1. Which 2 drugs are commonly associated with pre-renal failure?
    NSAID s and ACE inhibitors
  2. What is Acute Renal Failure?
    • Loss of renal function due to decrease in GFR.
    • often reversible.
  3. What are some of the clinical pesentations in renal failure?
    Fluid Overload

    Hormones: low EPO, low active vitamin D.

    Hyperkalemia, hyperphosphatemia, metabolic acidois.

    Uremia (less excretion of nitrogenous waste)
  4. what is one thing i can do to determine if this is Pre-renal or Acute Tubular necrosis????
    Check the Fractional Excretion of Sodium!

    % FENa= (U/PNa ) / (U/Pcreatinine )
  5. what is the treatment for Acute tubular necrosis?
    there is no treatment, just support and watch their electrolytes, monitor BLOOD PRESSURE,
  6. what are the INDICATIONS for dialysis??
    • 1. Fluid Overload
    • 2. Severe metabolic acidosis
    • 3. Hyperkalemia
    • 4. Uremic syndrome
  7. How do we mostly stage Chronic Kidney disease?
    Based on the GFR.
  8. how does hypertension damage the kidneys?
    Because the hyperfiltration causes the tubules to work more to re-absorb more. This, and deposits of calcium phosphates leads to glomerulosclerosis.
  9. What has been experimentally shown to reduce development of glomerulosclerosis and slow down the progression of renal disease?
    Adequate control of Blood PRESSURE with ACE inhibitors or ARBS
  10. what changes in sodium do you see in patient with Chronic Kidney disease?
    since they are filtering less out in the first place, they have HIGHER FRACTIONAL excretion of Sodium!
  11. do we give ACE inhibitors to someone with CKD?
    No, because they already have high potassium.

    (remember, aldosterone not only promotes potassium excretion in the kidney, but ALSO promotes potassium excretion in the GI).
  12. causes of Low Calcium in CKD?
    • the increased phosphate binds onto the calcium
    • 2. there is less intestinal absorption due to reduced 1, 25- vitamin D (remember, hydroxylation requires normal proximal tubules).
  13. why do diabetics with CKD have less need for insulin?
    Because the insulin is normally metabolized by the proximal tubule, thus in kidney disease, the half life of the insulin will be prolonged.
  14. What do we give to treat someone with CKD?
    1. Blood Pressure: Loop diuretics to control systemic blood pressure (Remember, hypertension is the single most important factor in the progression of the renal disease)

    2. Potassium: Loop diuretics. or temporarily Kayexalate resins to bind the potassium.

    3. Metabolic acidosis: give Sodium Citrate (which will convert to bicarb in the body)

    4. Phosphates: Tums (calcium carbonate salts) to bind the phosphates

    5. Calcium: Calciferol (orally active vitamin D)

    6. Limit protein intake to slow uremia (has been show to slow down progression of renal disease)

    7. Anemia: EPO once a week.
  15. In diabetics, what is the early sign of nephropathy?
    MICROalbuminuria (which can soon become pvert proteinuria).

    • Indicates the need for better glucose and blood pressure control.
    • --and that they need ACE Inhibitor to reduce progression!!
  16. for diabetics, what drug can reduce the progression of nephropathy?
    ACE inhibitors.
  17. What is the normal concentration for serum sodium?
    135-145 mEq/L
  18. osmolality versus tonicity
    Tonicity refers to particles which can lead to water movement across cell membranes.

    Osmolality is all particles.
  19. major site for urinary dilution
  20. what is the normal range for potassium
    3.5-5.5 mEq/L
  21. what is the Henderson-Hasselbach equation
    pH= 6.1 + log 10 (bicarb/(0.03x pCO2)
  22. what is the normal value for pH and for HCO3-
    pH= 7.4

