Kern Kidneys 2

Card Set Information

Kern Kidneys 2
2011-10-03 21:54:16
Kern Kidneys

Kern Kidneys 2
Show Answers:

  1. In acute kidney injury (acute renal failure), which is more common: pre-renal (decreased perfusion), renal (intrinsic to the kidney) or post-renal (obstruction)?
  2. Acute kidney injury can be divided into anuric, oliguric, and non-oliguric forms. Which is characterized by < 100 mL urine output per 24 hours? This is rare, and suggests complete obstruction or a major vascular event.
  3. Acute kidney injury can be divided into anuric, oliguric, and non-oliguric forms. Which is characterized by < 400 mL urine output per 24 hours? This form is common with obstruction and pre-renal azotemia. It is characterized by fluid retention and volume overload, together with increasing BUN and creatinine. The fluid overload itself can be a major problem (pulmonary edema, anasarca).
  4. Acute kidney injury can be divided into anuric, oliguric, and non-oliguric forms. Which is characterized by > 400 mL urine output per 24 hours? This form is common with nephrotoxins, acute glomerulonephritis, and acute interstitial nephritis. It is characterized by increasing BUN and creatinine, without fluid retention and volume overload. In general, this is a little easier to manage, and has a slightly better prognosis than the other forms
  5. Identify the syndrome:
    Common cause of acute renal insufficiency
    Morphologic changes often subtle
    Two main types: ischemic and toxic
    Diagnosed through elevated BUN and creatinine, plus/minus oliguria
    Key feature is to recognize the presence of clinical circumstances which predispose the patient to this (must be an initiating event) -- hypotension, hypovolemia, administration of toxic drugs or chemicals, etc
    Urinalysis: granular casts plus/minus tubular epithelial cells
    Exclude pre-renal azotemia
    Exclude obstruction
    Treatment consists of treating the underlying cause
    Overall mortality rate is high (~50%)
    Most deaths due to infection or primary disease process
    Acute Tubular Necrosis
  6. What predisposes to acute tubular necrosis (ie, shock, severe volume contraction)?
    Renal Hypoperfusion
  7. Ischemic ATN is characterized by ______ ________, usually with an additional insult -- sepsis, nephrotoxic agent, or NSAIDs, for example.
    Renal Hypoperfusion
  8. What two drugs are notorious for causing Toxic ATN?
    • Aminoglycosides (antibiotic)
    • NSAIDs
    • Also caused by cephalosporins, ampho B, radiographic contrast agents, chemo drugs, hemoglobin, myoglobin, and anesthetics
  9. Which type of acute tubular necrosis tends to cause "skip" lesions at various levels of the nephron; many different areas of the tubules can be affected, including both proximal and distal tubules?
    Ischemic ATN
  10. Which type of acute tubular necrosis tends to primarily affect the proximal tubules (proximal convoluted and proximal straight tubules)? Other portions of the tubules can also be involved
    Toxic ATN
  11. What are the three main factors that determine the pathophysiology of ATN?
    • Vasoconstriction
    • Obstruction of tubules by casts
    • Tubular Backleak through damaged tubular walls
  12. What are the following things predisposing factors for?

    High metabolic rate in tubular cells
    Limited capacity for anaerobic metabolism
    Low oxygen tension
    Disproportional ischemia due to congestion and leukocyte "plugging" in vessels
    Ischemic ATN
  13. Identify the pathology below:
    • Acute Tubular Necrosis
    • Dilated tubules with loss of tubular cells, thinning of the epithelium, irregular spacing of tubular cell nuclei and numerous casts and debris obstructing the tubular lumens. There is also interstitial edema and mild interstitial inflammation
