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Renal Flashcards

1
Q

What is the clinical classification of glomerular nephrotic syndrome?

A
  1. Proteinuria (>3.5 g/d)

2. Hypoalbuminemia (

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2
Q

What is the clinical classification of glomerular nephritic syndrome?

A
  1. Decreased renal function (elevated creatinine)
  2. Hypertension
  3. Dysmorphic RBCs and RBC casts
  4. Edema
  5. Proteinuria (
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3
Q

What is the general management of nephrotic syndrome?

A

Low salt diet, diuretics, BP control, +/- cholesterol-lowering drugs, ACE-inhibitors, and Vitamin D replacement

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4
Q

What are the 5 primary renal nephrotic syndromes?

A
  1. Hereditary Nephrotic Syndromes
  2. Minimal Change Disease (MCD)
  3. Focal Segmental Glomerulosclerosis
  4. Membranous Nephropathy (MN)
  5. Membranoproliferative GN (MPGN)
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5
Q

What are some systemic diseases that can cause nephrotic syndromes?

A

Diabetes
Amyloid and light chain disease
SLE (membranous)

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6
Q

What is the Maltese Cross sign?

A

In nephrotic syndrome, you get lipoproteins in the urine. You see refractile bodies in the urine under polarized light – oval fat (lipid) bodies

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7
Q

What are other complications of nephrotic syndrome?

A
  1. Hypercoagulability - increased coag factors, decreased AT3, increased platelet aggregation to stimuli
  2. Increased risk for bacterial infections (peritonitis, pneumonia) - loss of IgG and complement components
  3. Decreased Vitamin D levels - loss of Vit D binding protein into urine
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8
Q

Where in the circulation are people with nephrotic syndrome at highest risk of developing a blood clot?

A

Renal veins

The venous return has the highest coag factors, because ATIII gets filtered out into the urine. Can kill ppl (PE).

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9
Q

What are the differences in edema between nephrotic syndrome and heart failure?

A

Nephrotic syndrome - edema is central, so they can lie flat. They get periorbital edema.

Heart failure - cannot lie flat

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10
Q

What is the most common nephrotic syndrome in children?

A

Minimal Change Disease (70%)

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11
Q

What is the most common nephrotic syndrome among people in their 20s and African Americans?

A

Focal Segmental Glomerulosclerosis

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12
Q

How is Minimal Change Disease treated?

A

Corticosteroids (prednisone), short course of oral cytoxan (12 wks) for frequent relapsers

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13
Q

What is one of the pathogenic mechanisms of Minimal Change Disease?

A

Podocytes can become antigen-presenting cells. Can express receptors that are normally present on dendritic cells - one of them is CD80.

Some circulating factor is activating the podocyte - associated with shape change, proteinuria.

High CD80 levels in the urine is associated with MCD

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14
Q

What are the pathophysiologic mechanisms associated with Focal Segmental Glomerulosclerosis?

A
  1. Circulating factor idiopathic – soluble uPAR (suPAR)
  2. Viral factor – HIV infection of podocyte
  3. Pathology factor in African Americans – APOL1
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15
Q

What disease is associated with Focal Segmental Glomerulosclerosis?

A

HIV

5-10% of all AIDS patients; may precede AIDS
80% black, 50% IVDA

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16
Q

What are the etiologies of membranous nephropathy (MN)?

A
  1. Primary - due to antibodies to phospholipase A2 on the podocyte
  2. Secondary - Hep B, gold, mercury, SLE, cancer

Mercury-based skin-lightening creams…

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17
Q

If someone presents with this nephrotic syndrome in their 50s+, you need to screen them for cancer

A

Membranous nephropathy

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18
Q

What are the differences between Membranoproliferative GN Types 1 and 2?

A

Type 1:

  • IgG under IF
  • subendothelial deposits (EM)
  • associated with Hep C infection

Type 2:

  • “dense” intramembranous deposits (ribbon-like deposits in the BM)
  • complement disorder
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19
Q

RBC cast is pathognomonic for?

A

Glomerulonephritis

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20
Q

What are the syndromes associated with aggressive nephritic disease?

