1. Formula for Osmolal gap
    Calculated Osm = 2 (Na) + BUN/2.8 + Glucose/18

    Osm gap = Measured - Calculated

    Normal OG < 10
  2. Briefyly discuss Isopropyl alcohol ingestion

    What is it metabolized to?
    What acid-base characteristic does it have?
    • Metabolized to acetone.
    • Causes Osmolar Gap and Ketosis, but no AG
  3. Briefly discuss Ethylene glycol ingestion

    How is it ingested as?
    What is its acid-base feature?
    What can it cause?
    What is the treatment?
    • Ingested as antifreeze
    • Can cause profound shock
    • Anion gap metabolic acidosis, osmolar gap
    • Metabolized to calcium oxalate crystals in urine
    • Treatment: fomepizole, folic acid, dialysis
  4. Briefly discuss Propylene Glycol:

    Where is it found?
    What can it cause?
    Solvent in IV lorazepam, diazepam, and propofol which can cause lactic acidosis
  5. What are the mechanisms of Non-AG Metabolic Acidosis?
    • Loss of HCO3: Diarrhea, Ureteroenterostomy (ileal loops)
    • Inability to excrete H+: RTA
    • Exogenous Acid: TPN
    • -- Addition of lysine, arginine
  6. Discuss Non-Anion Gap Metabolic Acidosis:

    When is it seen?
    How do you differentiate from its causes?
    • Seen in Diarrhea and RTA
    • Differentiate the two above by measuring Urine AG
    • UAG = (UNa + UK) - UCl
    • Serves as a measure of kidney's ability to generate ammonium
    • In non-AG acidosis, calculate UAG:
    • Negative UAG = Diarrhea: kidney generates NH4, urine Cl increases
    • Positive UAG = RTA: NH4 production is impaired
  7. What are the Distal RTAs?
    Type 4 or Type 1
  8. What RTA is proximal?
    Type 2
  9. Which RTAs are hypokalemic?
    Type 1 and 2
  10. Which RTA is hyperkalemic
    Type 4
  11. Discuss Distal, Type 1 RTA:

    What is the defect?
    What is the urine pH?
    What are its associations?
    • Can't excrete H+ ions across concentration gradient
    • Urine pH never less than 5.5, despite presence of acidemia
    • Associated with hypercalcemia, stones, nephrocalcinosis
    • Etiologies: Amphotericin, toluene, hypergammaglobulinemia
    • Treatment: Potassium and HCO3 replacement, Shohl's solution
  12. What are possible etiologies of Distal Type I RTA?
    • Amphotericin
    • Toluene
    • Hypergammaglobulinemia
  13. What is the treatment for Distal Type I RTA?
    K and HCO3 replacement
  14. What disorders are associated with Distal Type I RTA?
    • Hypercalcemia
    • Nephrolithiasis
    • Nephrocalcinosis
  15. Discuss Proximal, Type II RTA:

    What is the urine pH?
    • Mechanism: Bicarb wasting
    • Urine pH is high early in course, then falls as serum pH falls
    • Etiologies: Drugs - CA inhibitors, amphotericin, heavy metals, myeloma, Sjogren's syndrome
    • Look for Fanconi Syndrome: hypophos, hypouricemia, glycosuria, AAuria (coal -- cysteine, ornithine, arginine, lysine)
    • Treatment: lots of HCO3
  16. What are the etiologies of Proximal Type II RTA?
    • Carbonic Anhydrase inhibitors
    • Amphotericin
    • Heavy metals
    • Myeloma
    • Sjogren's syndrome
  17. Discuss Distal, Type 4 RTA:

    • Hyperkalemic, hyperchloremic metabolic acidosis
    • Mechanism: usually hyporenin, hypoaldo
    • Etiology:
    • - DM, most common
    • - Obstructive uropathy
    • - Interstitial renal disease, sickle cell disease
    • - Drugs: cyclosporine
    • Treatment: HCO3, furosemide, Florinef
  18. Metabolic alkalosis that is Chloride sensitive (UCl < 10) is caused by?
    • Vomiting: UGI losses
    • Diuretics
    • Post-hypercapnia
    • CF
  19. Metabolic alkalosis with UCl > 10 (Chloride Resistant) without HTN is likely caused by?
    • Bartter syndrome
    • Gitelman syndrome
    • Surrptitious diuretics
  20. Metabolic alkalosis that is chloride resistant (UCl > 10) with HTN is likely caused by?
    • Exogenous steroids
    • Endogenous steroids
    • 10 hyperaldo
    • Cushing's
    • 11-OH defic
    • Liddle syndrome
  21. Discuss Bartter Syndrome:

    Acid-base characteristic?
    Electrolyte characteristics?
    What is the renin and ado level?
    What is the calcium level?
    Where is the defect?
    What is the treatment?
    • Hypokalemia
    • Metabolic alkalosis and normal BP
    • Low mag, high renin and aldo
    • Hypercalciuria
    • No chondrocalcinosis
    • Defect in the Ascending Loop
    • Looks like the pt is taking a loop diuretic
    • Rx: NSAIDs, K
  22. Discuss Gitelman syndrome