    [HCO3-]= 25 mEq/L
  23. if the pCO2 is providing compensation, expect the 2 digits to =
    the last 2 digits of the pH.
  24. What is the main site of H+ excretion?
    • In the proximal tubule we have the NHE exchanger.
    • and
    • in the Distal Tubule (H+/ATPase. )
  25. what is the serum "anion gap" and what should it normally be?
    [Na] - [Cl-] +
  26. what are Mudpiles?
    • Methanol
    • Uremia
    • diabetic ketoacidosis
    • Paraldehyde
    • Isoniazid
    • Lactic acidosis
    • Ethylene glycol
  27. What are some ways we can loose Bicarb?
    • GI (diarrhea)
    • Renal=
    • *Type 2 RTA : unable to reabsorb bicarb
    • Carbonic anhydrase inhibitors
  28. when someone is hyperglycemic, how do we calculate what their "true" sodium levels are?
    for every 100 mg glucose he is ABOVE from 100, then we add 1.6 mEq/ liter

    Hence, if 1800 = glucose, that is 1700 above, so 17 X 1.6 mEq === 27. 2 mEq/L (we add this amount to the current mEq/L of sodium.
  29. In a person with hyperglycemia, how do we treat them?
    • 1. Saline isotonic (once you give insulin , all the glucose will rush in and drag the water with it)
    • 2. Insulin
    • 3. Potassium.
  30. how do you calculate pOSM?
    • Calculated Posm= (2 x Serum Na) + (serum glucose/18) +
    • (BUN/2.8) =
  31. what is "effective" osm?
    Effective osm= (2 x serum Na) + (serum glucose/18)

    BUN is not included, it can easily go across membranes, not an osmotic agent.
  32. What can you give to lower Potassium in body?
    Kayaxalit (potassium binding resin)= patients hate this!! diarrhea!

    fastest way is to give glucose with insulin (in normal person), in a diabetic you could just give them insulin.
  33. patient has HYPERKALEMIA and he is already showing the peaked T waves and the lengthened QRS and the shortened QT. It will take a few minutes to get the dialysis machine, what can I do to prevent the attacks on the myocardium????
    • give Calcium Gluconate!
    • Ca directly antagonizes effects of hyperkalemia on
    • myocardium.
  34. how can you check his TTKG to see if has normal or abnormal response to potassium
    • (U/P K+)
    • /
    • (U/P osm)
  35. What is MAP=
    MAP= diastolic pressure + 1/3 (pulse pressure)
  36. what is the hallmark for established hypertension?
    Increased SVR
  37. What are the fundoscopic findings in hypertension?
    Hemorrhage, exudates, and papilledema.
  38. What is the Diastolic in HYPERTENSIVE EMERGENCY?
    Diastolic> 140
  39. what is pathologic finding in Malignant Hypertension?
    fibrinoid necrosis.
  40. What is the best single test for the Pheochromocytoma?
  41. what can you use to find the hard-2-localize ectopic pheochromocytomas:
  42. what are adverse effects of thiazides
    • Be careful, increased cholesterol and glucose levels.
    • increased uric acid.
  43. these drugs useful when the GFR and Creatinine is really low and/or the hypertension is complicated by the edema.
    Loop Diuretics
  44. Which drug must you always give with a beta blocker?
  45. Nifedipine
    Calcium channel blocker with VERY Strong vasodilator effects. Increased CO, headache, flushing.
  46. Any of the 4 drugs can be used as initial therapy for treating Hypertension...
    • 1. Thiazides
    • 2. Ace inhibitors
    • 3. beta blockers
    • 4. Calcium channel blockers
  47. Which of the drugs for initial therapy of hypertension have been shown to be the MOST effective at minimizing end organ damage?
    • 1. Beta blockers
    • 2. Thiazides
  48. What are 2 main factors to consider when trying to figure out which anti-hypertensive drug to give?
    Age and Ethnicity
  49. If greater then 50 , which antihypertensive?

