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CRP- Renal > Proteinuria and Glomerular Disease > Flashcards

Proteinuria and Glomerular Disease Flashcards

1
Q

Where are the sialoproteins found and what do they do?

A

they line the outside and undersurface of the ENDOTHELIAL layer of the glomerulus and line the external surface of the EPITHELIAL layer. These are negatively charged proteins which will repel like negatively charged proteins from passing through.

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2
Q

Does beta-2-microglobulin get through the glomerular membrane?

A

YES it passes unrestricted.

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3
Q

Can albumin get through the glomerular membrane?

A

NO because it is negatively charged and will thus be repelled by the sialoproteins; a little does pass naturally though, but 98% is reabsorbed.
*about 30 mg of albumin will be excreted in the urine (very very little).

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4
Q

What is normal serum albumin?

A

4.0 g/dl

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5
Q

How much total protein is found in the urine/day?

A

up to 130 mg/day= largely globulins (TAMM-HORSFALL glycoprotein, small MW plasma proteins, intracellular lysozymes and debris), albumin (30 mg), and B2-microglobulin (5 mg).

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6
Q

Is Tamm-Horsfall glycoprotein found naturally in the blood?

A

NO it is manufactured by the renal epithelial cells and secreted into the tubular space. It is a normal finding and the protein that makes up the matrix of CASTS.

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7
Q

Can exercise cause transient proteinuria?

A

YES

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8
Q

What else can cause transient proteinuria?

A

fever, increased glucose, or increased BP

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9
Q

What is orthostatic proteinuria?

A

you spill more protein when you are ambulatory than when you are supine. Not pathologic :)

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10
Q

What are the 3 types of abnormal proteinuria?

A
  1. glomerular proteinuria (size, charge, hemodynamics, functional).
  2. tubular proteinuria (B-2 microglobulin)
  3. overflow proteinuria (light chain overproduction, myoblobinuria, or hemoglobinuria; aka things that should not be in the blood, but are and are making it into the urine).
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11
Q

** Because B-2 microglobulin is freely filterable and 99% reabsorbed, if you see a lot in the urine, where must your problem be?

A

in the tubules (not the glomerulus) and this points you toward the tubular interstitial diseases.

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12
Q

What protein does the dipstick measure and what is does a positive test indicate?

A

albumin and if it is positive this corresponds to > 300 mg. (normal is 20-30 mg). In between these two is microalbuminuria.

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13
Q

*** What is important not to confuse?

A
  • clinical PROTEINuria= greater than 500 mg

- clinical ALBUMINuria= greater than 300 mg/day (normal is 30mg, so microabluminuria is between these two).

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14
Q

What is the sulfosalicylic acid test?

A

if your dipstick is negative, but this SSA is positive, it means you have a nonalbumin protein in the urine. This points you away from the glomerular diseases and toward the tubular interstitial diseases.

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15
Q

How much creatinine do males vs females excrete per day?

A
  • males excrete 20-25 mg in urine

- females excrete 15-20 mg in urine

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16
Q

What is the urine protein:creatinine ratio?

A

mg of protein per gram of creatinine

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17
Q

What is the range of quantified proteinuria?

A

mild= 3 .5 g/day

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18
Q

What does normal urine electrophoresis look like?

A

generally flat

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19
Q

What does glomerular proteinuria electrophoresis look like?

A

almost like serum electrophoresis, with a tall spike for albumin!

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20
Q

What does tubular proteinuria electrophoresis look like?

A

higher spike at the beta globulin

21
Q

What does overproduction proteinuria electrophoresis look like?

A

tall spike at the gamma globulin (light chain disease; likely multiple myeloma).

22
Q

What are the 5 major syndromes of glomerular disease?

A
  1. nephrotic syndrome
  2. acute glomerulonephritis
  3. chronic glomerulonephritis
  4. rapidly progressive glomerulonephritis
  5. asymptomatic hematuria and/or proteinuria
23
Q

** What is asymptomatic hematuria and/or proteinuria?

A
  • diagnosis of exclusion when you can’t find any clinical evidence for renal or urologic disease process.
  • usually NOT worthy of renal biopsy.
24
Q

** What is nephrotic syndrome?

A
  • a constellation of clinical and laboratory abnormalities occurring as a result of increased permeability of the glomerular capillary wall to plasma proteins (> 3.5 g).
  • HYPOALBUMINEMIA
  • EDEMA (due to plasma hypoosmotic state from losing albumin).
  • HYPERLIPIDEMIA (due to loss of osmotic pressure leading to increased liver production of albumin, which incidentally increases production of cholesterol and TGs. Will see maltese cross of fatty casts in urine).
  • HYPERCOAGULABLE state (due to increased hepatic synthesis of clotting factors, and increased platelet aggregation due to lack of albumin).
25
Q

What else raises serum cholesterol and TGs in nephrotic syndrome due to loss of albumin?

A

urinary loss of LCAT (normally clears lipids from the blood)= increased cholesterol, and because you’ve lost the binding proteins (albumin) there are now more FFAs in circulation leading to increased LPL activity= increased TGs.

26
Q

What are some complications of nephrotic syndrome?