    Acid-base characteristic?
    Is the BP high or low?
    What is the calcium level
    What is it associated with?
    Where is the defect?
    The pt looks like he is taking what medication?
    What is the treatment?
    • Metabolic alkalosis and normal BP
    • Low K, low Mg
    • Hypocalciuria
    • Associated with Chrondrocalcinosis
    • Defect in the Distal Convoluted Tubule
    • Looks like the pt is taking a thiazide diuretic
    • Tx: Magnesium, K, sometimes amiloride or spironolactone
  23. What is the best intervention in Hypotonic hyponatremia associated with Edema states (CHF, cirrhosis, nephrotic syndrome) and RF? (High ECF Volume)
    • Restrict water
    • Diuretics
  24. Discuss SIADH:

    What urine and serum studies are you going to look for and how will they look?
    What do you always rule out?
    What is the treatment?
    • UOsm inappropriately high for low SOsm, low uric acid levels
    • Always R/O Addison disease
    • Rx: Demeclocycline, Lithium, Vasopressin receptor antagonists (cornivaptan)
  25. Etiologies of Nephrogenic Diabetes Insipidus:
    • Hereditary: X-linked defect in V2 receptot gene
    • Drugs: Lithium, Demeclocycline, Amphotericin
    • Electrolytes: Hypercalcemia, hypokalemia
    • Sjogren's
  26. Treatment for Nephrogenic Insipidus?
  27. What is the treatment for Nephrogenic DI caused by Lithium toxicity?
    • Amiloride
    • Thiazides
    • NSAIDs
  28. What are the ECG changes of hyperkalemia?
    • Peaked T waves
    • Widened QRS
    • Loss of P waves
    • Bradyarrhythmias
  29. Causes of Hypocalcemia:
    • CKD
    • Hypoparathyroidism
    • Pseudohypoparathyroidism
    • Hypomag
    • Acute Pancreatitis
    • Rhabdomyolysis
    • Vitamin D Deficiency
  30. What are causes of Hypercalcemia?
    • 1. Endo causes:
    • - High PTH
    • - Hyperthyroidism
    • - Addison's
    • 2. Granulomatous Dis -- Sarcoid, TB
    • 3. Malignancy
    • 4. Toxicity -- Vitamin A or D, Thiazides, Milk-Alkali syndrome
    • 5. Familial Hypocalciuric Hypercalcemia
  31. What drugs cause Hypomagnesemia?
    "The Amish Pay Cash for their Penthouse"

    • Thiazides
    • Aminoglycosides
    • Cisplatinum
    • Cyclosporine
    • Pentamidine
  32. Etiologies of Hypophosphatemia
    • Alcoholic Ketoacidosis
    • DKA
    • Refeeding/Hyperal
    • Phosphate binders
    • HyperPTH
  33. Complications of Hypophosphatemia:
    • Hemolysis, Thrombocytopenia, Poor WBC function
    • Rhabdo
    • Muscle paralysis
  34. Discuss effect and use of Carbonic Anhydrase Inhibitors

    Where does it work?
    What can it cause?
    What is it used for?
    • Works in the proximal tubule
    • Causes a Type II RTA
    • Causes a metabolic acidosis, so used for treatment of met. alkalosis, mountain sickness, glaucoma
  35. Discuss effect and uses of Loop diuretics:
    • Inhibit Na-K:2Cl channel
    • Useful in hypercalcemia, Type 4 RTA
  36. Range of Pre-HTN BP?
  37. Stage I HTN ?
  38. Stage 2 HTN
    ≥160 / ≥100
  39. Discuss Primary Hyperaldosteronism:
  40. Discuss hypertension secondary to 11-OH deficiency:
    • There is high cortisol, low renin and low aldosterone.
    • Glycyrrhizic acid also inhibits 11-hydroxysteroid dehydrogenase
  41. What is Liddle syndrome?
    What pertinent labs point toward this diagnosis?
    What is the treatment?
    • HTN with low K and metabolic alkalosis
    • Abnormality is in salt absorption
    • Defect in the amiloride sensitive Na channel results in chronic volume expansion
    • Low renin, Low aldo levels
    • Autosomal dominant
    • Treatment: triamterene and Na restriction
  42. What is the normal Protein level in a 24-hour urinc collection?
    How about in a normal "spot" urine protein/creatinine ration?
    • <150 mg/day
    • < 200 mg/g (.2) in a spot urine
  43. What are the causes of sterile pyuria?
    • TB
    • prostatitis
    • analgesic abuse nephropathy
  44. In a pt with hematuria, what would make you suspect an upper tract source?
    • RBC casts
    • Proteinuria
    • Elevated creatinine
  45. What are the diseases associated with the ff casts?
    1. RBC casts
    2. WBC casts
    3. RTC casts
    4. Granular ("dirty brown") casts
    5. Waxy casts
    • 1. Glomerulonephritis
    • 2. Pyelo
    • 3. Interstitial inflammation
    • 4. ATN
    • 5. CKD
  46. Discuss Diagnostic studies for ARF
    • UA
    • FEN
    • U/S of kidney
    • Renal bx if ARF unresolved or unexplained
  47. Discuss Acute Interstitial Nephritis
    • Always consider when ARF occurs with patient on a new medication
    • Clinical clues: rash, fever, eosinophilia
    • UA: renal tubular cells +/- casts
    • Eosinophils in the urine (Wright or Hansel stain)
  48. Drugs that can cause Acute Interstitial Nephritis
    • NSAIDs
    • Antibiotics: PCN, sulfa, cephalosporins, rifampin, quinolones
  49. Discuss AIN (Acute Interstitial Nephritis) secondary to NSAIDs
    • May occur months after beginning NSAID in patients with normal renal fxn
    • AIN with nephrotic range proteinuria
    • This is different than the pre-renal ARF that NSAIDs cause in patients with pre-existing renal disease
  50. ARF with FEN > 2% point toward what diagnosis?
    What casts is assoc with this?
    • ATN
    • Muddy brown cast
  51. What type patient is at risk for Radiocontrast Nephropathy?
    • DM
    • CKD
    • CHF
  52. Interventions to reduce risk of Radiocontrast Nephropathy?
    • .9 NS 1 ml/kg/kg for 24 hour
    • Low osmolality contrast, lowest dose
    • Prevention: N-acetylcysteine, NaHCO3
    • Stop metformin, diuretics, NSAIDs

