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UA Spring > Renal disease pt 2 > Flashcards

Renal disease pt 2 Flashcards

1
Q

How does the liver compensate for loss of albumin? Caveat?

A

Make lipoproteins/lipids to restore oncotic pressure, but lipids are small and can end up in urine

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2
Q

Nephrotic syndrome UA findings

A
  • Massive proteinuria > 3.5 g/dL
  • Low levels of serum albumin
  • High levels of serum lipids
  • Pronounced edema
  • RBC
  • Fat droplets
  • RTE
  • Epithelial casts
  • Fatty casts
  • Waxy casts
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3
Q

Why is there edema in nephrotic syndrome?

A
  • Loss of albumin reduces oncotic pressure such that water leaves capillaries to the tissues
  • Tissues are hypertonic to blood, so water leaves to tissues
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4
Q

Minimal Change Disease aka

A

Liver nephrosis

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5
Q

What happens in minimal change disease?

A

Little cellular change, thus allowing some proteins to pass through glomerulus

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6
Q

Minimal change disease typically found in

A

Children

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7
Q

Minimal change disease clinical findings

A
  • Edema
  • Fat droplets
  • Marked proteinuria
  • Transient hematuria
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8
Q

Focal Segmental Glomerulosclerosis (FSGS)

A

Affects only certain glomeruli, others can stay normal

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9
Q

FSGS features what kind of deposits?

A

Immune deposits of IgM and C3 (complement)

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10
Q

FSGS UA findings

A
  • Elevated protein
  • RBC
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11
Q

Alport Syndrome

A
  • Inherited disorder affecting glomerular basement membrane (GBM)
  • GBM thin, no antibody effect
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12
Q

Alport syndrome symptoms

A
  • Same as nephrotic syndrome
  • Massive proteinuria > 3.5 g/dL
  • Low levels of serum albumin
  • High levels of serum lipids
  • Pronounced edema
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13
Q

Most common cause of end-stage renal disease

A

Diabetic Nephropathy

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14
Q

How does damage occur in diabetic nephropathy?

A
  1. Glomerular membrane thickening
  2. Mesangial cell proliferation
  3. Increased deposition of cellular material
  4. Vascular sclerosis
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15
Q

Diabetic nephropathy features what kind of deposits and where?

A

Glycosylated proteins deposit in capillary tufts

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16
Q

List tubular disorders

A
  • Fanconi Syndrome
  • Nephrogenic diabetes insipidus
  • Renal glycosuria
  • Acute tubular necrosis
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17
Q

Acute tubular necrosis features

A

RTE cell damage

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18
Q

Causes of acute tubular necrosis

A
  • Ischemia (reduced blood flow/lack of oxygen) due to surgery, trauma, or shock
  • Toxic substances (aminoglycosides, anti-fungals, radiographic dye, anti-freeze, heavy metals, Hgb, Mgb
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19
Q

Acute tubular necrosis UA findings

A
  • Hallmark: RTE cells and RTE casts
  • Mild proteinuria
  • Wide variety of casts (granular, waxy, broad)
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20
Q

Fanconi’s syndrome

A

Failure of tubular reabsorption in PCT, which means there’s disrupted transport, cellular energy, and membrane permeability

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21
Q

Substances affected in Fanconi’s syndrome

A
  • Glucose
  • Amino acids
  • Phosphorus
  • Sodium
  • Potassium
  • Bicarb
  • Water
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22
Q

List an inherited cause of Fanconi’s syndrome

A

Wilson’s disease

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23
Q

List an acquired cause of Fanconi’s syndrome

A

Multiple Myeloma

24
Q

List an exogenous cause of Fanconi’s syndrome

A

Heavy metals

25
Q

Nephrogenic Diabetes Insipidus

A

Inability of tubules to respond to ADH

26
Q

Nephrogenic Diabetes Insipidus UA findings

A
  • Low specific gravity
  • Frequent urination
27
Q

Renal glycosuria

A
  • Inherited disorder where glucose receptor on PCT cell won’t work or not enough expressed
  • Only glucose reabsorption affected
28
Q

