
Q

What condition is due to abnormally high bone turnover that occurs with secondary hyperparathyroidism? How does it appear on x-ray?

A
  1. Osteotitis fibrosa cystica

2. Subperiosteal resorption of bone, most prominently at phalanges of hands; radiolucent bone cysts of long bones

44
Q

What levels of transferrin sat and ferritin are diagnostic of IDA in ESRD? What are the goal transferrin sat and ferritin in patients with CKD and anemia?

A
  1. Transferrin sat <20% and ferritin <200

2. Transferrin sat >30%, serum ferritin >500 ng/mL

45
Q

Name 3 side effects for each of the following: cyclosporine, tacrolimus, mycophenolate?

A

Cyclosporine: HTN, ginvigal hyperplasia, dyslipidemia, hirsutism, hyperkalemia, osteoporosis
Tacrolimus: new onset DM, HTN, hyperkalemia, GI sx, osteoporosis
Mycophenolate: diarrhea, leukopenia, anemia

46
Q

Name 5 glomerular diseases associated w/ low complement levels.

A

SLE, post-infectious GN, cryoglobulinemia, membranoproliferative GN, atheroembolic disease

47
Q

What kidney diseases are the following associated with? HIV, hepatitis B, hepatitis C.

A

HIV - FSGS
Hepatitis B - membranous glomerulopathy
Hepatitis C - MGPN with immune complex deposition (both Ig and complements on immunofluorescence)

48
Q

How do you differentiate HELLP from pre-eclampsia?

A

Need microangiopathic hemolytic anemia with elevated bilirubin and schisocytes on peripheral blood smear in HELLP

49
Q

What disease presents w/ elevated UPC ratio with minimal proteinuria by urine dipstick?

A

Light chain cast nephropathy

50
Q

What is the treatment for sulfonylurea toxicity?

A

Dextrose + octreotide, glucagon IM

51
Q

What can be used for severe SSRI/SNRI toxicity?

A

Cyproheptadine

52
Q

Name 3 side effects for the following: azathioprine, sirolimus?

A

Azathioprine: hepatitis, pancreatitis, leukopenia
Sirolimus: dyslipidemia, new onset DM, anemia, leukopenia, proteinuria

53
Q

What is the most accurate equation for adjusting medication dosages in older adults (to estimate GFR)?

A

Cockgroft-gault equation

54
Q

What condition should be suspected in a patient w/ gross hematuria, no active urine sediment, and no other systemic symptoms?

A

Sickle cell trait

55
Q

What presents with pain in low back, flank, or abdomen, weight loss, anorexia, gross hematuria, claudication, and IVC obstruction leading to edema or DVT? What are some associated lab findings? What are some causes? What is the treatment?

A
  1. Retroperitoneal fibrosis
  2. Elevated ESR & CRP, elevated ANA (60% of patients), anemia, normal urine sediment
  3. Idiopathic, drugs (beta blockers, bromocriptine, ergots), malignancy (lymphoma), infection (TB), radiation
  4. Steroids, relief of ureteral obstruction, treat underlying disorder
56
Q

What presents w/ hematuria, R flank pain, dysuria, history of recurrent UTIs, and alkaline urine (pH >8)?

A

Struvite stones w/ urease-producing bacteria (proteus, klebsiella)

57
Q

What are some lab findings in rhabdomyolysis? Name 5.

A

Hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia, AKI, falsely low FENa, blood on U/A w/ no RBCs

58
Q

What are some medications that reduce proximal tubule secretion of creatinine? Name 3.

A

Cimetidine, trimethoprim, cobicistat, dolutegravir

59
Q

What electrolyte disturbance can present w/ ST segment depression, decreased T wave amplitude, and increased U wave amplitude? What electrolyte disturbance can present w/ peaked T wavs, shortened QT interval, prolonged PR interval, and wide QRS?

A
  1. Hypokalemia

2. Hyperkalemia

60
Q

What are some drugs that can cause drug-induced associated vasculitis? Name 3. What antibodies is it associated with?

A
  1. Hydralazine, minocycline, antithyroid drugs

2. High titers of anti-MPO, and can also have concomitantly positive low titer anti-proteinase 3 antibodies

61
Q

What is used as a solvent in IV medications and can lead to agitation, hypotension, tachycardia, coma, seizures, and increased anion gap metabolic acidosis in toxicity? What is the management?

A
  1. Propylene glycol

2. Discontinue IV infusion; hemodialysis

62
Q

What presents as gross hematuria, flank pain, and occasionally obstruction and infection in a patient taking pain medication? What may the CT show?

A
  1. Renal papillary necrosis

2. Microcalcifiations at the papillary tips

63
Q

What glomerular disease can be seen in those w/ hx of premature birth, solitary kidney, or use of lithium, interferon, and pamidronate?

A

Secondary FSGS

64
Q

Tuberous sclerosis complex is associated w/ tumors in the brain, eyes, heart, kidney, skin, and lungs as well as seizures and developmental delay. What renal disease is found in tuberous sclerosis? What screening is required?

A
  1. Renal angiomyolipomas

2. Abdominal MRI every 1-3 years, screening for RCC

65
Q

What disease has prominent thickening and lamellation of the GBM in a “basket-wave” appearance on electron microscopy?

A

Alport syndrome/Hereditary nephritis

66
Q

What condition should be considered in a patient w/ normal renal function, microscopic hematuria, and a family history of isolated hematuria w/o kidney failure?

A

Thin glomerular basement membrane disease

67
Q

What should be given to pregnant women with acute HTN besides anti-hypertensives?

A

Magnesium sulfate as seizure ppx

68
Q

Kidney transplant recipients on immunosuppressive agents are at the greatest risk for what malignancy?

A

Non-melanoma skin cancer - need regular skin exams

69
Q

Are tacrolimus and cyclosporine safe in pregnancy?

A

Yes

70
Q

What electrolyte disorder can cause ST elevation (mimicking STEMI), shortened QT interval, and flattened T waves?

A

Hypercalcemia

71
Q

What presents w/ hyperphosphatemia, increased renal tubular absorption of phosphate, and metastatic calcium deposits usually in periarticular locations?

A

Tumoral calcinosis, an autosomal recessive disorder associated w/ mutations in FGF-23

72
Q

What can be used to reduce calcium oxalate stone recurrence?

A

HCTZ - reduces calcium excretion in the urine

73
Q

What diagnosis should be considered in an older male patient that presents w/ a varicocele and a recent episode of hematuria and flank pain?

A

Renal cell carcinoma

74
Q

What is the treatment for patients w/ relapse of GPA, besides steroids?

A

Rituximab (is superior to cyclophosphamide)

75
Q

What pattern of renal injury is seen in IV zoledronic acid? Pamidronate?

A
  1. Acute tubular necrosis

2. Nephrotic syndrome, most commonly collapsing FSGS

76
Q

What is the management for renal cysts that have regular borders, no septa/calcifications/solid components, posterior enhancement on U/S, and no contrast enhancement on CT/MRI? What is the management for cysts w/ few septa, calcifications, no contrast enhancement on CT/MRI that are <3 cm vs. >3 cm?

A
  1. Reassurance
  2. Reassurance if <3 cm
  3. Follow up imaging in 6-12 months if >3 cm
77
Q

How does polyoma virus (BK) present on cytology? What is needed for diagnosis?

A
  1. Atypical cells w/ intranuclear inclusions

2. Renal biopsy showing characteristic cytopathology (at least 2 biopsy cores) plus positive antibodies against BK