  14. What are the red things in the picture below:
    Hemoglobin Casts
  15. What are the main diseases of the interstitium?
    • Interstitial Nephritis
    • Fibrosis
  16. Identify the syndrome:
    ~10-15% of cases of acute kidney injury
    Hallmarks: interstitial edema and inflammation, predominantly of lymphocytes
    Tubular injury common
    Glomeruli and vessels spared
    Immune-mediated mechanisms prominent
    Cell-mediated immunity (T-cells)
    Some cases: anti-tubular basement membrane antibodies (rifampin, systemic autoimmune disease)
    Immune reaction may be stimulated by drug or infection
    Four Major Clinical Scenarios: drug or toxin exposure; infection -- systemic or local; immunologic diseases; idiopathic lesion without apparent precipitating cause (10-20% of cases)
    Symptoms (if any) often due to primary illness -- not this per se
    Acute renal insufficiency (azotemia)
    Allergic: may have eosinophilia, skin rash, fever, arthralgias
    Urinalysis: hematuria, sterile pyuria, WBC casts may be present
    Treatment is to treat the underlying illness or discontinue the drug/toxin which is causing the interstitial nephritis
    Acute Interstitial Nephritis
  17. What is the most common cause of Acute Interstitial Nephritis?
    Drug-Related AIN
  18. Drug-related AIN is idiosyncratic, not dose-related. There are a wide variety of drugs involved. What are three common causes?
    • Beta-lactam antibiotics
    • NSAIDs
    • Sulfonamides
  19. Identify the syndrome:
    Often associated with proteinuria or nephrotic syndrome
    Glomerular pathology identical to minimal change disease: diffuse effacement of foot processes
    Occasionally associated with membranous nephropathy (subepithelial deposits)
    Acute Interstital Nephritis due to NSAIDs
  20. If a patient presents with acute renal insufficiency and nephrotic proteinuria, always question him about ________ ingestion.
  21. What is the second most common cause of Acute Interstitial Nephritis?
    Infection-related AIN
  22. What type of virus infects urothelial cells, and can cause serious infection-related acute interstitial nephritis in immunocompromised individuals?
    BK Polyoma Virus
  23. Identify the pathology below:
    • Acute Interstitial Nephritis
    • Note marked widening of the interstitium due to edema; there is also interstitial inflammation, predominantly lymphocytes; there are also some eosinophils. There is also some injury to the tubules.
  24. Identify the pathology below:
    • Allergic Interstitial Nephritis due to a drug
    • Note the striking infiltrate of eosinophils in the interstitium
  25. Identify the syndrome below:
    Main histological features: interstitial fibrosis and scarring, tubular damage, mononuclear inflammation
    Glomeruli and vessels initially spared; later become sclerotic
    Many different causes
    Presentation: variable
    Treatment: primarily supportive
    Renal replacement therapy when/if needed
    Chronic Interstitial Nephritis (CIN)
  26. The presence of __________ indicates chronic interstitial nephritis; acute interstitial nephritis features _________.
    • Fibrosis
    • Edema
  27. What is an infection of the bladder known as? This is common, particularly among young, sexually active women. There are usually no major consequences; may lead to spread to the kidney.
  28. What is an infection of the kidney known as? May be associated with serious sequelae. Variants: non-obtrusive versus complicated; acute versus chronic
  29. The majority of cases of pyelonephritis are due to what? What type of organisms are usually involved? What type of organisms are involved by hematogenous spread?
    • Reflux from bladder -- this occurs due to a combination of infection of the bladder and incompetent vesico-ureteral valves, allowing reflux of the infected urine up into the kidney
    • Low virulence
    • Virulent organisms
  30. Dysuria, urgency, and frequency are common symptoms of cystitis. Presence of chills, fever, back pain, and costovertebral angle tenderness suggest progression to what?
  31. What is by far the most common bacterium causing UTIs?
    E. coli
  32. Identify the pathology below:
    • Pyelonephritis
    • Note the dense collections of cells within tubular lumens -- there is also interstitial edema and inflammation
  33. Identify the pathology below:
    • Acute Pyelonephritis
    • Note the large accumulation of neutrophils within tubule lumens ("pus in tubules"). There may also be neutrophils in the interstitium -- but the glomeruli are characteristics spared (at least at first)
  34. Identify the syndrome:
    Chronic inflammation and tubulointerstitial damage
    Scarring of renal pelvis and calyces
    Two forms: reflux nephropathy (typically occurs in early childhood) and chronic obstruction
    Upper and lower poles of kidneys usually involved -- compound papillae there allow reflux into kidney