Serum and urine glucose levels in renal glycosuria

A
  • Serum glucose = normal
  • Urine glucose = increased
29
Q

Most common renal disease

A

UTI (upper or lower)

30
Q

Interstitial disease affects

A

The interstitium and tubules

31
Q

Most common interstitial disorder

A

Cystitis (bladder infection)

32
Q

Cystitis UA findings

A
  • Numerous WBC
  • Numerous bacteria
  • Mild proteinuria
  • RBC (not from glomerulus)
33
Q

Pyelonephritis

A

Upper UTI

34
Q

Acute pyelonephritis result of

A

Bacteria ascending upwards from lower UTI due to renal calculi, pregnancy, or reflux of urine

35
Q

Acute pyelonephritis symptoms

A
  • Urination frequency
  • Burning
  • Lower back pain
  • Correlation btwn acute pyelonephritis and bacteremia
36
Q

Acute pyelonephritis UA findings

A
  • Numerous WBC
  • Numerous bacteria
  • Proteinuria
  • WBC casts (tubule infection)
37
Q

How to distinguish between upper and lower UTI?

A

Upper UTI = casts present (WBC) because only nephron makes casts and bladder (lower UTI) can’t

38
Q

More serious form of pyelonephritis

A

Chronic

39
Q

Chronic pyelonephritis often diagnosed in

A

Children (poorly formed kidneys)

40
Q

Chronic pyelonephritis congenital urinary structural defect effects

A
  • Bladder reflux to ureters or renal pelvis
  • Cannot empty collecting ducts
41
Q

What can lead to chronic renal failure?

A

Permanent tubular damage

42
Q

UA findings in chronic pyelonephritis

A
  • Numerous WBC
  • Bacteria
  • WBC casts
  • Granular casts
  • Waxy casts
  • Broad casts
43
Q

Acute interstitial nephritis

A
  • Inflammation of renal interstitium or tubules
  • Associated with allergic reaction to meds (penicillin class, sulfonamides, cephalosporin, NSAIDs)
44
Q

Acute interstitial nephritis UA findings

A
  • No bacteria
  • Eosinophils (do Hansel stain)
  • RBC
  • Proteinuria
  • Numerous WBC
  • WBC casts
45
Q

Final progression to end-stage renal failure looks like:

A
  • Marked GFR reduction (<25ml/min)
  • Steady increase serum BUN/creatinine
  • Electrolyte imbalance
  • Lack of renal concentrating ability
  • Positive urine protein/glucose
  • Increase granular, waxy, and broad casts
46
Q

Acute vs chronic renal failure

A

Acute renal failure shows sudden loss of renal function and is frequently reversible

47
Q

Pre-renal causes of renal failure

A

Sudden reduction in blood flow

48
Q

Renal causes of renal failure

A

Acute glomerular or tubular disease

49
Q

Post-renal causes of renal failure

A

Renal calculi or tumor obstructions

50
Q

Acute renal failure general rule of thumb UA findings

A
  • RTE cells + casts = acute tubular necrosis
  • WBC casts = interstitial infection of inflammation
  • Abnormal cells = malignancy
51
Q

Renal lithiasis

A
  • Kidney stones that form in the kidney, ureters, and bladder
  • Calculi vary in size
52
Q

Conditions favoring kidney stone formation

A
  • pH
  • Chem concentration
  • Urinary stasis
  • Presence of certain crystals
53
Q

75% of kidney stones consist of

A

Calcium oxalate or phosphates

54
Q

Other kidney stones may consist of

A

Mag-ammonium phosphate, uric acid, cystine

55
Q

Patient management of kidney stones

A
  • Maintaining urine pH to prevent crystallization
  • Hydration
  • Dietary restrictions
56
Q

Renal lithiasis UA findings

A

Microscopic RBC due to irritation of the tissue by kidney stone (aka calculus)

UA Spring (8 decks)

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