    *Please note that this is an exception -- FENa may be low
  53. Who is at risk for Gadolinium Contrast induced Nephrogenic Systemic Fibrosis?
    • ARF or CKD with GFR < 30 ml/min
    • ARF due to hepatorenal syndrome or post-op liver transplant
  54. What is Nephrogenic Systemic Fibrosis?
    • Tightening of the skin of trunk and extremities, unlike scleroderma, spares face.
    • May affect internal organs
  55. Discuss Minimal Change Disease
    • Presentation: Sudden onset, severe nephrtoic syndrome
    • Most common in children, but 10-15% of adult cases of NS
    • Usually GFR is normal, no HTN
    • Most cases are idiopathic
    • May be caused by NSAIDs, also assoc with Hodgkin Disease
    • Treatment: steroids, especially in children, may need cytotoxics in adults
  56. What is the only pathologic finding in Minimal Change Disease?
    Foot process fusion along the GBM seen on EM
  57. Discuss FSGS
    • Most common cause of idiopathic nephrotic syndrome in African-Americans
    • Frequently associated with reduced GFR, HTN and progressive renal failure
    • Most common etiology is idiopathic
    • - HIV-associated Nephropathy
    • - Reflux nephropathy
    • - Obesity
    • Tx: ACE-I, ARB, steroids
  58. What would you suspect in an elderly pt with severe nephrotic syndrome?
    • Suspect Primary (AL) Amyloidosis
    • Usually rapidly progress to end-stage disease
    • Associated with overproduction of light chains
    • Assoc with other organ involvement, i.e., hepatomegaly, restrictive CMP
    • Diagnosis: SPEP, UIEP, Biopsy
    • Responds poorly to treatment
  59. What other differential diagnosis would you have on a pt with nephrotic syndrome with long-standing inflammation, i.e., Familial Mediterranean Fever, TB, RA?
    • Secondary Amyloidosis
    • In FMF, colchicine prevents amyloidosis
    • Always consider MM as etiolgy
    • Rate of progression slowed with eprodisate
  60. In Familial Mediterranean Fever, what medication can prevent amyloidosis?
  61. What can slow the rate of progression of nephrotic syndrome in a pt with Secondary Amyloidosis?
  62. Which Nephritic syndrome has low complement?
    • 10
    • Post-infectious GN
    • MPGN

    • 20
    • SLE
    • Endocarditis
    • Cryoglobulinemia
  63. Which Nephritic Syndrome has normal complement?
    • 10
    • ANCA (+) RPGN
    • IgA Nephropathy
    • Alport syndrome

    • 20
    • Goodpasture's
    • Vasculitis
    • TTP/HUS
  64. Briefly describe the presentation of a pt with Nephritic Syndrome
    • Proteinuria
    • Hematuria
    • ± RBC casts
    • Reduced GFR
    • Salt and water retention
  65. Briefly discuss Post-infectious Glormerulonephritis
    • Post-infectious GN: occurs after many types of infections. Classic is post-strep
    • Latent period: PSGN occurs 7-10 days after URI and up to 30 days after skin infection
    • Requires nephritogenic strain of strep
    • Most commonly presents with gross hematura
    • Labs:
    • ASO positive
    • C3 falls and returns to normal after 6-8 weeks
    • Generally self-limited
  66. What are characteristic pathology features in the renal bx of a pt with Post-infectious GN?
    Subepithelial humps on EM, which are immune complexes
  67. What are the clinical features of Lupus Nephritis?
    • Proteinuria -- 100%
    • Nephrotic syndrome -- 45 - 65%
    • RBC casts -- 10%
    • Microscopic hematuria -- 80%
    • Decreased GFR -- 40-80%
  68. WHO Classification for Lupus Nephritis
    • I Normal Glomeruli
    • II Mesangial
    • III Focal proliferative
    • IV Diffuse proliferative
    • V Membranous
  69. What is the treatment of Lupus Nephritis with proliferative lesions?
    Steroids with cyclophosphamide or MMF
  70. What is the treatment for lupus nephritis with Mesangial (class II) classification?
    What about Proliferative (class II or IV)?
    • Steroids for Mesangial lupus nephritis
    • Pulse steroids and cyclophosphamide, or later MMF, or just MMF and steroids for Proliferative lupus nephritis
  71. Briefly discuss Mixed Essential Cryoglobulinemia
    • Typically associated with HCV
    • Clinical presentation: purpuric skin lesions, polyarthralgias, glomerulonephritis
    • Labs: C4 low, RF +, "mixed" IgG-IgM cryoglobulins+
    • 25% will be mixed "nephritic" and "nephrotic"
    • Renal disease may improve with treatment of HCV, relapses common
  72. What is the usual clinical presentation in Mixed Essential Cryogobulinemia
    • purpuric skin lesions
    • polyarthralgias
    • glomerulonephritis
  73. What lab result would you expect to see in a pt with Mixed Essential Cryoglobulinemia
    • C4 low
    • RF +
    • "mixed" IgG-IgM cryoglobulins+
    • 25% will be mixed "nephritic" and "nephrotic"
  74. What are the three types of Rapidly Progressive GN (RPGN)?
    Histologic hallmark is the "crescent"

