Pocket Medicine




Definition (CJASN 2008;3:844; KI Suppl 2012;2:19)

•  AKI: abrupt (<48 h) ↑ Cr ≥0.3 mg/dL, ↑ Cr ≥50%, or UOP <0.5 mL/kg/h for ≥6 h additional gradations based on further ↑ Cr & ↓ UOP, but not used clinically

•  Cannot estimate GFR using Cr in setting of AKI or D’ing Cr (requires steady state)

Workup (Lancet 2012;380:756)

•  H&P: recent procedures & meds; thirst; VS & vol status; s/s of obstruction, vasc or systemic dis.; ischemia (prerenal & ATN) accounts for >50% of in-hospital AKI

•  Urine evaluation: output, urinalysis, sediment, electrolytes, and osmolality

•  Fractional excretion of sodium (FENa) = (UNa/PNa)/(UCr/PCr)

<1% → prerenal, contrast, HRS or glomerulonephritis; >2% → ATN In setting of diuretics, ✓ FEUN = (UUN/PUN)/(UCr/PCr); <35% → prerenal

•  Renal U/S or CT: r/o obstruction & eval kidney size to estimate chronicity of kidney disease

•  Serologies (if indicated): see “Glomerular Disease”

• Renal bx: may be necessary if cause remains unclear (esp if hematuria and/or proteinuria)

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); NaHCO3 ? more effective than NaCl (Annals 2009;151:631)

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

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 Med2012;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.


•  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, ↑ PO4), & 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)

Acid-base disturbance: acidemia

Electrolyte disorder: generally hyperkalemia; occasionally hypercalcemia, tumor lysis

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

Overload of volume (CHF)

Uremia: pericarditis, encephalopathy, bleeding

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


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), PO4, ? 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 HCO3 (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: ↑ PO4, ↓ Ca, ↓ calcitriol → ↑ PTH → renal osteodystrophy

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

if ↑ PO4 and ↓ Ca → calcium acetate (PhosLo) or calcium carbonate

if refractory ↑ PO4 or in setting of ↑ Ca → sevelamer (Renagel), lanthanum (Fosrenol)

if severe ↑ PO4 → 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-PO4 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


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)

? ↑ diuresis w/ co-administration of albumin if ↓ serum albumin (Crit Care Med 2005;33:1681)

Thiazide diuretics (NEJM 2009;361:2153)

•  Drugs: hydrochlorothiazide (HCTZ), chlorothiazide (Diuril), metolazone (Zaroxolyn)

•  Mechanism: inhibit Na-Cl cotransporter in the distal convoluted tubule (DCT)

synergistic with loop diuretic, esp. if chronic loop use

↓ effect when GFR <30, except metolazone which is still effective in renal insufficiency

•  Dosing: give prior to loop diuretic, typically ~30 min before

K-sparing diuretics

•  Drugs: spironolactone (Aldactone), amiloride, triamterene, eplerenone

•  Mechanism: ↓ Na reabsorption in collecting duct (amiloride/triamterene inhibit principal cell Na channel [ENaC]; spironolactone/eplerenone inhibit mineralocorticoid receptor). Relatively weak natriuretic activity, useful in combination with thiazide or in cirrhosis.

Disease state specific regimens

•  Renal insufficiency: loop diuretic (↑ dose to achieve effective delivery to ThAL) ± thiazide

•  CHF: loop diuretic (↑ frequency over ↑ dose) + thiazide (watch K & Mg)

•  Nephrotic syndrome: urinary albumin binds secreted loop diuretic, use 2–3 × normal dose

•  Cirrhosis: spironolactone (blocks 2° hyperaldosteronism) + lasix in 2.5:1 ratio

•  Severe metabolic alkalosis: acetazolamide & treat underlying cause

Adverse effects

•  Loop: ± ↑ Na, ↓ K, ↓ Mg, ↓ Ca, hyperuricemia, ototoxicity, hypersensitivity (sulfa)

•  Thiazide: ↓ Na, ↓ K, ↓ Mg, ↑ Ca, hyperlipidemia, pancreatitis, ↑ glucose

•  K-sparing: ↑ K (esp. w/ ACEI), metabolic acidosis, gynecomastia (spironolactone)