A
  1. Rapidly progressive GN
  2. Crescentic GN
  3. Pulmonary-renal syndrome
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21
Q

SNGFR is proportional to?

A

Pgc = glomerular capillary hydrostatic pressure

SNGFR = single nephron GFR

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22
Q

How is vasodilation of afferent arterioles generally maintained?

A

Prostaglandins (E2 and I2) and NO

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23
Q

How is vasoconstriction of efferent arterioles generally maintained?

A

Angiotensin II

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24
Q

What do NSAIDs and ACE-inhibitors do to RBF?

A

NSAIDs cause vasoconstriction of afferent arterioles by blocking prostaglandins.
ACE-inhibitors cause vasodilation of efferent arterioles by blocking Ang II formation.

If taken together = bad :(

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25
Urea routinely ____estimates the GFR
Underestimates - it is reabsorbed in the tubules
26
What is pyelonephritis?
Inflammation of the kidney tissue, calyces, and pelvis
27
What is pyonephrosis?
Pus accumulation in the renal pelvis due to an infection in the kidney's collecting system. Etiology: Upper UTI in combination with obstruction and hydronephrosis
28
What is hydronephrosis?
Distension and dilation of the renal pelvis and calyces, usually caused by obstruction of the free flow of urine from the kidney
29
What is pyelitis?
Inflammation of the renal pelvis and calyces
30
What are the normal values for K+ ?
3.5 - 5
31
What are the normal values for Na+ ?
135 - 145
32
What are the normal values for phosphorus?
2.4 - 4.8
33
What are the normal values for Cl- ?
94 - 105
34
What are the normal values for Cr?
0.7 - 1.4
35
What are the normal values for BUN?
8 - 20
36
What are the normal values for glucose?
60 - 120
37
What are the normal values for cholesterol?
140 - 200
38
What are the normal values for serum osmolality?
275 - 295
39
What are the normal values for GFR?
125 ml/min
40
What cells secrete renin?
Granular cells, which a specialized subset of smooth muscle cells in afferent arterioles. These cells are part of the juxtaglomerular apparatus (JGA).
41
What is the order of the renal arteries in order of descending size?
Renal artery --> interlobar --> arcuate --> interlobular --> afferent arterioles
42
Creatinine routinely _____estimates the GFR
Over It is freely filtered by the glomerulus, not reabsorbed, but secreted to some degree
43
What is the Cockgroft and Gault formula for creatinine clearance?
Creatinine clearance = [(A) x (140 - age) x weight] / (72 x SC) ``` A = 1 if male, 0.85 if female SC = serum creatinine (mg/dL) ```
44
What is the equation for creatinine clearance using a 24-hour urine sample?
CLcr = (Ucr/Pcr) x V ``` Ucr = urine Cr Pcr = plasma Cr V = urine flow rate; obtained by dividing (volume collected in 24 hours) / (1440 min) ```
45
What compounds cause dilation of the afferent arterioles?
NO, prostaglandins
46
What compound causes constriction of the efferent arteriole?
Angiotensin II
47
What compounds cause constriction of the afferent arterioles?
NSAIDs, adenosine, norepinephrine, endothelin, thromboxane
48
What compounds cause dilation of the efferent arteriole?
ACE-inhibitors & ARBs
49
What is the specific gravity of urine?
1.010 is isotonic | than this is concentrated
50
What is azotemia?
Build up of nitrogen (nitrogenous wastes) in the blood (i.e., increase in serum BUN and Cr)
51
What is FENa and what is it used for?
FENa = Fractional excretion of sodium FENa = (Una / Pna) / (Ucr / Pcr) x 100% If 2% = AKI is caused by other pathologies
52
What are some of the immunosuppressive drugs used to treat glomerulonephritis?
Prednisone, cyclophosphamide, mycophenolate mofetil, azathioprine, chlorambucil, rituximab, IVIG
53
What is the pathophysiology of IgA nephropathy?