    • 1. ANCA (+) = Pauci-immune GN (No immune deposits)
    • 2. Anti-GBM Antibody disease
    • - Goodpasture Syndrome
    • - Idiopathic Anti-GBM Ab GN
    • 3. Immune Complex-Mediated RPGN
    • - SLE, Post-infectious GN (some cases only)
    • - IgA Nephropathy
  75. Briefly discuss ANCA (+) RPGN (Pauci-immune RPGN):
    What needs to be urgently done?
    • Presents as insidious, rapidly progressive GN with HTN
    • Represents a "microscopic" polyangiitis
    • Serology (-) except ANCA
    • Requires urgent renal bx: Only finding is extracapillary proliferation -- "crescents"
    • Treatment: "pulse" methylprednisolone, cyclophosphamide
  76. What typically presents with gross hematuria immediately after URI? (no latent period like PSGN)
    IgA Nephropathy
  77. Briefly discuss IgA Nephropathy
    • Very common form of GN world-wide
    • Typically presents with gross hematuria immediately after URI
    • Pts frequently have normal GU eval before referral for renal biopsy
    • Rare in Af-Am
    • Progressive renal failure in some patients, especially if severe proteinuria and/or hypertension
  78. How do you confirm the diagnosis of IgA Nephropathy?
    kidney biopsy
  79. What renal disease is associated with nerve deafness?
    • Hereditary nephritis: Alport Syndrome
    • Familial renal disease, usually X-linked
    • Patients typically present with hematuria immediately following URI (lack of latent period distinguishes from Post-Strep GN)
    • Ocular disorders may be associated
    • Primary abnormality is defect in alpha-5 subunit of Type IV collagen
  80. How do patients with Hereditary Nephritis typically present?
    • Patients typically present with hematuria immediately following URI (lack of latent period distinguishes from Post-Strep GN)
    • May come with nerve deafness, usually men (X-linked familial renal disease)
    • May also have ocular disorders
  81. Briefly discuss Goodpasture Syndrome
    • Anti-GBM antibodies, acute GN, pulmonary involvement
    • Usually present with hemoptysis, dyspnea
    • Treatment: Plasmapheresis, high-dose steroids
  82. What is you differential diagnosis for a patient who present with hemoptysis and dyspnea?
    • Goodpasture Syndrome
    • Wegener granulomatosis
    • Lupus and other vasculitides
    • Infcetious endocarditis (right sided)
    • Sarcoidosis
  83. What is a characteristic pathology of Goodpasture Syndrome?
    Anti-GBM antibodies
  84. Briefly discuss PAN
    • Affects medium-sized arteries, multi-system involvement
    • Renal involvement due to renal aneurysms leading to renal ischemia/infarction
  85. How do you diagnose PAN?
    Celiac arteriogram
  86. What is the treatment for PAN?
    • "pulse" steroids
    • cytotoxic drugs
  87. Briefly discuss Wegener Granulomatosis:
    • Present most commonly with renal disease associated with involvement of upper and lower respiratory tract.
    • Treatement: "pulse" steroids and cytotoxic drugs

