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Med School > CKD > Flashcards

CKD Flashcards

1
Q

Definition of CKD

A

Abnormality of kidney function or structure that is present for at least 3 months
- persistently abnormal function (GFR<60) due to intrinsic kidney disease
OR
- normal function but persistent structural abnoramility of the kidneys with markers of damage (proteinuria, hematuria, casts)

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2
Q

Screening for CKD
How often should you test after an abnormal result?

A
  1. Serum creatinine
  2. ACR
  3. Urinalysis
    +/- 4. U/S
  • repeat testing 3-6 months or sooner if severe
  • need to screen diabetics annually
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3
Q

Common causes of CKD
Higher risk ethnicities

A
  • Most common cause is DM
  • HTN, ischemic, glomerulonephritis, polycystic kidney disease, drugs, pyelonephritis, AKI, NSAIDs
  • Smoking, sleep apnea
  • South asian, pacific islanders, indigenous
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4
Q

Uremic syndrome
- when does it occur
- sx

A
  • Symptomatic around <30 eGFR, predominates at <15
  • fatigue, nausea, anorexia, amenorrhea, cold intolerance, leg cramps and restlessness, wasting, pruritis, constipation, edema/SOB, CHF, HTN
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5
Q

Common comorbidities with CKD

A
  • anemia, hyperkalemia, acidemia, hyperparathyroidism, hyperphosphatemia
  • ESRD is actually very uncommon in CKD/DKD as most patients will die before progressing to the need for dialysis
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6
Q

BP goals for CKD and CKD with DM
Careful rule to avoid with HTN drugs?
Which BP drug is first line?
Which BP drug has a risk of hyperkalemia?

A
  • under 135/85
  • under 130/80 if diabetic
  • DO NOT combine and ACEi and ARB
  • thiazides are first choice
  • spironolactone is effective but there is a risk of hyperkalemia
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7
Q

When is metformin contraindicated in CKD?

A

eGFR <30

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8
Q

Bacteria present but no WBC?

A

NOT an infection, likely contamination

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9
Q

What values would suggest severe CKD?
- ACR
- Protein dipstick
- PCR
- 24h protein

A
  • ACR 30+
  • 1+ or more protein
  • PCR 50+
  • 24h protein 300+
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10
Q

How do _____ affect the AA/EA?
- NSAIDs
- ACEIs/ARBs
- ANP/prostaglandin/ATII/NE

A
  • NSAIDs constrict the AA and ACEI/ARBs dilate the EA (decrease GFR)
  • ANP/prostaglandin dilates AA and ANP/ ATII/NE constricts EA (increase GFR)
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11
Q

How does PTH affect Bone/ Kidney/ Intestine?

A

Bone –> increases calcium and PO4 resorption

Kidney –> increases calcium resorption, increases PO4 excretion (indirect), increases calcitriol activation

Intestine –> indirectly increases calcium and PO4 absorption by increasing calcitriol

  • overall increases serum calcium and neutral/ mildly decreases serum PO4
  • PTH effect on PO4 renal excretion overrides its own bone and intestine effects as well as the calcitriol effect of increasing PO4 resorption
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12
Q

How does calcitriol affect Bone/ Kidney/ Intestine?

A

Bone –> increases calcium and PO4 resorption

Kidney –> increases calcium and PO4 resorption

Intestine –> increases calcium and PO4 absorption

  • overall increases serum calcium and PO4
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13
Q

How does FGF-23 affect Bone/ Kidney/ Intestine?

A

Bone –> unknown

Kidney –> increases PO4 excretion, decreases calcitriol activation

Intestine –> indirectly decreases calcium and PO4 absorption by decreasing calcitriol

*overall decreases serum PO4 and calcitriol

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14
Q

Stimulation vs inhibition of PTH?

A

(+) –> decreased calcium, increased PO4
(-) –> increased calcium, calcitriol, FGF-23

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15
Q

Stimulation vs inhibition of calcitriol?

A

(+) –> decreased PO4, increased PTH
(-) –> increased PO4, FGF-23

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16
Q

Stimulation of FGF-23?
(No knowledge on what inhibits it)

A

increased PO4, calcitriol, PTH

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17
Q

How does CKD mineral bone disease affect the balance of Ca/calcitriol/PTH, etc?