    If < 50??
    (as you age, your BP is less responsive to ACE-I or Beta blcokers, hence for above 50 years old, we give : Calcium channel blockers and thiazides. )
  50. African Americans: which antihypertensive drugs are not as effective?
    • Ace inhibitors
    • Beta blockers
    • (EXCEPT: Labetolol which is combined alpha and beta blocker)
  51. What is the initial goal for BP control when giving antihypertensive drugs?
    DBP < 90 mmHg.
  52. Why is Hydralazine only used as a 3rd step drug?
    Because it requires the patient to be on a diuretic and a beta blocker to block the effects of the drug on the kidney and sympathetic system.
  53. Malignant hypertension?
    • DBP> 140 mmHg
    • encephalopathy

    Treat immediately with Nitroprusside (vasodilator).
  54. Hypertensive Urgency
    DBP= 120-140

    give CLONIDINE
  55. Treatment of hypertension secondary to really bad renal disease
    Loop Diuretics.
  56. what is the best treatment for Goodpasture's disease?
    Plasmapharesis, Cyclophosphamide, and prednisone.
  57. What are 3 components of Nephritic?
    Red cell leakage

    Increased Renin

    Impaired Filtration
  58. Podocyte Foot fusion only
    Minimal Change Disease
  59. What about of Proteinuria classifies as Nephrotic Range?
    >3.5 mg/24 hr
  60. Nephrotic Syndrome
    Proteinuria sufficient to cause edema and hypoalbuminemia
  61. Abrupt onset of reduced urine volume and reduced GFR, usually with microscopic hematuria and often hypertension.
    Acute Nephritic Syndrome
  62. What are the Proliferative Types of GlomeruloNephritis?
    • 1. Membranoproliferative GN
    • 2. Mesangial IgA (IgA nephropathy)
    • 3. Acute Proliferative GN (acute post-streptococcal)
    • 4. Crescentic GN ( rapidly progressive GN)
  63. There Only structural abnormality is fusion of the foot processes of the podocytes. May be due to a nephrotoxic cytokine coming from T cells. Disease is Episodic and heals in between. Done by adulthood usually.

    How do We treat?
    Minimal Change Disease

    Treatment: Corticosteroids.
  64. Accumulation of hyaline material in mesangial region
    Most common in non-diabetic black men

    May be helped with steroids.
    Focal Segmental Glomerulosclerosis
  65. Image Upload 1
    Focal Segmental Glomerulosclerosis
  66. Image Upload 2
    • Membranous Glomerulonephritis (Light microscopy shows the thickening of the GBM)
    • on IF= granular ribbon like green pattern
    • EM= electron dense deposits in subepithelial position with intervening "Spikes" of GBM material

    • --Most common in non-diabetics
    • --Treat: steroids
  67. Membranoproliferative Glomerulonephritis? What is similar in both Type I and Type II.
    C3 deposition in glomeruli is so intense that blood levels of C3 are depleted. Often an autoantibody reacts with an antigen on the C3 path and stabilizes the enzyme in its active form.
  68. WHat do you we see on the different levels for the MembranoGlomerulonephritis diseases?
    I.F= granular

    • E.M. Type I= Subendothelial/mesangial
    • Type II= dense intramembranous deposits

    Light Micro" mesangial proliferation plus thickening of GBM.

    No benefit from steroids!!
  69. IgA nephropathy (Berger's Disease)
    • Disregulated mucosal immunity , Ig A precipitates in the glomerular mesangial regions, where they activate inflammatory systems.
    • I.F= IgA and C3 in granular pattern in mesangium.
    • E.M.= electron dense deposits in mesangium

    Often triggered by Fevers and URIs

    No specific treatment.
  70. Subepithelial IgG and C3 deposits with GBM thickening
    Membranous GN
  71. Low Serum C3
    seen in ....
    • Membranoproliferative glomerulnephritis
    • Post-streptococcal Acute Glomerulonephritis
  72. Endothelial and Mesangial hypercellularity.