    High dose steroids not effective with nephrities, so this is combined with cyclophosphamide and plasmapheresis
  88. How is Wegener's Granulomatosis diagnosed?
    • granulomas on biopsy
    • vasculitis
    • C-ANCA (+)
  89. In a pt with HUS or TTP, what would you expect to see on the renal biopsy?
    Thrombotic microangiopathy
  90. What are the essential labs needed in the initial workup of the Nephritic Syndrome?
    • Complement levels
    • ANA
    • Hepatitis studies
    • ANCA
    • Blood Cx
    • Lupus studies
    • ASO titers
    • Anti-GBM antibodies
    • And finally, Renal biopsy
  91. What is the standard initial treatment for Goodpasture's Syndrome?
  92. What is the classic presentation of a pt with Analgesic Abuse Nephropathy?
    • Chronic interstitial nephritis with little proteinuria
    • May present with acute flank pain due to papillary necrosis
    • Will have sterile pyuria
    • Imaging shows papillary necrosis
    • Can be contributed to by Tylenol
  93. What else can cause papillary necrosis?
    • sickle cell disease
    • DM with pyelo
  94. When do you screen for berry aneurysms in patients with Polycystic Kidney Disease?
    • Not done routinely
    • It is recommended for those with PCKD with symptoms suspicious for aneurysm and those with family history of PCKD and aneurysms
  95. Once a renal patient's GFR decreases to < 60 ml/min, what is your next intervention?
    • Monitor for Renal Osteodystrophy
    • Screen for secondary hyperparathyroidism
    • Monitor calcium and phosphorus
    • Measure iPTH
    • Alk phos may be elevated
    • Goal is to keep Ca X Pho < 55
  96. For pts at risk for renal osteodystrophy, what is the amount of Phosphorus you would recommend in their diet?
    750 - 1000 mg/day
  97. What interventions would you order to control phosphorus in a patient with renal osteodystrophy?
    • Dietary restriction of phosphorus (750-1000 mg/day)
    • Ca-containing phosphate binders: Calcium CO3 or Calcium acetate
    • Sevelamer or lanthanum
    • Al (OH)3
  98. What intervention would you order for a pt with Renal Osteodystrophy and elevated PTH?
    • Measure serum 25-OH Vitamin D level
    • 1, 25 Vit D3 (calcitriol) or Vit D analogues (zemplar, Hectorol)
    • Calcimimetic agent - Cinacalcet
  99. What is the appropriate intervention for CRF patients with metastatic calcifications and uncontolled hyperparathyroidism?
  100. Briefly discuss Anemia management in a pt with Stges 3,4,5 CKD:
    • Goal Hgb is 11-12
    • If Hgb is < 11, check for iron deficiency with Fe TIBC, Sat and Ferritin
    • Target ferritin value is >100
    • Target Iron saturation >20%
    • If Hgb < 11, give erythropoietin
  101. In patients with CKD, explain why you have to treat acid excess
    • It may exacerbate anorexia and bone disease.
    • Keep serum HCO3 > 20
  102. What are the absolute indications for dialysis in patients with GFR < 15 mL/min?
    • Pericarditis
    • Encephalopathy
  103. What is the diagnostic criteria for CAPD peritonitis?
    PD fluid WBC count > 100 with > 50% PMNs
  104. Recommended empiric therapy for CAPD peritonitis?
    IP Vancomycin or cefazolin and ceftazidime/cefepime (or gentamicin)
  105. In patients with kidney transplant, what is the usual immunosuppression regimen?
    • Triple therapy
    • Prednison
    • Cyclosporine or tacrolimus and/or sirolimus
    • Celcept
  106. What is the usual infection prophylaxis in pts with kidney transplant?
    • Bactrim
    • Ganciclovir
  107. What drugs can raise the levels of cyclosporine and tacrolimus?
    • "D-A-V-E-C"
    • erythromycin
    • clarithromycin
    • verapamil
    • diltiazem
    • azole anti-fungals
  108. What drugs can lower the levels of cyclosporine and tacrolimus?
    • rifampin
    • phenobarb
    • phenytoin
  109. What is the treatment of acute rejection in patients with renal transplant?
    • high dose steroids
    • Polyclonal or monoclonal antibodies
  110. What are the physiologic changes of the kidney in pregnancy?
    • Kidneys enlarge
    • Salt and water retention occur
    • Serum Na falls, BUN falls
    • Respiratory alkalosis
    • Uric acid falls, can have renal glycosuria
    • SVR falls: BP falls, normal always < 120/80
    • GFR rises: normal Scr < 0.8 mg/dL
  111. Define preeclampsia
    • HTN and proteinuria beginning after the 20th week of pregnancy
    • Edema no longer part of the definition
    • If these sx occur in early pregnancy, suspect underlying chronic renal disease
  112. Define Severe Preeclampsia with HELLP Syndrome
    • Hemolysis
    • - abnormal peripheral smear
    • - bilirubin > 1.2
    • - LDH > 600
    • Elevated LFT
    • - AST > 70
    • Low Platelets: < 100,000
  113. What is the clinical presentation of the Acute Fatty Liver of Pregnancy?
    • Primigravida (> 50%)
    • fever
    • abdominal pain
    • nausea and vomiting
    • after 35th week
  114. What is the exam and lab result in Acute Fatty Liver of Pregnancy?
    • Exam: jaundice, HTN, edema, abdominal pain
    • Lab: hyperbiliruvinemia, mild elevation of transminases, hepatic/renal failure
  115. What is the treatment of Acute Fatty Liver of Pregnancy?
    termination of pregnancy
  116. What is the diagnosis in a Post-partum pt with acute renal failure, anemia, HTN?
    • Idiopathic Post-Partum Renal Failure
    • Clinical Features:
    • - Microangiopathic hemolytic anemia
    • - Renal thrombotic microangiopathy
    • - Acute renal failure
    • - Malignant HTN
    • - Thrombocytopenia
    • Begins days to weeks following a normal pregnancy
    • Treatment: usually plasma exchange, ? steroids
  117. Calcium Stone Treatment
    • All patients
    • - increase water intake, reduce protein
    • - increase diet vegetables and fruit
    • - Reduce dietary NaCl
    • Hyercalciuria -- treat with HCTZ
    • Hypocitraturia -- treat with K-citrate
    • Hyperocaluria -- diet, pyridoxine
    • Hyperuricosuria -- allopurinol
  118. Uric Acid Stone Treatment
    • Hyperuricosuria?
    • - reduce dietary purines
    • - allopurinol
    • Persitently acid urine
    • - KHCO3, K citrate, NaHCO3 to keep urine pH > 6.5 - 7
    • - Reduce dietary protein
    • Chronnic volume depletion: chronic diarrhea
    • - correct it
  119. What are "Coffin-lid" crystals?
    Image Upload 1
    • Triple phosphate crystals that have coffin lid appearance
    • Usually due to recurrent UTI caused by urease splitters, i.e., proteus, providencia, klebsiella
    • Urolotic removal of stone
    • Appropriate antibiotics
  120. What are interventions to treat and prevent Cysteine stones?
    • Keep urine output > 2.5 - 3 L/day
    • KHCO3 to keep urine pH > 7 - 7.5
    • Treatment: D-penicillamine or tiopronin
    • -- forms more soluble mixed disulfides with cysteine that are more soluble than cysteine
  121. Describe Cystine stones
    • Octagonal
    • Look like "Stop signs."
  122. What are the characteristics of Immune complex-mediated glomerular nephritis?
    • Hypocomplementemia
    • Dysmorphic erythrocytes
    • Erythrocyte casts seen on urinalysis