A

hyperphosphatemia, hypocalcemia, decreased calcitriol, and PTH resistance to calcium ALL lead to SECONDARY HYPERPARATHYROIDISM

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17
Q

How does CKD mineral bone disease affect the balance of Ca/calcitriol/PTH, etc?

A

hyperphosphatemia, hypocalcemia, decreased calcitriol, and PTH resistance to calcium ALL lead to SECONDARY HYPERPARATHYROIDISM

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18
Q

Treatment for CKD mineral bone disease?

A
  • limit hyperPO4 using binders (Tums, Fe, Mg) and diet, consider supplementing calcitriol, consider calcimimetic if on dialysis ( will increase Ca sensitivity), maintain target PTH for CKD stage
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19
Q

What is calcitriol? What is its role in CKD?

A
  • main active vitamin D metabolite
  • helps overcome skeletal resistance to PTH that occurs with CKD
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20
Q

Describe process of Diabetic Kidney Disease
What is a good predictor of mortality?

A
  • GFR will initially increase (hyperfiltration) –> microalbuminuria –> proteinuria –> nephrotic syndrome –> decreased GFR
    –> ESRD
    *faster if diabetic

Silent –> mild GBM thickening, focal mesangial sclerosis
Incipient –> moderate GBM thickening, variable sclerosis, moderate albuminuria, mild GFR decrease
Overt –> severe albuminuria, HTN, decreased GFR, marked sclerosis
ESRD –> global sclerosis, GFR<15, HTN, decreasing albuminuria

*albuminuria predicts CV mortality - closely related to vascular disease due to endothelial dysfunction leading to protein leak

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21
Q

Describe pathology in the kidney with DKD

A
  • mesangial expansion and proliferation
  • GBM thickening
  • podocyte loss, hypertrophy, foot process effacement
  • glomerulosclerosis
  • increased ROS (TGF-B, IL1/6/18, TNF-a) from the PKC/ polyol/ RAAS pathways

*oxidative stress is central to the damage caused by hyperglycemia

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22
Q

SGLT2 Inhibitors

A
  • reduce glucose absorption in the kidneys thus reducing hyperglycemia
  • helps slow progression of DKD/ protects CVS
  • i.e. Empagliflozin
23
Q

What kind of drug is finerone?

A
  • Non-Steroidal Mineralocorticoid Receptor Antagonist
  • inhibits inflammation and fibrosis, slows CKD and CV morbidity
24
Q

What drugs should you give for DKD?

A
  • SGLT-2 inhibitors, MRAs, RAAS inhibitors for inflammation
  • GLP-1RAs for hyperglycemia
  • ACEis/ARBs/MRAs/SGLT2 inhibitors for hemodynamic dysregulation
25
Q

Which antihypertensive should be used if creatinine 150+ or eGFR<30?

A
  • ACEis/ ARBs always 1st line unless contraindicated, then CCB, then hydrochlorothiazide
  • Loop diuretic (furosemide) over thiazides if you need volume control
26
Q

What is anemia like in CKD? What causes anemia in CKD?

A
  • normocytic, normochromic, hypoproliferative (reticulocyte count)
  • <130 Hgb for men, <120 for women
  1. EPO deficiency/ lack of responsiveness to hypoxia (stabilization of HIF) which would normally stimulate EPO production
  2. Iron abnormalities (loss, decreased absorption, reticuloendothelial blockade)
  3. Decreased RBC survival (due to less EPO and inflammation)
27
Q

Role of EPO, why does it decrease in CKD?

A
  • prevents apoptosis of erythroblasts
  • made in peritubular capillary cells - loss of healthy cells in CKD leads to less EPO (though still minimal ability to make more in response to hypoxia)
28
Q

Describe the issues with iron caused by CKD

A
  • most iron is stored in Hgb/ as ferritin, main regulation is via absorption in the gut
  • Loss –> due to frequent sampling, procedures, hemodialysis, coagulopathy, uremic bleeds
  • Inflammation increases hepcidin which decreases gut absorption of Fe (absolute deficiency)
  • Hepcidin also blocks Fe transporters which locks ferritin storage (functional deficiency AKA reticuloendothelial iron blockade)
29
Q

Why treat anemia? How? When?

