Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (58 page)

Contrast-induced acute kidney injury (CIAKI)

• Risk factors: CKD, DM, CHF, age, hypotension, ↑ contrast volume (
JACC
2004;44:1393) • Clinical: Cr ↑ 25% or 0.5 mg/dL w/in 48 h, peaks in 3–5 d, resolves in 7–10 d • Prevention (
NEJM
2006;354:379;
JAMA
2006;295:2765;
KI Suppl
2012;2:69)

Isotonic IV fluids
(unless contraindic, eg, CHF): 3 mL/kg/h × 1 h before, 1 mL/kg/h × 6 h after (
JAMA
2004;291:2328); NaHCO
₃
? more effective than NaCl (
Annals
2009;151:631)

Hold ACEI
/
ARB
(
AJKD
2012;60:576),
NSAIDs
,
diuretics

N-acetylcysteine
1200 mg PO bid on day prior to & day of contrast; safe & ∴ reasonable in high-risk Pts, but benefit remains unclear (
JACC CV Interv
2009;2:1116;
Circ
2011;124:1250) Minimize contrast volume and consider iso-osmolar contrast (
JACC
2006;48:692) ? high-dose statin (
Circ
2012;126:3008) No proven benefit to Ppx RRT in addition to above, may be harmful (
Am J Med
2012;125:66)

• Gadolinium: can cause AKI in stage IV CKD (
Neph Dial Trans
2006;21:697), no effective Ppx Nephrogenic systemic fibrosis: fibrosis of skin, joints, eyes, and internal organs ~2–4 wk post exposure in Pts w/ mod-severe CKD (
JACC
2009;53:1621). ? role of postgado HD (
Radiat Med
2006;24:445). Rx is ↑ renal function, physical therapy. Can be irreversible.

Treatment

• Treat underlying disorder (see relevant sections); ? steroids if AIN (
KI
2008;73:940) • Prerenal: Isotonic IVF
alb (
NEJM
2004;350:22), HES (starch) nephrotoxic (
NEJM
2012;367:124) • Avoid nephrotoxic insults; review dosing of renally cleared drugs • Optimize hemodynamics (both MAP & CO); may take 1–2 wk to recover from ATN

• Watch for and correct volume overload, electrolyte (↑ K, ↑ PO
₄
), & acid/base status • If obstruction is diagnosed and relieved, watch for:

Hypotonic diuresis (2° buildup of BUN, tubular damage); Rx w/ IVF (eg,
¹
/
₂
NS)

Hemorrhagic cystitis (rapid Δ in size of bladder vessels); avoid by decompressing slowly

• Indications for urgent dialysis (when condition refractory to conventional therapy)

A
cid-base disturbance: acidemia

E
lectrolyte disorder: generally hyperkalemia; occasionally hypercalcemia, tumor lysis

I
ntoxication: methanol, ethylene glycol, lithium, salicylates (
Kid Int
2009;75:1349)

O
verload of volume (CHF)

U
remia: pericarditis, encephalopathy, bleeding

•
No
benefit to dopamine (
Annals
2005;142:510), diuretics (
JAMA
2002;288:2547), or mannitol

CHRONIC KIDNEY DISEASE (CKD)

Definition and etiologies
(
Lancet
2012;379:165)

• ≥3 mo of
reduced GFR
(<60)
and
/
or
kidney damage
(path, markers, imaging)

• Prevalence 13% in U.S.; Cr poor estimate of GFR; ∴ use prediction equation, eg, MDRD or CKD-EPI:
www.kidney.org/professionals/KDOQI/gfr_calculator.cfm
nb, equation may underestimate GFR in Pts w/ normal renal fxn, esp MDRD

• Etiologies: DM (45%), HTN/RAS (27%), glomerular (10%), interstitial (5%), PKD (2%) (
NEJM
2008;359:1477), congenital, drugs, myeloma, progression of AKI (
JAMA
2009;302:1179)

• Presence and degree of albuminuria a/w worse outcomes independent of GFR

• Rates of all-cause mortality and CV events increase with each stage of CKD and are significantly higher than the rate of progression to kidney failure (
NEJM
2004;351:1296)

