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Renal II Exam Three > Renal CIS - Nephrotic stuffs > Flashcards

Renal CIS - Nephrotic stuffs Flashcards

1
Q

What is the GFR associated with stage 5 CKD?

A

< 15 (or dialysis)

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2
Q

Stage 3 for 3 months is considered to be?

A

Chronic kidney disease

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3
Q

As GFR decreases what are the big impacts that occur (6 things) and in what order to they arise?

A
  1. HTN
  2. Increased PTH
  3. Anemia
  4. Increased phosphorous
  5. Acidosis/hyperkalemia
  6. Uremic syndrome
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4
Q

70% of chronic renal disease cases are caused by diabetes or HTN, with GN and the cystic diseases accounting for another 12%. What makes up the rest?

A

Prostatic obstruction and tubulointerstitial diseases

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5
Q

What are nine common presentations with chronic renal disease? And give the reason for each!

A

. Hypertension, edema, CHF (Na and H2O retention)

  1. Bone disease (Increased phosphate = decreased Ca++ = increased PTH = bone break down)
  2. Anemia (decreased EPO)
  3. Isosthenuria and broad waxy casts (problems concentrating urine and lipoprotein production by the liver)
  4. Acidosis (inability to secrete H+ normally)
  5. Hyperkalemia (inability to secrete K+)
  6. Progressive azotemia over months to years (end stage: fatigue weakness, malaise, nausea, vomiting, etc.)
  7. Paresthesias - (accumulation of toxic metabolites damages nerves)
  8. Bilateral small kidneys - (with fibrosis)
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6
Q

Riddle me the main three nephrotic spectrum diseases in primary renal disease.

A

Minimal change disease

Focal segmental glomerulosclerosis (FSGS)

Membranous

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7
Q

An AfroAmerican HIV patient on heroin is referred to you from the ED after presenting with pedal, periorbital edema, hypertension, and urine analysis showing oval fat bodies.

Renal biopsy shows podocyte injury with areas of sclerosis. What is the most likely diagnosis?

A

FSGS

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8
Q

What is cryoglobulin associated glomerulonephritis seen in, and due to?

A

Hepatitic C infection, and Type I MPGN (also secondary membranous glomerulopathy)

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9
Q

Idiopathic FSGS disease may be related to heritable abnormalities of any of several podocyte proteins, to polymorphisms in APOL1 gene * in those of African descent, or to increased levels of soluble urokinase receptors.

In what patients will you see FSGS?

A
  1. hispanic and black
  2. UV reflux
  3. Morbidly obese
  4. heroin users
  5. HIV
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10
Q

A 55 y/o male with non-Hodkins lymphoma presents with peripheral edema, 40 pound weight gain, and a history of recurrent infections over the past 6 months. The patient’s abdomen is prominent and he complains of dyspnea.

Urinalysis is shown. Serum vitamin D levels are low and albumin is 1.6 gm/dL. Spot urine for protein/creatinine ratio is 6.5 (6.5 gm/24 hours). Kidney biopsy shows thickened GBM with “spike and dome pattern” of subepithelial deposits. This patient has which type of renal nephrotic pathology?

A

Membranous

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11
Q

Membranous nephropathy is caused by immune complex deposition in the subepithelial area. What is the characteristic pattern of IgG and C3 deposition here?

A

“spike and dome”

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12
Q

What are ten causes of secondary membranous nephropathy?

A
  1. lymphoma
  2. carcinoma
  3. penicillamine
  4. gold
  5. SLE
  6. MCTD
  7. Thyroiditis
  8. Hep B or C
  9. Endocarditis
  10. syphilis
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13
Q

What is causing the characteristic depositions shown at points 1-5 in the attached image?

A
  1. Acute proliferative Gomerulonephritis (Post infections glomerulonephritis) (I think also)
  2. Membranous nephropathy
  3. Type I membranoproliferative glomerulopathy
  4. IgA nephropathy or Henoch Schonlein Purpura
  5. Minimal Change disease (I think)
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14
Q

What is the antigen in primary membranous nephropathy?

A

Phospholipase A2 receptor on the podocyte membrane.

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15
Q

A patient with membranous glomerulonephropathy suddenly develops nausea and vomiting with flank pain. Ultrasound shows bilateral kidney enlargement. The patient has developed renal:

A.infarction.
B.hemorrhage.
C.Infection.
D.vein thrombosis.
E.pelviceal obstruction

A

Vein Thrombosis

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16
Q

Fill in the labels on the arrows.

A
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17
Q

Is this serum electrophoresis normal or not?

A

No, the albumin is significantly decreased, with increased macroglobulin at alpha 2 and increased lipoprotein and fibrinogen at the Beta point.