A
  • improved exercise tolerance, improved QoL, receive fewer transfusions which can potentially sensitize someone to a transplant
  • if ferritin <100 or hemodialysis patient –> IV iron
  • if ferritin >100 or no response –> EPO or darbopoietin
  • adjust ESA until Hb is in target range of 11-13

Supplement iron if TSAT <30% and ferritin <500

30
Q

Transferrin vs Ferritin

A

Transferrin –> form available for erythropoiesis, made in the liver so will increase with inflammation and decrease with malnutrition and cirrhosis
- transferrin saturation (TSAT) tells you amount of Fe bound to transferrin

Ferritin –> best marker of iron deficiency (under 100)
- acute phase reactant so will increase with infxn/ malignancy
- tells you if there is enough room to supplement iron without causing an overload

31
Q

When should you not give iron?
When should you not give ESAs?
What is the goal for iron?

A
  • Do not give iron with active infection
  • Do not give ESAs with cancer (EPO is anti-apoptotic)
  • give enough to maintain erythropoiesis and avoid transfusion (target between 95-115) but DO NOT overload (over 130)
32
Q

Kidney Function effect on absorption

A
  • no major impact
  • may have gut edema leading to decreased absorption
  • oral iron and PO4 binders may chelate other drugs
33
Q

Kidney Function effect on distribution
Explain the concept of Vd

A
  • if hypoalbuminemia need to monitor highly protein bound (>80%) drugs i.e. phenytoin, digoxin
  • will need to halve dose

Vd –> theoretical volume of fluid total drug would need to be diluted to produce the concentration in the blood
- Low Vd (under 1) –> more water soluble, more likely to be eliminated by dialysis
- High Vd (over 2) –> more lipid soluble, less likely to be eliminated by dialysis

34
Q

Describe the two phases of drug metabolism?

A

Phase I –> functionalization –> loss of activity
Phase II –> conjugation with highly polar compounds to aid in rapid excretion

35
Q

Kidney Function effect on excretion

A
  • if non-renal clearance is over 70%, can use normal drug dosing even if there is renal insufficiency
  • if renal clearance is over 30%, adjust the dose
36
Q

What type of proteins are filtered by hemodialysis vs glomerulus?

A

HD –> smaller and unbound
Glomerulus –> bigger proteins

*PD is mostly small pores but some larger ones

37
Q

Belmont Report

A
  • beneficence, nonmaleficence, autonomy, justice
38
Q

Alport Syndrome

A
  • type IV collagen variants, affects the GBM
  • 2nd most common inherited kidney disease after polycystic
  • hearing and ocular issues
39
Q

Indications for chronic dialysis w ESRD

A
  • metabolic abnormalities (hyperK/PO4, acidemia, severe anemia)
  • clinical abnormalities (fluid overload, uremic symptoms)
40
Q

How does hemodialysis work? What are the types of access?

A
  • uremic blood (K, PO4, toxins) is run against diasylate (purified water w individualized electrolytes and dextrose)

Diffusion –> passive movement of solutes down a concentration gradient, affected by size of solute/pores, SA of membrane, gradient, and flow rate
- more for small molecules (K, Na, urea)

Convection –> active movement of solutes dragged by water movement/ pressure gradient, affected by the same factors as diffusion plus amount of H20 removed
- more for medium/ large molecules (B12, glucose, PO4, uric acid, cretainine)

  • Av Fistula/graft –> preferred
  • Tunneled IJ catheter –> tip in RA, risk of infection/ endocarditis, cannot shower/ swim
  • Can be done in facilities (3x week for 4h or 8h nocturnal)
  • Can be done at home (trained, no cost, travel)
41
Q

How does peritoneal dialysis work? Different types?

A
  • peritoneal lining acts as the membrane
  • fill bag, tubing, drainage bag (cannot get wet)
  • similar mechanisms as HD except also ONCOTIC pressure (convection) for larger molecules as diasylate is glucose based
  • Continuous Ambulatory - 3-4 exchanges a day with last fill at night with icodextrin, drained in the morning
  • only free inbetween exchanges
  • Continuous Cycler - hooks up to machine that does 4-8 exchanges while asleep, last fill in the morning with icodextrin and drain at night
  • ambulatory and free during the whole day

*HD and PD outcomes are similar and you can switch between the two

42
Q

Diagnostic vs Carrier vs Screening vs Predictive Testing
Which age group is most likely to do predictive testing?