    Associated with HIV infection, syphilis, Hep C, or any chronic infection
  123. Muddy brown casts on urinalysis point toward what kind of pathology?
    Pigment nephropathy
  124. What is pigment nephropathy?
    It is a form of AKI that results after muscle injury leads to the release of myoglobin and other intracellular muscle contents into the circulation. Myoglobin is known to cause nephrotoxicity by induction of kidney ischemia and tubular obstruction that results in a form of AKI known as pigment nephropathy.
  125. When should you consider a diagnosis of rhabdomyolysis?
    A diagnosis of rhabdomyolysis should be considered in patients with a serum creatine kinase level above 5000 U/L (83.5 µkat/L) who demonstrate heme positivity on urine dipstick testing in the absence of hematuria
  126. What are complications of rhabdomyolysis?
    • Hypocalcemia
    • Hyperphosphatemia
    • Hyperuricemia
    • Metabolic acidosis
    • Atue muscle compartment syndrome
    • Limb ischemia
  127. How do you manage a pt with ADPKD who present with BP 140/90?
    • BP target in pts with ADPKD is less than 125/75
    • Frontline med is ACE-I or ARB
  128. What intervention would you recommend on a pt with ADPKD who present with low-grade fever and gross hematuria?
    • Rule out infection which usually present with flank pain and bland urine.
    • Low-grade fever and flank pain are the usual presentation in patients with cyst hemorrhage.
    • These episodes are most often self-limited and bed rest and increased fluid intake shorten the duratio of gross hematuria.
  129. In a pt with ADPKD, what is associated with low risk for disease progression?
    • Small kidney size
    • Absence of HTN or proteinuria
  130. What is the gold standard for diagnosis renovascular hypertension due to fibromuscular dysplasia?
    intra-arterial digital subtraction angiography
  131. In a pt with Stage IV CKD and anemia, what level of ferritin and transferrin saturation is diagnostic of iron deficiency?
    A transferrin saturation below 20% and a serum ferritin level below 100 ng/mL (100 µg/L) are diagnostic of iron deficiency in predialysis patients with CKD.
  132. What is the treatment for patients with myeloma kidney?
    • Chemo and plasmapheresis
    • Dialysis also if with symptomatic uremia
  133. What is the initial management of a pt with myeloma cast nephropathy?
    • volume expansion
    • alkalinization of the urine
    • discontinuation of nephrotoxic agents
    • avoidance of radiocontrast agents
  134. What is Tumor Lysis Syndrome?
    • It is caused by urate deposition and calcium phosphate ppt within the renal tubules
    • Develop after initiation of chemo and can occur spontaneously in pts with a hign tumor burden
    • Can manifest as acute oliguric kidney injury accompanied by increased serum uric acid, phos, and potassium levels
  135. What patients are at high risk for Tumor Lysis Syndrome, and what is the recommended treatment?
    • High risks are:
    • 1. Burkitt lymphoma
    • 2. NHL lymphoblastic
    • 3. Burkitt acute lymphoblastic leukemia
    • 4. ALL with leukocyte count ≥100,000/uL
    • 5. AML with leukocyte count ≥50,000/uL
    • 6. serum uric acid levels higher than 7.5 mg/dL (0.4 mmol/L)