Mesangial deposition of IgA immune complexes --> mesangial expansion Associated with an aberrant glycosylation of IgA
54
Lupus nephritis is usually caused by what? Where?
Immune complex depositions In the: - mesangium (hematuria; not treated) - subendothelium (nephritic; high dose chemo tx for 6 mos) - subepithelium (nephrotic; mimics membranous)
55
What does Henoch-Schoenlein purpura have to do with the kidneys?
It's a systemic IgA vasculitis Leads to IgA complex depositions in the kidneys, GI tract, skin, and joints
56
Normal urine pH?
Varies from 4.6 - 8.0, normal 6.0
57
What is the equation for serum osmolality?
Sosm = 2 x Na + BUN/2.8 + Glu/18
58
If you add plasma, what compartment of fluid does it get added to?
ECF - specifically, intravascular
59
If you add saline, what compartment of fluid does it get added to?
ECF - both intravascular (25%) and extravascular (75%)
60
If you add D5W (water), what compartment of fluid does it get added to?
All of them - 2/3 intracellular, 1/3 ECF
61
Alkalosis leads to _____kalemia via what mechanism?
Hypokalemia High pH leads to K+ being pushed into cells --> in epithelial cells lining lumen in the nephron, high K+ will flow out into lumen along concentration gradient. Apical K+ channels are also inhibited to some extent by H+, so higher pH --> more channel usage.
62
How do some diuretics lead to hypokalemia via GFR?
One of the mechanisms is that they cause increased flow in the tubule --> more loss of K+, because it is harder for a K+ concentration to build up in the lumen
63
High potassium is a stimulus for ______ secretion
Insulin Insulin moves K into cells even without glucose via increase in Na/K pump quantity.
64
Catecholamines do what to K+ ?
They move K+ from extra-cellular to intra-cellular space B2 adrenergic receptors block this, so non-selective B-blockers (propranolol) will do this but selective (metoprolol) will not
65
How does black licorice cause hypokalemia?
The mineralocorticoid receptor that binds aldosterone (and upregulates Na/K exchange, apical K channels) will also bind cortisol, which has a concentration 1000x greater than aldo. 11BOH-SDH is an enzyme that converts cortisol --> cortisone = protects the receptor. Black licorice inactivates 11BOH-SDH :(
66
What are normal Hg A1C levels?
67
What is the mnemonic for remembering α and β receptors + insulin and renin stuff?
``` Alpha = decrease (attack) Beta = increase (build) ``` ``` Renin = 1 i Insulin = 2 i's ``` Thus, α1 = ↓ renin = ↓ aldo = hyperkalemia α2 = ↓ insulin = hyperkalemia ``` β1 = ↑ renin = ↑ aldo = hypokalemia β2 = ↑ insulin = hypokalemia ``` Thus, β-blockers (nonspecific) --> hyperkalemia α-blocker --> hypokalemia Beta-BLOCKER BLOCKS K from going into cells
68
How do you determine whether a metabolic acidosis is compensated?
ΔpCO2 = 1 - 1.5 x ΔHCO3-
69
How do you determine whether a metabolic alkalosis is compensated?
ΔpCO2 = 0.25 - 1 x ΔHCO3- Averaged as 0.7 x ΔHCO3-
70
How do you determine whether a respiratory acidosis is acute or chronic?
Acute: 1 ΔHCO3- = 10 ↑ ΔpCO2 1:10 Chronic: 4 ΔHCO3- = 10 ↑ ΔpCO2 4:10
71
How do you determine whether a respiratory alkalosis is compensated?
Acute: 2 ΔHCO3- = 10 ↓ ΔpCO2 2:10 Chronic: 4 ΔHCO3- = 10 ↓ ΔpCO2 4:10
72
Equation for MAP?
MAP = CO x PVR
73
Second equation for MAP?
MAP = [(2 x diastolic) + systolic] / 3
74
What effect do calcium channel blockers have on the kidney?
They dilate the afferent arteriole, and improve RBF and natriuresis
75
When should you start with a 2-drug regimen in a hypertensive patient?
When systolic >= 160 or diastolic >= 100
76
What is the only oral drug for urinary incontinence that the professor talked about in class?
Oxybutynin immediate release (OXY-IR) Smooth muscle relaxant; facilitates storage Side effects: can't see, can't pee, can't spit, can't shit (anticholinergic agent)

CVPR (3 decks)

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