    Usually caused by a combination of infection plus reflux and/or obstruction
    Chronic Pyelonephritis
  35. Identify the pathology below:
    • Chronic Pyelonephritis
    • Note the interstitial fibrosis with tubular atrophy and inflammation
  36. What are the three complications of Urinary Tract Obstruction?
    • Susceptibility to infection
    • Susceptibility to stone formation
    • Renal atrophy
  37. What is dilatation of renal calyces and pelvis due to obstruction?
  38. What is the major difference between chronic pyelonephritis without obstruction and chronic pyelonephritis due to obstruction?
    • Without: damage is primarily limited to the upper and lower poles of the kidneys
    • With: all parts of the kidney are involved
  39. Approximately 25% of patients with SLE have what?
    Signs of renal disease
  40. What virus has been suggested to precipitate SLE? What is the best known drug for causing drug-related lupus?
    • Epstein-Barr
    • Procainamide
  41. Which class of SLE is characterized by minimal mesangial LN; normal by light; mesangial deposits on IF and EM?
    Class I
  42. Which class of SLE is characterized by mesangial proliferation of LN: mesangial hyperceullularity; mesangial deposits; capillary loops are open?
    Class II
  43. Which class of SLE is characterized by focal lupus nephritis; segmental or global proliferation <50% of gloms?
    Class III
  44. Which class of SLE is characterized by diffuse lupus nephritis; segmental or global proliferation in >50% of gloms?
    Class IV
  45. Which class of SLE is characterized by membranous lupus nephritis; subepithelial deposits plus/minus mesangial deposits; capillary loops open?
    Class V
  46. Which class of SLE is characterized by advanced sclerosis lupus nephritis; >90% of glomeruli globally sclerotic, with no residual activity; basically, with this class, should just give up and start dialysis?
    Class VI
  47. In Lupus Nephritis, what do the activity and chronicity scores indicate?
    • Activity: determines how aggressively to treat
    • Chronicity: reflects prognosis
  48. Identify the pathology below:
    • Karyorrhectic Nuclear Debris (darker pink)
    • Seen in Lupus Nephritis
  49. Identify the pathology below:
    • Karyorrhectic Nuclear Debris (small dark dots); probably foci of necrosis on the right and left
    • Seen in Lupus Nephritis
  50. Identify the pathology below:
    • Hyaline Thrombi (lower left); they probably represent massive subendothelial deposits that bulge into the lumen of the capillary
    • Seen in Lupus Nephritis
  51. Identify the pathology below:
    • Wire Loop Lesions
    • Thick, rigid capillary loops; they represent massive subendothelial immune complex deposits
    • Seen in Lupus Nephritis
  52. Identify the pathology below:
    • Lupus Nephritis
    • Note massive capillary wall deposits
  53. Identify the pathology below:
    • Lupus Nephritis
    • Note the hyaline thrombi and wire loop lesions, particularly on the right of the glomerulus
  54. Identify the pathology below:
    • Lupus Nephritis
    • Note the subendothelial and mesangial deposits
  55. Identify the pathology below:
    • Lupus Nephritis
    • Massive subendothelial immune complex deposits as would be seen in a "wire loop" lesion. There are also mesangial deposits present
  56. What are the classic therapies for active proliferative lupus nephritis (class III or IV)?
    Cyclophosphamide (Cytoxan) and prednisone or other corticosteroids
  57. Almost all diabetics with nephropathy also have what (~90%)?
    Diabetic Retinopathy
  58. What is now the most common cause of patients starting dialysis therapy?
    Diabetic Nephropathy
  59. Control of what two things can decrease the risk of diabetic nephropathy, as well as slow the progression of diabetic nephropathy once it begins?
    Hyperglycemia and BP
  60. What is the number one cause of end-stage renal disease in the US?
  61. What is the goal of BP in diabetics?
    < 130/80
  62. What is the earliest detectable change to signal diabetic nephropathy? What is the first clinical sign of renal disease? What two things indicate the onset of overt renal disease?