    Treatment: Hydration + Allopurinol + rasburicase
  136. What patients are at Intermediate risk for Tumor Lysis Syndrome, and what is the recommended treatment?
    • Diffuse large B-cell lymphoma
    • ALL with leukocyte count 50,000-100,000/uL (50-100 × 109/L)
    • Acute myeloid leukemia with leukocyte count 10,000-50,000/µL (10-50 × 109/L)
    • Chronic lymphocytic leukemia with Leukocyte count 10,000-100,000/µL (10-100 × 109/L) treated with fludarabine
    • Other hematologic malignancies (including chronic myeloid leukemia and multiple myeloma) with rapid proliferation with expected rapid response to therapy

    Treatment: Hydration + Allopurinol therapy
  137. What patients are at Low risk for Tumor Lysis Syndrome, and what is the recommended treatment
    • Non-Hodgkin lymphoma with indolent non-Hodgkin lymphoma
    • Acute lymphoblastic leukemia with leukocyte count ≤50,000/µL (50 × 109/L)
    • Acute myeloid leukemia with leukocyte count ≤10,000/µL (10 × 109/L)
    • Chronic lymphocytic leukemia with Leukocyte count ≤10,000/µL (10 × 109/L) and solid tumors
  138. What kind of hydration is used to treat tumor lysis syndrome?
    Urinary alkalinization has historically been used to treat tumor lysis syndrome but has been shown to increase the risk of calcium phosphate deposition in the renal tubules, leading to worsening kidney dysfunction. Hydration with isotonic saline is therefore preferred.
  139. When is dialysis recommended in tumor lysis syndrome?
    • oliguric
    • life-threatening hyperkalemia
  140. What medication is contraindicated in pts with myeloma cast nephropathy and GFR is below 30 mL/min/1.73 m2?
    Oral bisphosphonates
  141. In a chemo patient who is receiving cisplatin, what can you give to attenuate direct tubular toxicity?
  142. What is the treatment for IgA nephropathy?
    • ACE inhibitor or an ARB is indicated for patients with IgA nephropathy who have good prognostic indicators such as normal kidney function, normal blood pressure, and a urine protein-creatinine ratio less than 1 mg/mg.
    • Those with progressive disease who have elevated serum creatinine levels should receive pulse corticosteroid therapy or, if kidney insufficiency is present, corticosteroids and an alkylating agent.
  143. How do you manage a pt with staghorn calculi?
    • In patients with staghorn calculi, stone removal is indicated to prevent obstructive nephropathy, loss of kidney function, or pyelonephritis and sepsis. Percutaneous nephrolithotomy is the initial treatment of choice for staghorn calculi, particularly those that are larger than 4 cm in diameter.
    • Extracorporeal shock-wave lithotripsy (ESWL) is associated with a high risk for residual stone fragmentation that may cause future infection and stone growth. Therefore, ESWL is recommended only for patients with stones smaller than 4 cm in diameter and is often combined with percutaneous nephrolithotomy to allow for direct visualization of stone removal.
  144. Cisplatin nephrotoxicity
    When does it usually occur?
    What is the manifestation?
    Typically occurs within the first 2 weeks after drug administration and manifests as a Fanconi-like syndrome of glycosuria, phosphaturia, aminoaciduria, and renal wasting of magnesium and hypomagnesemia.
  145. What is an important point to remember in kidney transplant recipients who had a previous FSGS?
    Focal segmental glomerulosclerosis can recur soon after kidney transplantation, sometimes within minutes or hours of this procedure.
  146. How do you manage a pt with a complex kidney cyst?
    Surgical resection is indicated for patients with Bosniak category III and IV kidney cysts.
  147. What is adynamic bone disease?