    Subepithelial C3 and IgG
    Acute Glomerulonephritis (Post-strep)
  73. how can SLE present with kidney damage?
    • In the first 4 types, it would be a Diffuse Proliferative Glomerulonephritis
    • (due to SLE)

    and then it could be Membranous Nephropathy
  74. How is Alport's syndrome different from Good pasture's disease?
    genetic mutation in the Type 4 collagen for Alport's
  75. In diabetic nephropathy, what sign correlates to the the extent of the disease?
    the amount of mesangial thickening.
  76. what are the earliest signs of diabetic nephropathy?
    • Microhematuria
    • due to increased pressure rates.
  77. Why are blacks more likley to have increase risk of developing glomerular damage from hypertension because ....
    they have a tendency to vasodilate at the afferent arteriole.
  78. name the Mixed nephrotic/nephritic syndrome
    • Membranoproliferative glomerulonephritis
    • SLE

  79. How can we lessen tubular damage from glomerular disease?
    lower the amount of proteinuria
  80. What factors make sure that there is no protein in the urine?
    a highly selective glomerular capillary wall with negative charge

    low molecular weight proteins reabsorbed by the PT
  81. what is the best way of detecting proteinuria and what is its flaw?
    • The best method is through Urine Dipstick.
    • However, it only Detects ALBUMIN!!

    hence, it will be negative even if you had a lot of Bench Jones proteins from Multiple Myeloma.
  82. what is the best way to quanitify the amount of protein loss?
    you "estimate" a 24 hour protein collection using a protein/creatinine ratio in grams per body surface.
  83. What ratio of protein/creatinine would suggest the presence of nephrotic range?
  84. what are the non-renal complications of proteinuria?
    • PE (loss of Anti-thrombin III)
    • Malnutrition
    • Loss of immunoglobulins (infection)
    • edema= skin breakdown, more infection
    • hyperlipidemia , increased atheosclerosis
  85. What is a distinctive property of Renal adenocarcinoma?
    It likes to stick to endothelial cells.

    It proliferates along the luminal surfaces of large veins, such as renal vein or inferior vena cavae. (it likes to sticks to endothelial cells)
  86. classic traid of Renal cell carcinoma
    • Flank pain
    • hematuria
    • abdominal mass
  87. what do you see on histology for Renal Cell carcinoma?
    nests of uniform clear cells
  88. What are the paraneoplastic signs of Renal cell carcinoma?
    • EPO (polycythemia)
    • Renin
    • hypercalciuria (Parathromone)
    • Sex hormones
    • cortisol
  89. Oncocytoma
    • asymptomatic.
    • encapsulated tan nodule
    • with brown look,
  90. what do waxy casts indicate?
    advanced renal failure
  91. Granular casts?

    Image Upload 3
    muddy brown

    acute tubular necrosis
  92. WBC casts

    Image Upload 4
    tubulointerstitial inflammation

    acute pyelonephritis

    transplant rejection
  93. what types of situations will lead you to have calcium oxalate crystals?
    ethylene glycol (antifreeze) or vitamin C abuse, sarcoidosis.
  94. What is WAGR?
    • Wilms tumor
    • Aniridia (no iris)
    • Genitourinary
    • mental motor Retardation
  95. Thyroidization of kidney?
    tubules can contain eosinophillic casts (thyroidization of kidney) because they look like colloid.

    Seen in Chronic Peylonephritis.
  96. what are the 4 things associated with Renal Papillary necrosis?
    • 1. diabetes mellitus
    • 2. acute pyelonephritis
    • 3. sickle cell disease
    • 4. chronic use of phenacetin (acetaminophen)
  97. what are 2 main ways you can tell the difference between prerenal kidney failure versus intrinsic?
    In Intrinsic, there is granular muddy brown casts (acute tubular necrosis). Also, the BUM/Creatinine is less than 20
  98. What is the BUN/creatinine ratio for post-renal?
    Initially, it is > 20, because the backup pressure pushes BUN into the urine,