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18
Q

Is this serum electrophoresis normal?

What is represented at Y?

A

Normal

Gamma Globulins

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19
Q

How do nephrotic syndromes influence the coagulation cascade?

A

Due to the loss of antithrombin III, proteins C and S, as well as increased fibrinogen, there is increased platelet aggregation and a hypercoagulable state.

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20
Q

This specimen was taken from a patient with non-selective proteinuria in excess of 3.5 g/day. On the left is a PAS stain, and on the right the specimen shows apple green birefringence. What stain was used on the right, and what is causing this nephrotic syndrome?

A

Congo red stain revealing apple green birefringence is indicative of amyloidosis.

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21
Q

In what three places will you likely see amyloid deposits in amyloidosis related nephrotic syndrome?

A

Glomeruli

Wall of arteries

wall of arterioles

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22
Q

A significantly overweight middle aged patient comes to you complaining of significant lower extremity edema. Urine dipstick is positive for glucose. Unable to live with themselves they decide to take their own life by eating themselves to death. On autopsy you take a sample of renal tissue and see the attached findings. What are the pink nodules shown here? What was the process by which this damage occured?

A

Kimmelstein-wilson nodules

  1. Non-enzymatic glycosylation of the glomerular basement membrane
  2. hyalinization of efferent arterioles
  3. hyalinization of mesangial matrix in the glomerulus
23
Q

This specimen was taken from the famous athlete pictured. What do you see here? What is the major risk factor for this condition?

A

Collapsing glomerulopathy

Version of FSGS that is specific to HIV patients

24
Q

In the attached image try to identify the diseases based on the deposition patterns shown. Then indicate what the main point of injury is, the normal findings, if it will progress to CKD and major associated disease processes.

A
25
Q

A 68 y/o male presents with polyuria alternating with oliguria and

1g/d proteinuria. History is positive for working with lead base paint.

The patient recently finished a course of tetracycline for a UTI. BP is

164/90 and the patient has a suprapubic mass. Labs are as follows:

Na+ 138 meq/L, K+ 5.6 meq/L, HCO3- 18 meq/L, Cl- 110 meq/L

Urine: no eosinophils, no crystals, SG 1.010, casts as shown.

BUN 52 mg/dL, Creatinine 2.2 mg/dL

Calcium 7.5 mg/dL, Phosphorus 5 mg/dL

Uric acid 4.5 mg/dL (3.5-7.7)

This man is most likely suffering from:

A

Prostatic Obstruction

26
Q

What is chronic tubulointerstitial disease characterized by?

A
  1. isosthenuria with polyuria
  2. moderate proteinuria
  3. very few cells
  4. type I, II or IV RTA
  5. broad waxy casts
  6. small kidneys
27
Q

What are the causes of chronic tubulointerstitial disease?

TQ here almost for sure

A
  1. Prostate (obstructive uropathy)
  2. Analgesics (NSAIDs)
  3. VU reflux
  4. Lead (heavy metals)
  5. Gout
  6. Myeloma
28
Q

One more time! What are the causes of chronic tubulointerstitial disease?

A

Prostate (obstructive uropathy)

Analgesics (NSAIDs)

VU reflux

Lead (heavy metals)

Gout

Myeloma

**Proud American Veterans Love GM**

29
Q

A 55 y/o male presents with back pain and weight loss. He takes hydrochlorthiazide for hypertension. Lab reports reveal a hemoglobin of 8 grams and a sed rate of 90 compatible with multiple myeloma. Further lab tests show:

Na+ 138 meq/L, K- 3.2 meq/L

Cl- 121 meq/L, HCO3- 16 meq/L

BUN 20 mg/dL, Creatinine 1.8 mg/dL

Urine pH is 5.0.

This patient has which type of acid base problem?

A

Type II RTA

30
Q

A 55 y/o male presents with back pain and weight loss. He takes hydrochlorthiazide for hypertension. Lab reports reveal a hemoglobin of 8 grams and a sed rate of 90 compatible with multiple myeloma. Further lab tests show:

Na+ 138 meq/L, K- 3.2 meq/L

Cl- 121 meq/L, HCO3- 16 meq/L

BUN 20 mg/dL, Creatinine 1.8 mg/dL

Urine pH is 5.0.

How do you know this patient does not have Type IV RTA?

A

hyporeninemic hypoaldosteronism would yield a high potassium

31
Q

A 55 y/o male presents with back pain and weight loss. He takes hydrochlorthiazide for hypertension. Lab reports reveal a hemoglobin of 8 grams and a sed rate of 90 compatible with multiple myeloma. Further lab tests show:

Na+ 138 meq/L, K- 3.2 meq/L

Cl- 121 meq/L, HCO3- 16 meq/L

BUN 20 mg/dL, Creatinine 1.8 mg/dL

Urine pH is 5.0.