    In what group of patients does it occur?
    How is it different from bone disease secondary to hyperparathyrodisim?
    Adynamic bone disease commonly occurs in patients with ESKD and may cause fractures. However, unlike bone disease associated with secondary hyperparathyroidism, adynamic bone disease is often associated with hypoparathyroidism caused by excess vitamin D intake and/or calcium loading. This condition usually manifests as bone pain accompanied by a serum parathyroid hormone level below 100 pg/mL (100 ng/L) and a normal alkaline phosphatase level.
  148. Explain why pts with ESRD may develop "bone disease due to secondary hyperparathyrodism?
    • Chronic kidney disease (CKD) is associated with progressive alterations in mineral and bone metabolism that can cause bone disease. In patients with end-stage kidney disease (ESKD), the kidney’s inability to excrete phosphorus leads to hyperphosphatemia.
    • Loss of kidney function also is associated with 1,25-dihydroxyvitamin D deficiency. Hyperphosphatemia along with decreased 1,25 dihydroxy-vitamin D levels result in hypocalcemia, which leads to direct stimulation of parathyroid hormone secretion. Furthermore, decreased 1,25 dihydroxyvitamin D levels cause increased production of parathyroid hormone.
  149. What is adynamic bone disease?
    Adynamic bone disease is a major cause of bone disease in patients with stage 5 chronic kidney disease and usually manifests as osteopenia, fractures, and bone pain accompanied by a serum parathyroid hormone level below 100 pg/mL (100 ng/L) and a normal alkaline phosphatase level.
  150. How do you evaluate suspected hyeraldosteronism in a pt with resistant hypertension?
    • Patients with hypertension should be screened for primary hyperaldosteronism if they are young, have hypokalemia, or have difficult-to-control blood pressure; such screening includes determination of the serum aldosterone to plasma renin activity ratio, with a ratio greater than 20 strongly suggesting the diagnosis.
    • The best screening test for primary hyperaldosteronism is a determination of the ratio of serum aldosterone (in ng/dL) to plasma renin activity (in ng/mL/min). A ratio greater than 20, particularly when the serum aldosterone level is greater than 15 ng/dL (414 pmol/L), is consistent with the diagnosis of primary hyperaldosteronism.
    • After biochemical confirmation of hyperaldosteronism, localization procedures are appropriate to differentiate aldosterone-producing adenomas, which are amenable to surgical resection, from bilateral hyperplasia, which is medically treated. Given the high incidence of incidental adrenal lesions, however, imaging studies, such as CT of the adrenal glands, should not be performed before autonomous production of aldosterone is confirmed through biochemical testing.
  151. How do you manage recurrent uric acid nephrolithiasis?
    • Alkalinization of the urine with potassium citrate thera;y to obtain a urine pH above 6.0 decreased the risk of recurrent uric acid stones.
    • Consumption of more than 2 L of fluid daily and restriction of sodium inatake are recommended for all patients with a history of nephrolithiasis, and targeted therayp is recommended for patients with a metabolic abnormality that favors stone formation. Because the solubility of uric acid increases in alkaline urine, use of potassium citrate to obtain a urine pH above 6.0 would decrease this patient’s risk for recurrent uric acid stones.
  152. How do you manage a pt with an acute attack of nephrolithiasis?
    Kidney stones may take several days to weeks to pass spontaneously. If a stone does not pass within 2 to 4 weeks, rapid stone removal is indicated. This intervention also is recommended for patients with infection, intractable nausea and vomiting, complete obstruction or anuria, and stones greater than 1 cm in diameter. Extracorporeal shock-wave lithotripsy would be warranted in these settings or in a patient with a stone that is less than 1 cm in diameter located within the kidney or higher than mid ureter, which is not consistent with this patient’s presentation. Furthermore, even if stone removal were indicated for this patient, flexible ureteroscopy would be a more appropriate method than extracorporeal shock-wave lithotripsy to remove a stone located in the distal ureter.
  153. When is Extracorporeal shock-wave lithotripsy (ESWL) indicated?
    ESWL is indicated for stones less than 1 cm in diameter located in the kidney and upper urinary tract and in conjunction with with percutaneous nephrolithotomy to help break apart large stones or staghorn calculi.
  154. When is percutaneous nephrolithotomy indicated?
    Percutaneous nephrolithotomy is indicated for stones larger than 1 cm in diameter, staghorn calculi, and cystine stones that are resistant to ESWL. This intervention also is indicated for patients with urinary tract abnormalities such as horseshoe kidney.
  155. When is ureteronoscopy recommended in the treatment of kidney stones?
    It is recommended to remove stone in the distal ureter or to remove stone fragmens caused by ESWL.
  156. What urinalysis result point toward acute tubular necrosis?
    What conditions usually point toward the development of ATN?
    • Elevated serum creatinine level, minimal proteinuria, and muddy brown casts.
    • This condition usually develops after a sustained period of ischemia or exposure to nephrotoxic agents such as cisplatin, intravenous aminoglycosides, or radiocontrast.
  157. When does acute interstitial nephritis commonly develop?
    • It commonly develops after exposure to certain medications, including bactrim.
    • Manifestations of this condition may include rash, pruritus, eosinophilia, and fever. Urine sediment findings include pyuria, leukocyte casts, microscopic hematuria, and tubular-range proteinuria.
  158. Trimethoprim can increase serum creatinine by how much?
    0.5 mg/dL or less
  159. Chronic calcineurin inhibitor nephrotoxicity is characterized by what?
    Cyclosporine and tacrolimus, even when present in the serum at nontoxic levels, can cause kidney injury. Chronic calcineurin inhibitor nephrotoxicity is characterized by an elevated serum creatinine level, hyperkalemia, hyperuricemia and gout, and a normal anion gap metabolic acidosis.
  160. How do you diagnose isopropyl alcohol poisoing?
    • It is characterized by an increased osmolal gap in the setting of positive serum and urine ketones, and does not cause metabolic acidosis
  161. A pt appears intoxicated and unconscious, with elevated osmolal gap. How do you differentiate the causes?
    An elevated osmolal gap suggests the presence of an unmeasured osmole and is most commonly caused by ethanol. The osmolal gap is also elevated in the presence of ethylene glycol, methanol, and isopropyl alcohol. However, isopropyl alcohol does not cause an elevated anion gap metabolic acidosis (methanol and ethylene glycol poisoning) and is not associated with retinal abnormalities (methanol poisoning) or kidney failure (ethylene glycol poisoning).
  162. A pt with a history of "glue sniffing (inhalant abuse)" was brought to the ED with MS change. Describe the lab findings that you would expect.
    metabolic acidosis, hypokalemia, hypophosphatemia, rhabdomyolysis, and elevated creatine kinase level.
Card Set
Kidney problems