Slide Nephrology
Slide Nephrology
Slide Nephrology
Agenda
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Acute Kidney Injury (AKI)
A. Definitions and Background
1. AKI is defined as an acute decrease in kidney
function. Associated with accumulation of waste
products and (usually volume).
b. Acute Kidney Injury Network (AKIN)
a. An abrupt (<48 hr) increase in SCr of more
than 0.3 mg/L OR a 50% increase in
baseline OR
b. Urine output less than 0.5 ml/kg/hr for more
than 6 hours
c. Rifle Criteria. Used to stage AKI. (Risk, Injury,
Failure, Loss or ESRD)
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Patient Case – Question 2
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A. Prerenal
B. Intrinsic
C. Postrenal
D. Functional
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Rapid Increase
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Patient Case – Question 2
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A. Prerenal
B. Intrinsic (most likely ATN)
C. Postrenal
D. Functional
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D. Prevention of AKI
1. Avoid nephrotoxic drugs when possible.
2. Ensure adequate hydration (2L/day). If
intravenous, 0.9% sodium chloride (NaCl) is
preferred.
3. Patient education
4. Drug therapies to decrease incidence of
contrast- induced nephropathy – see drug
nephrotoxicity section.
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Acute Kidney Injury
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Patient Case – Question 5
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E.P. is a 67-year-old man referred to cardiology for
intermittent chest pain. The patient has a medical history
significant for CKD, type 2 diabetes mellitus, and
hypertension. Medications include enalapril,
hydrochlorothiazide, and pioglitazone. Laboratory values
include SCr 1.8 mg/dL, glucose 189 mg/dL, hemoglobin
12mg/dL, and hematocrit 36%. His physical examination is
normal. The plan is to undergo elective cardiac
catheterization.
Which one of the following approaches is the best choice for
hydration?
A. 0.45% NaCl.
B. 0.9% NaCl.
C. D5 (5% dextrose) / 0.45% NaCl.
D. Oral hydration with water.
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Drug-Induced Kidney Damage
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Contrast-Induced Kidney Damage
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e. Prevention
i. Medications used to prevent contrast-induced
nephropathy:
a) Acetylcysteine – antioxidant and vasodilatory
mechanism. Accumulation of glutathione takes time
and may not be as effective in emergency cases.
Various dosing recommendations. Safe.
b) Ascorbic acid – antioxidant. One large study showed
benefit when used immediately before. Not
confirmed. Give ascorbic acid 3 g before procedure
and 2 g 2 times/day x two doses after procedure.
May have role in emergency cases
c) Fenoldopam - avoid
d) Theophylline/Aminophylline – Avoid
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Chronic Kidney Disease
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A. Background
2. Definition. Kidney damage for more than 3 months
as defined by structural or functional abnormalities of
the kidney, without or without decreased GFR OR
GFR < 60 ml/min/1.73m2 for 3 months
3. Stages of CKD
1 Kidney damage with GFR > 90 mL/minute/1.73m2
2 Kidney damage with GFR 60-89 ml/minute/1.73m2
3 GFR 30-59 mL/minute/1.73m2
4 GFR 15-29 mL/minute/1.73m2
5 GFR < 15 mL/minute/1.73m2 or on dialysis
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Chronic Kidney Disease
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F. Diabetic Nephropathy
4. Management / slowing progression
a. Aggressive blood pressure management
i. Target BP < 130/80 mm Hg.
ii. ACE and ARB’s are preferred (often in
combination with a diuretic) and should be used
with any degree of proteinuria (even if not
hypertensive). Combine with diuretic if needed.
Hold if K is greater than 5.6 mEq/L or with a >
30% rise in Scr.
iii. Calcium channel blockers are an add-on option.
Data are emerging for combined
iv. Dietary Na less than 2.4 g/day. Modify DASH to
limit K.
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F. Diabetic Nephropathy
4. Management / slowing progression
b. Intensive blood glucose control.
Glycosylated hemoglobin less than 7%.
Less aggressive with more advanced
CKD
c. Protein restriction – There are
insufficient data in diabetes but 0.8 g/kg
day might slightly reduce progression.
Patients should avoid high-protein diets.
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Case – Questions 12 and 13
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R.T. is a 60-year-old HD patient who has had ESRD…
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A. Anemia
1. Several factors are responsible for anemia in CKD:
decreased erythropoietin production (most important),
shorter life span of red blood cells, blood loss during
dialysis, iron deficiency, anemia of chronic disease, and
renal osteodystrophy.
3. Signs and symptoms. Symptoms of anemia of CKD are
similar to anemia associated with other causes.