    overtime, there is damage to tubular epithelium and thus there is decrease in BUN
  99. how does the clearance of creatinine change in diabetic glomerulopathy?
    • tje efferent arteriole becomes constricted due to hyaline arteriosclerosis which causes an increase in the GFR and clearance of creatinine
    • (the increased GFR overtime damages the glomerulus)
  100. alkaline pH, smells like ammonia....what is it?
    proteus mirabilis
  101. someone has normal serum glucose, but there is increased glucose in the urine
    • pregnant lady
    • (low renal threshold for glucose)
  102. increased urine urobilinogen, absent urine bilirubin
    extravascular hemolysis (hemolytic anemia: hereditary spherocytosis)
  103. Increased urine UBG, increased urine bilirubin?
  104. hemoglobinuria
    intravascular hemolysis
  105. hexagonal crystal stones causing obstructions
    Cystine stone (cystinuria)
  106. dysmorphic RBCs
    indicate hematuria of glomerular origin.
  107. maltese cross
    are due to cholesterol which is almost always increased in nephrotic syndrome
  108. in diabetes mellitus, why is the GBM thickened?
    because they have increased synthesis of type 4 collagen
  109. what creates the negative charge in GBM
    heparan sulfate
  110. crescents consist of
    proliferation of parietal epithelial cells
  111. what is the most common cystic disease in children?
    renal dysplasia
  112. striations in the papillary ducts of the medulla,
    "swiss cheese appearance"
    Medullary Sponge Kidney
  113. what is the key finding in Nephritis syndrome?
    Red blood cell casts
  114. "wire looping" with neutrophil infiltration
    SLE (diffuse proliferative glomerulonephritis)
  115. While in Nephritic syndrome most of the damage was due to neutrophils, in nephrotic syndrome......
    it is is mostly due to cytokines
  116. what are 2 key findings in Nephrotic syndrome?
    proteinuria > 3.5 g/24 hours


    fatty casts with maltese crosses and oval bodies
  117. HIV, heroin abuse
    Focal Segmental glomerulosclerosis
  118. tram tracks caused by splitting of the GBM by ingrowth of the mesangium
    Type I MPGN

    subendothelial IC with granular IF
  119. HBV, HCV
    Type I MPGN
  120. Initial laboratory manifestation of diabetic glomerulopathy
  121. what happens in diabetic glomerulopathy?
    nonenzymatic glycosylation of the GBM->increases vessel and tubular cell permeability to proteins

    *NEG of the efferent more than afferent= hyaline arteriosclerosis which increases GFR

    *glucose becomes sorbitol, osmotic damage

    *hyperfiltration damages the mesangium and causes proliferation of type 4 collagen
  122. where is the most common site of ischemic damage?
    straight segment of proximal tubule (most susceptible to hypoxia)

    Medullary segment of the TAL
  123. what do we see on histology for Chronic Pyelonephritis?
    eosinophillic material resembling thyroid tissue "thyroidization"
  124. gross hematuria, proteinuria, and colicky flank pain
    ring defect

    Renal Papillary Necrosis
  125. waxy/broad casts
    sign of Chronic renal failure
  126. hyperplastic arteriosclerosis with "onion skin"appearance
    Malignant hypertension
  127. what are the symptoms of Malignant hypertension and what is treatment?
    BP: 210/120

    • Hypertensive encephalopathy: cerebral edema
    • Papilledema (loss of normal optic disk margin)
    • Retinopathy: flame hemorrhages, exudates
    • oliguric acute renal failure

    Treatment: sodium nitroprusside
  128. what vasculitis gives you renal infarcts?
    polyarteritis nodosa
  129. abruptio placentae can lead to
    diffuse corticol necrosis due to DIC limited to the renal cortex.
  130. what is essential in preventing stone formation
  131. urine is alkaline and smells lime ammonium
    • Proteus
    • Staghorn calculi (struvite stones)

    magnesium ammonium phosphate
  132. What is an Angiomyolipoma?
    hamartoma that is composed of blood vessels, smooth muscles, adipose tissue
  133. large necrotic gray tan tumor
    Wilms tumor
  134. exstrophy of bladder
  135. causes of adenocarcinoma of the bladder
    • urachal remnants
    • exstrophy of the bladder
  136. mesangial deposits of IgG, IgM and complement. Mesangial proliferation
  137. what are the 2 most common outcomes from renal stones?
    • Hydronephrosis
    • and
    • Pyelonephritis
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