A

Diagnostic –> symptomatic patients who need a diagnosis

Carrier –> asymptomatic patients who are not at risk of disease, inform risk for future kids

Screening –> asymptomatic patients at risk for a treatable genetic condition based on general population (CF)

Predictive –> asymptomatic patients at risk for an inherited disease based on family history (Huntingtons, BRCA1/2)
- most common in 20-30s and 55-60s

43
Q

Gene positive vs gene negative?

A

Positive - asymptomatic but will LIKELY develop condition

Negative - asymptomatic but not at risk of developing condition

44
Q

Reasons not to pursue predictive testing

A

too young, anticipated negative psychological effects, no preventative therapy, potential for discrimination

*most will have decreased anxiety and depression regardless of the outcome a year later, but will have worse outcomes for (+) eventually (depression is most common)

45
Q

What does a purpuric rash indicate?

A
  • secondary glomerulonephritis
  • caused by ANCA vasculitis (ANCA MPO will be (+))
46
Q

Kidney Friendly Diet

Sodium limit if stage 3-5 CKD or post-transplant?

A
  • plant based diet, unsaturated fats, nuts, avoid processed meats/ refined carbs/ sweetened drinks
  • increase protein intake if on dialysis, but avoid excess protein and malnutrition (protein energy wasting common in late stage CKD)
  • avoid restaurants as they have a lot of excess sodium
  • less than 2300mg Na per day
47
Q

Fluid requirements if transplant/ PKD/ HD/PD?

PO4 requirements if stage 3-5 vs stage 5 dialysis?

A

transplant - no fluid restriction
PKD - at least 3 L
HD - 750ml - 1L plus urine output
PD - 1.5 - 2L or to thirst

Stage 3-5 - 0.8-1.5
Stage 5 Dialysis - 1.1 - 1.8
*PO4 is more bioavailable in processed foods than legumes/grains, want to avoid hyperPO4

48
Q

What aspects of diet can cause hyperkalemia?

A
  • inadequate fiber, excess proteins, lots of coffee, juice
49
Q

Who should you NOT give a transplant to? Who can?

A
  • active infection/ malignancy/ psych illness, high peri-operative risk, high comorbidity burden (dementia)
  • even Hep C/ HIV patients have been able to donate kidneys
  • pigs can! (zenotransplantation)
50
Q

Living vs dead donor

A
  • living is better –> shorter time, decreased perioperative risk, better graft longevity
51
Q

Barriers to transplant?

A
  • T cell and B cell mediated graft rejection
  • APC presents Ag to T cell via MHC/TCR and B7/CD28 connections (CTLA4 inactivates T cells)
  • ABO blood group and HLA Abs
  • Ab-mediated rejection is the #1 cause of graft failure
  • Acute rejection is becoming less common but long term outcomes are still relatively the same
52
Q

Examples of immunosuppresants

A
  • belatacept - better renal toxicity outcomes comapred to cyclosporine
  • anti-thymocyte globulins ( get slow recovery of CD4/8 cells)
53
Q

How do blood groups work

A

Group A –> Anti B Abs, A antigen
Group B –> Anti A Abs, B antigen
Group AB –> no Abs, A and B antigens
Group O –> Anti A and B Abs, no antigens

*AB group most likely to receive transplants

54
Q

HLA Antibodies

A
  • HLA Abs are present on all nucleated cells
  • They are formed in pregnancy, blood transfusions, transplantation, infection (all sensitizing events)
  • Less important for liver transplant
55
Q

Declaration of Istanbul

A

Made organ trafficking illegal (except Iran)

56
Q

Criteria for Donation after Death

A
  • neurologic death –> coma with no responsiveness, absence of brainstem reflexes, apnea test, must be no reversible cause
  • if irreversible but doesnt meet the above criteria, can donate after cardiac death (heart stops for more than 5 minutes)

Med School (21 decks)

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