    • Increase in GFR
    • Microalbuminuria (30-300 mg albumin per 24 hours)
    • Overt proteinuria and increase in creatinine/BUN
  63. What is the earliest histologic abnormality associated with diabetic nephropathy?
    • Hypertrophy (glomerular and tubular)
    • (this requires sophisticated measurements to detect)
  64. What is the first routinely recognizable abnormality in diabetic nephropathy (seen in incipient/progressive disease)?
    Diffuse thickening of teh glomerular capillary basement membranes. There is also expansion of the mesangial area by deposition of extracellular mesangial matrix material
  65. What are the overt changes associated with diabetic nephropathy (pathologically)?
    • Glomerulosclerosis
    • Tubulointerstitial fibrosis
    • Tubular atrophy
    • Vascular changes (hyaline arteriosclerosis)
  66. What indicates the end-stage renal disease of diabetic nephropathy?
    Global glomerulosclerosis involving the majority of glomeruli, marked interstitial fibrosis, and tubular atrophy
  67. What is the most characteristic change of diabetic nephropathy?
    Nodular Diabetic Glomerulosclerosis (aka Kimmelstiel-Wilson Nodules)
  68. What is the gross appearance of a kidney with diabetic nephropathy?
    • Enlarged and appears pale, with a smooth surface
    • (Diabetic nephropathy is one of a limited # of causes of renal failure associated with large kidneys -- others = polycystic kidney disease, myeloma kidney, and amyloidosis)
  69. Identify the pathology below:
    • Diabetic Nephropathy
    • The mesangium shows diffuse expansion. This is a common pathologic change in diabetic nephropathy, although not diagnostic for it
  70. What are the most characteristic EM findings in diabetic nephropathy?
    Marked thickening of the GBM, with expansion of the mesangium
  71. Identify the pathology below:
    • Nodular Glomerulosclerosis (Kimmelstiel-Wilson Lesions)
    • Seen in diabetic nephropathy
  72. Identify the pathology below:
    • Nodular Glomerulosclerosis (Kimmelstiel-Wilson Lesions) (purple stuff)
    • Seen in Diabetic Nephropathy
  73. Identify the pathology below:
    • Diabetic Nephropathy
    • Shows nodular deposits in the mesangium; the capillary lumens appear dilated (microaneurysms)
  74. Identify the pathology below:
    • Diabetic Nephropathy
    • Marked thickening of the GBM and expansion of the mesangium by finely granular, slightly electron-dense material (Kimmelstiel-Wilson lesions)
  75. What are insudative/exudative vascular lesions (hyaline arteriolosclerosis, fibrin cap, and capsular drop) associated with?
    Diabetic Nephropathy
  76. Identify the pathology below:
    • Hyaline Deposits in arterioles (both afferent and efferent)
    • Characteristic feature of Diabetic Nephropathy -- seeing deposits in both the afferent and efferent arterioles to a glomerulus is virtually pathognomonic
  77. Seeing prominent hyaline deposits in both the afferent and efferent arterioles to a glomerulus is considered virtually pathognomonic of what?
    Diabetic Nephropathy
  78. Identify the pathology below:
    • Diabetic Nephropathy
    • "Hyaline" deposits in glomerular capillaries -- probably represent plasma protein that has leaked beneath the endothelium into the damaged capillary wall
    • Not specific for diabetic nephropathy (also seen in FSGS)
  79. Identify the pathology below:
    • "Capsular Drop"
    • Hyaline deposit in Bowman's capsule basement membrane -- considered virtually diagnostic for Diabetic Nephropathy
  80. What is characteristic on immunofluorescence for diabetic nephropathy?
    Linear staining of glomerular and tubular basement membranes for IgG and albumin
  81. Identify the pathology below:
    • Diabetic Nephropathy
    • Linear staining of the GBM, along with staining of the mesangial nodules
  82. Identify the pathology below:
    • Diabetic Nephropathy
    • Shows linear staining of the tubular basement membranes
  83. What are the three main complications of Diabetic Nephropathy?
    • Nephrosclerosis
    • Pyelonephritis
    • Papillary Necrosis (necrotizing papillitis)
  84. What are microaneurysm formation (especially in the capillaries), thick basement membranes, and "leaky" vessels and basement membranes associated with?