How do you know this patient does not have Type I RTA?

A

Urine pH is 5.0, thus he can secrete H+; type I pH is >5.5

32
Q

What is the primary defect in type I RTA?

A

Impaired distal acidification

33
Q

What is the primary defect in type 2 RTA?

A

Reduced proximal bicarbonate reabsorption

34
Q

What is the primary defect in type 3 RTA?

A

No type three RTA

35
Q

What is the primary defect in type IV RTA?

A

Decreased aldosterone secretion or effect

36
Q

What is the bicarb level in type 1 RTA?

A

variable, may be below 10 meq/L

37
Q

What is the plasma bicarb level in type 2 RTA?

A

usually 12 to 20 meq/L

38
Q

What is the plasma bicarbonate level in type 4 RTA?

A

Greater than 17 meq/L

39
Q

What is the urine pH for type I RTA?

A

Greater than 5.3

40
Q

What is the urine pH for type 2 RTA?

A

Variable, greater than 5.3

Apparently can acidify the urine to below 5.3 per Dr. Darrows addition to the chart.

41
Q

What is the urine pH for type 4 RTA?

A

Usually less than 5.3

42
Q

What does Type 1 RTA do to plasma potassium?

A

Usually reduced (hyperkalemic forms do exist though)

43
Q

How would you correct hypokalemia from type 1 RTA?

A

largely correctible with alkali therapy

44
Q

What are plasma potassium levels like in type 2 RTA? What impact does alkali therapy have?

A

Reduced, made worse by bicarbonaturia induced by alkali therapy

45
Q

What are the plasma potassium levels like in type 4 RTA?

A

Increased

46
Q

What are 4 causes of Type I RTA?

A

Amphoteracin B,

HyperparaT,

Sjogrens syndrome,

Medullary sponge kidney

47
Q

What are 7 causes of type 2 RTA?

A
  1. Myeloma protein,
  2. Fanconi syndrome,
  3. Drugs-tenovofir
  4. toluene,
  5. acetazolamide,
  6. toperimate,
  7. zonisamide
48
Q

What are eight causes of type 4 RTA?

A
  1. Diabetes,
  2. ACE inhibitors,
  3. K sparing diuretics,
  4. Obstruction,
  5. Interstitial
  6. Nephritis,
  7. HIV,
  8. NSAIDs.
49
Q

A 55 y/o male presents with back pain and weight loss. He takes hydrochlorthiazide for hypertension. Lab reports reveal a hemoglobin of 8 grams and a sed rate of 90 compatible with multiple myeloma. Further lab tests show:

Na+ 138 meq/L, K- 3.2 meq/L

Cl- 121 meq/L, HCO3- 16 meq/L

BUN 20 mg/dL, Creatinine 1.8 mg/dL

Urine pH is 5.1.

What is true of the CL/HCO3 relationship in this patient?

A

Chloride and bicarb should move in balance with each other. Here, chloride is increased by 21 but HCO3- is decreased by only 9 meq. This reveals that there is, in addition to the metabolic acidosis, an underlyind metabolic alkalosis.

50
Q

A 55 y/o male presents with back pain and weight loss. He takes hydrochlorthiazide for hypertension. Lab reports reveal a hemoglobin of 8 grams and a sed rate of 90 compatible with multiple myeloma. Further lab tests show:

Na+ 138 meq/L, K- 3.2 meq/L

Cl- 121 meq/L, HCO3- 16 meq/L

BUN 20 mg/dL, Creatinine 1.8 mg/dL

Urine pH is 5.1.

What is the cause of the low anion gap hyperchloremic metabolic acidosis and the occult metabolic alkalosis?

A

Myeloma protein (bence jones protein) have damaged the proximal tubule, causing it to leak HCO3 (as in fanconi syndrome).

The patient also has a chronic metabolic alkalosis induced by his Thiazide diuretic use.

51
Q

What do bence jones proteins join forces with?

A

They join up with Tamm Horsfall proteins and clog the renal tubules

52
Q

What are the six causes of renal failure from multiple myeloma?

A
  • “Myeloma kidney” (produces IL-1)
  • Hypercalcemia
  • Hyperuricemia
  • Amyloidosis
  • B cell infiltration
  • Hyperviscosity
53
Q

What is Gitelman’s syndrome?

A

Mutation in the NCC (Na+ Cl- cotransporter), leads to a thiazide effect.

54
Q

How do diuretics cause hypokalemic alkalosis?

A

Both by decreased plasma volume (contraction alkalosis) and, even in the formers absence, by presenting increased luminal Na to the collecting duct principle cells.

Renal II Exam Three (13 decks)

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