4. Treatment-Treatment of anemia in CKD can decrease
morbidity/mortality, reduce LVH, increase exercise
tolerance, and increase quality of life. Recent studies
have suggested that treatment to high hemoglobin
concentrations (greater than 13 g/dL) increases
cardiovascular events. TREAT trial failed to show a
benefit in outcomes but was associated with increased
stroke in CKD.
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Anemia
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Anemia
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Anemia
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Anemia
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g. Common causes of inadequate response to ESA
therapy:
i. Iron deficiency is the most common cause of
erythropoietin resistance. Increased use of
intravenous iron products has reduced this
problem, however.
ii. Infection and inflammation
iii. Other causes in patients with adequate iron
stores (the first three are the most common)
Chronic blood loss
Osteitis fibrosa
Others (see notes)
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Anemia
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g. Iron therapy
i. Most patients with CKD who are receiving ESA
therapy require parenteral iron therapy to meet
needs (increased requirements, decreased oral
absorption).
ii. For adult patients who undergo dialysis, an
empiric 1000-mg dose is usually given and
equations are rarely used.
iii. Follow transferrin saturation and ferritin as noted
during ESA therapy.
iv. Four commercial iron preparations are approved
in the United States (Table 2).
v. Oral iron not recommended in CKD patients on
HD.
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CKD – Bone Dz
B. Renal Osteodystrophy and Secondary
Hyperparathyroidism
4.Treatment
a. Therapy goals - (Table 3)
b. Nondrug therapy
a. Dietary phosphorus restriction
b. Dialysis
c. Parathyroidectomy
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CKD – Bone Dz
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c. Drug therapy.
i. Phosphate binders: (Can combine different binders).
Take prior to meals.
a) Aluminum-containing phosphate binders Avoid
(see notes).
b) Calcium-containing phosphate binders
1) Widely used binder. Considered initial binder of
choice for stage 3 and 4 CKD. Carbonate is
relatively inexpensive
2) Calcium acetate. Better binder than carbonate,
so less calcium given
3) Use may be limited by development of
hypercalcemia.
4) Total elemental calcium per day = 2000 mg/day
(1500-mg binder; 500-mg diet)
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CKD – Bone Dz
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c. Drug therapy.
a. Phosphate binders: (Can combine different binders).
c) Sevelamer: a nonabsorbable phosphate binder
1) Effectively binds phosphorus.
2) Indicated especially if calcium-phosphorus factor
is greater than 55 mg2/dL2.
3) Decreases cholesterol. As sole binder, may get
hypocalemia and acidosis (HCl salt).
4) Available as sevelamer HCl (Renagel) and
sevelamer carbonate (Renvela)
d) Lanthanum carbonate: chewable wafer. Similar
place in therapy as sevelamer.
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CKD – Bone Dz
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3. Drug therapy.
ii. Vitamin D analogs: Suppress PTH synthesis and
reduce PTH concentrations; therapy is limited by
resultant hypercalcemia, hyperphosphatemia and
elevated calcium-phosphorus product. Products
include Calcitrol, doxercalciferol, and paricalcitol.
iii. Cinacalcet HCL: A calcimimetic that attaches to
the calcium receptor on the parathyroid gland and
increases the sensitivity of receptors to serum
calcium concentrations, thus reducing PTH.
Especially useful in patients with high
calcium/phosphate concentrations and high PTH
concentrations when vitamin D analogs cannot be
used
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Patient Case – Question 14
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Patient Case – Question 14
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The End
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Renal Replacement Therapy
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Page 466
C. Hemodialysis (continued)
4. Common complications of hemodialysis
a. Intradialytic
i. Hypotension – primarily related to fluid removal. Tx: limit fluid
gains between sessions; give normal or hypertonic saline,
midodrine. Less well-studied agents include fludrocortisone,
selective serotonin reuptake inhibitors
ii. Cramps – vitamin E or quinine (controversial because of
side effect profile). Associated with rapid fluid removal.
iii. Nausea/vomiting
iv. Headache/chest pain/backpain
b. Vascular access complications – most common with catheters.
i. Infection – S. aureus. Need to treat aggressively. May need
to pull catheter
ii. Thrombosis - suspected with low blood flows. Oral
antiplatelets for prevention not used because of lack of
efficacy. Can treat with alteplase 1 mg per lumen.
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Patient Cases – 10 and 11
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9. R.R. is a 70-year-old man being evaluated for hemodialysis
access. He has a history of diabetes mellitus and
hypertension but is otherwise healthy. Which of the following
dialysis accesses has the lowest rate of complications and
longest life span?
A. Subclavian catheter
B. Tenckhoff catheter
C. Arteriovenous graft
D. Arteriovenous fistula
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The End
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