A
  • acute renal failure (ARF)
  • thrombo-embolic events (renal vein thrombosis= really only caused by something wrong with the kidney; this could break off and cause DVT or PE).
  • accelerated arteriosclerosis
  • anemia (from losing transferrin in the urine)
  • immunodeficiency (losing IgG and complement in urine)
  • hypocalcemia (losing vitamin D in urine and stimulate hyperparathyroidism).
27
Q

Can proteinuria cause problems for the kidney itself?

A

YES due to increased mesangial traffic and tubulotoxicity and secondary interstitial inflammation/scarring

28
Q

Does GFR normally decline with aging?

A

YES

29
Q

How do we manage nephrotic syndrome?

A
  • sodium restriction (2 g Na+ diet)
  • fluid restriction
  • diuretic therapy
  • anti-gravity measures (aka support stockings)
  • modest protein restriction
  • ACE inhibitors, ARBs or even diltiazem
  • anti-platelet Rx
  • vitamin/mineral supplement
30
Q

What are the 3 causes of nephrotic syndrome?

picmonic for all of these

A
  1. minimal change disease (in children and precipitated by lymphomas or infections often; often clinically normal though. Treat with corticosteroids).
  2. focal and segmental glomerulosclerosis (#1 nephrotic cause in adults; associated with HIV and heroin use).
  3. membranous glomerulopathy (#2 nephrotic cause in adults; HBV, SLE, gold, and tumor associated).
31
Q

Why are the membranes thick in membranous glomerulopathy?

A

because you have immune complex deposition in them leading to a SPIKE AND DOME appearance on EM and granular on immunofluorescence.

32
Q

Is membranous glomerulopathy a proliferative disease?

A

NO it is not cellular

33
Q

Is FSGS more common in blacks or whites?

A

blacks.

34
Q

What is the final common pathway of all immunologic and non-immunologic glomerular injury?

A

Focal segmental glomerulosclerosis (FSGS)

*Remember focal means

35
Q

** What is the #1 cause of pts starting dialysis (ESRD) today?

A

DM, which is broken into MACROvascular (ATHEROsclerosis) and MICROvascular (ARTERIOLOsclerosis; retinopathy, neuropathy, nephropathy) disease.

36
Q

** What are the 5 stages of diabetic nephropathy and what happens at each stage?
(TEST QUESTION)

A
  • Stage 1= diabetes begins (hyperglycemia causing increased GFR; hyperfiltration and increased kidney size). This lasts about 2 years (reversible up to this point).
  • Stage 2= structural changes start to occur (glomerular basement membrane thickening and mesangial expansion).
  • Stage 3 (incipient nephropathy)= microalbuminuria, increased BP and occurs due to poor glycemic control.
  • Stage 4= onset of clinical PROTEINURIA and involves rising creatinine.
  • Stage 5= ESRD (dialysis required).
37
Q

What is the amount of protein in the urine that defines MICROalbuminuria?

A
  • 30-300 mg/day
38
Q

How do you diagnose diabetic nephropathy?

A
  • clinical HX
  • diabetic retinopathy (END OF STORY IF YOU FIND THIS. Without this you need a renal biopsy)
  • proteinuria
  • relatively large kidney size
39
Q

How do we manage diabetic nephropathy?

A
  • glycemic control= A1C
40
Q

What are the 3 types of glomerulonephritis?

A
  1. acute glomerulonephritis
  2. chronic glomerulonephritis
  3. rapidly progressive glomerulonephritis
41
Q

** What is NEPHRITIC syndrome?

A
  • HEMATURIA, HTN, and AZOTEMIA +/- ARF.

* has edema and proteinuria (but

42
Q

Is glomerulonephritis almost universally immunologically mediated?

A

YES leading to inflammation of the glomerular basement membrane.

43
Q

Is glomerulonephritis due to impaired Na+ and water excretion?

A

YES leading to HTN and edema

44
Q

What is the prototype of acute post-infectious glomerulonephritis?

A

post-streptococcal glomerulonephritis (group A beta-hemolytic strep) causing diffuse proliferative glomerulonephritis. More in children; LUMPY BUMPY.

  • Diagnosis via ASO and anti-DNAse B
  • Hallmark is trilobed nucleus cells in the glomerulus.
45
Q

How do you treat post-streptococcal glomerulonephritis?

picmonic

A

supportive only with fluids bc it is self-limiting. Don’t give antibiotics bc the strep throat is already over by this point.

46
Q

What is IgA mesangiopathy (Berger’s disease)?

A
  • Most common cause of nephritic syndrome caused by deposits of IgA in the mesangium of the kidney.
  • presents most often with GROSS HEMATURIA after upper respiratory infection or acute gastroenteritis.
47
Q

What is membranoproliferative glomerulonephritis?

picmonic

A
  • mixed NEPHRITIC/NEPHROTIC disease. Mesangium splits the membrane in two (TRAM TRACK appearance)!
  • hep C is common cause
  • no treatment :(
48
Q

What is rapidly progressive glomerulonephritis?

picmonic

A
  • NEPHRITIC syndrome characterized by crescents of the glomerulus on biopsy.
  • caused by goodpasture’s, wegners, or microscopic polyangiitis.
  • Must treat with CORTICOSTEROIDS.

CRP- Renal (19 decks)

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