Treatment
(
Annals
2009;150:ITC2-1;
NEJM
2010;362:57)

•
General
: nephrology referral when GFR <30 and access planning (avoid subclavian lines; preserve an arm for access by avoiding blood draws, BP measurements, IVs); Rx CV risk factors (eg, smoking, LDL-C;
Lancet
2011;377:2181), vaccines (flu, PNA, HBV)

•
Dietary restrictions
: Na (if HTN), K (if oliguric or hyperkalemic), PO
₄
, ? moderate protein restriction, strict glc control in DM

•
BP Control
: goal <130/80, start with ACEI (or ARB), effective in DM & nondiabetic CKD (
NEJM
2004;351:1952); likely no benefit of ACEI + ARB (
BMJ
2013;346:f360). For outPts, ✓ Cr & K in 1–2 wk, d/c if Cr ↑ 30% or K >5.4 (after dietary Δ & loop diuretic).

•
Metabolic acidosis
: sodium bicarbonate or sodium citrate if low HCO
₃
(
JASN
2009;20:2075)

•
Anemia
: goal Hb ~10 g/dL, worse outcomes if higher (
NEJM
2006;355:2085 & 2009;361:2019) epoetin (start 80–120 U/kg SC, divided 3×/wk) or darbepoetin (0.45 µg/kg q wk) iron supplementation to keep transferrin sat >20% (often given IV in HD Pts)

•
Uremic bleeding
: desmopressin (dDAVP) 0.3 µg/kg IV or 3 µg/kg intranasally

•
2
°
Hyperparathyroidism
: ↑ PO
₄
, ↓ Ca, ↓ calcitriol → ↑ PTH → renal osteodystrophy

phosphorus binders (
take with meals!
) (
NEJM
2010;362:1312)

if ↑ PO
₄
and ↓ Ca → calcium acetate (PhosLo) or calcium carbonate

if refractory ↑ PO
₄
or in setting of ↑ Ca → sevelamer (Renagel), lanthanum (Fosrenol)

if severe ↑ PO
₄
→ aluminum hydroxide (Amphojel),
short-term use only

vit. Δ or analogue (paricalcitol) if 25-(OH)D <30, stop if ↑ Ca (
AJKD
2009;53:408) calcitriol or paricalcitol if Ca-PO
₄
product <55 (? ↑ survival in HD Pts,
NEJM
2003;349:446) cinacalcet (parathyroid calcium-sensing receptor agonist) if PTH remains elevated despite phosphorus binders ± vit. Δ analogue (
NEJM
2004;350:1516;
NDT
2011;26:1327) parathyroidectomy

•
Consider transplant evaluation

DIURESIS

General considerations

• Increases Na excretion for treatment of HTN or edema in CHF, renal failure, and cirrhosis • Daily wt most effective method of documenting successful diuresis
Loop diuretics
(
NEJM
1998;339:387)
•
Drugs
: furosemide (Lasix), torsemide, bumetanide (Bumex), ethacrynic acid •
Mechanism
: inhibit Na-K-2Cl transporter in thick ascending limb (ThAL) Transient, immediate venodilation may aid in pulmonary congestion (
NEJM
1973;288:1087) Response is fxn of amt of drug excreted; ∴ ↑ dose needed in renal insufficiency, CHF Sigmoidal dose response curve; ∴ ↑ dose until induce diuresis, ↑↑ dose beyond that point yields diminishing returns compared with ↑ frequency of dosing •
Dosing
: PO bioavailability of furosemide ~50%, ∴ IV dose ~2× as potent as PO dose torsemide & bumetanide ~90% bioavailability; use ethacrynic acid if sulfa allergy 40 mg furosemide PO
20 mg furosemide IV
20 mg torsemide PO
1 mg bumetanide dose furosemide bid-qid; qd dosing can lead to initial diuresis → antinatriuresis Continuous vs. bolus IV: similar results in acute CHF (
NEJM
2011;364:797)