    Diabetic Microangiopathy
  85. Identify the pathology below:
    • Capillary Microaneurysms, associated with Diabetic Microangiopathy
    • Several of the glomerular capillaries appear dilated, particularly the capillary on the upper right which is also congested with RBCs
  86. What is the following pathogenesis associated with?
    Glycosylation of various proteins -- advanced glycation end-products --> oxidative damage
    Genetic predisposition
    Conversion of glucose to sorbitol by aldose reductase
    Hemodynamic alterations
    Diabetic Nephropathy
  87. What area of the kidney is at greatest risk for ischemia?
    Superficial Cortex
  88. In "malignant" hypertension, defined as severe hypertension associated with acute end-organ damage, the diastolic BP is usually greater than what?
    >120 mmHg
  89. What are the two main determinants of blood pressure?
    • Cardiac Output
    • Peripheral Vascular Resistance
  90. What are the major causes of secondary hypertension?
    • R: renal disease
    • E: estrogens & eclampsia/preeclampsia
    • C: coarctation of the aorta
    • A: aldosteronism
    • P: pheochromocytoma
    • S: sleep apnea

    • A: alcoholism
    • B: brain lesions
    • C: cushing syndrome
    • D: drugs
    • E: endocrine diseases -- esp hyperthyroidism
  91. Malignant hypertension is defined by the clinical presentation, not by the blood pressure per se. What are the defining characteristics?
    • Severe hypertension: diastolic usually > 120 mm Hg
    • Retinal hemorrhages & exudates
    • Neurological changes
    • Hematuria & proteinuria, often oliguria
    • Papilledema
    • May cause acute renal failure, CHF; may be lethal
  92. What is the second leading cause of end-stage renal disease, following diabetes?
  93. What are two pathophysiological consequences of hypertension?
    • Hypoperfusion: progressive arterial and arteriolar narrowing
    • Glomerular Hyperperfusion: causes focal segmental glomerulosclerosis --> eventual global glomerulosclerosis
  94. What is hypertensive renal disease also known as?
    Hypertensive Nephrosclerosis
  95. What are the following clinical features associated with?
    Renal insufficiency/ESRD
    Urinalysis: proteinuria, normal sediment (typically <1 gram -- mild to moderate)
    EKG: left ventricular hypertrophy
    Arteriolar hyalinosis
    Arterial intimal fibrosis
    Tubulointerstitial fibrosis
    Tubular atrophy
    Hypertensive Renal Disease/ Hypertensive Nephrosclerosis
  96. What does the gross kidney look like in a patient who was hypertensive?
    Slightly pale surface with numerous small indentations; the indentations are where glomeruli have become obsolescent. The appearance has been described as "leathery."
  97. Identify the pathology below:
    • Arteriolar Hyalinosis (seen in Hypertensive Nephrosclerosis)
    • Darker material is the hyaline; it probably represents leakage of plasma proteins into the wall of the blood vessel, due to damage to the vessel wall by the hypertension; it narrows the lumen of the arteriole
  98. Identify the pathology below:
    • Arterial Intimal Fibrosis and Medial Fibrosis (as seen in Hypertensive Nephrosclerosis)
    • Collage = blue. There is collagen deposition in the intima (between the muscularis [stained red] and the endothelium), which is normally very thin; there is also collagen deposition in the muscularis. There is significant narrowing of the lumen of the artery, which decreases blood flow through the artery. In hypertension, this is occurring in arteries all over the body
  99. Identify the pathology below:
    • Interstitial Fibrosis
    • Collagen = blue. Shows marked interstitial fibrosis which is usually also associated with tubular atrophy. There is an artery on the left which shows marked fibrous thickening of the intima, which severely compromises the lumen of the artery. The glomeruli appear to show collapse of the glomerular capillaries and expansion of the mesangium, consistent with chronic hypertension