•  Substitutes for renal solute and fluid removal; Acute: CVVH vs. HD; Chronic: PD vs. HD

Hemodialysis (HD) (NEJM 2010;363:1833)

•  Physiology: blood flows along one side of semipermeable membrane, dialysate along other

Fluid removal (ie, Na + H2O) via transmembrane pressure (TMP) gradient

Solute removal via transmembrane concentration gradient and inversely proportional to size (∴ effective removal of K, urea, and Cr, but not PO4)

•  Typical orders: duration, volume removal goals, K and Ca in dialysate bath, anticoagulation

•  6× vs. 3×/wk improved HTN, LV mass, QoL, but ↑ vasc issues (NEJM 2010;363:2287); w/ 3×/wk HD, ↑ adverse outcomes after 2 d interval (NEJM 2011;365:1099)

• Complications: HoTN, arrhythmia, access issues (clot, stenosis, infxn, recirculation), disequilibrium syndrome (sx of cerebral edema due to H2O shifts after removal of plasma urea during dialysis, esp. in new HD Pts w/ ↑ ↑ BUN), high output HF

• Fever w/ catheter: empiric abx (vanc + AG qHD). GPC > GNR > mixed/fungal. Catheter removal, replacement, or “lock” abx. Consider metastatic infxn w/u (AJKD 2004;44:779).

Continuous veno-venous hemofiltration (CVVH) (NEJM 2012;367:26)

•  Physiology: hemofiltration rather than dialysis. Blood under pressure passes down one side of highly permeable membrane allowing H2O and solutes to pass across membrane via TMP gradient (convective clearance). Filtrate discarded. Replacement fluid infused (solute concentrations similar to plasma, except no K, urea, Cr, PO4). Fluid balance precisely controlled by adjusting filtrate/replacement fluid.

•  Access: double-lumen central venous catheter

•  Typical orders: volume goals, replacement fluid buffer: HCO3 (requires heparin to prevent machine from clotting) vs. citrate (hepatically metabolized to HCO3; provides anticoagulation w/ in machine via Ca chelation; ∴ requires Ca infusion)

•  Complications: hypotension, ↓ PO4, access complications; ↓ ICa (citrate toxicity in Pts with hepatic dysfunction → look for ↓ ICa but normal/ ↑ serum Ca and AG met acidosis)

•  Potential advantages over HD: less hypotension, better volume control, removal of inflammatory mediators; however, no survival advantage (Lancet 2006;368:379)

•  No advantage for high intensity CVVH over standard intensity (NEJM 2008;359:7)

Peritoneal dialysis (PD) (Perit Dial Int 2001;21:25)

•  Physiology: peritoneum acts as membrane. Fluid balance controlled by choosing dialysate [glc] (higher concentrations pull more fluid into peritoneum); longer dwell times pull less fluid as glc equilibrates across peritoneum

•  Access: permanent catheter inserted in OR

•  Typical orders for CAPD (continuous ambulatory peritoneal dialysis):

PD fluid = dextrose (1.5%, 2.5%, or 4.25%), buffer (lactate), Na+, Ca2+, Mg2+

infuse 10 min, dwell 90 min–5.5 h, drain 20 min

•  Can use overnight cycler device that infuses & drains more rapidly, with shorter dwells, while Pt sleeps. Called automated or continuous cycling peritoneal dialysis (APD, CCPD).

•   Complications: hypoalbuminemia; right-sided pleural effusion Peritonitis: abd pain, tenderness, cloudy drainage (WBC >100 and >50% PMNs) spectrum: 60–70% GPC, 15–20% GNR, remainder no bacteria or fungal Rx: abx IV or in PD, catheter removal for certain pathogens (eg, yeast, Pseudomonas) Hyperglycemia: exacerbated by inflammation, long dwell times, and higher [glc]

Kidney transplantation (NEJM 1994;331:365)

•  Rx of choice for ESRD; contraindic: active malig, infxn, ischemia, noncompl, subst abuse

•  Immunosuppression: calcineurin inhib (tacrolimus, CsA), antimetabolite (AZA, MMF), prednisone, ± mTOR inhibitor (sirolimus) (NEJM 2004;351:2715)

•  Late renal dysfxn: usual AKI causes + calcineurin tox, rejection, BK virus, recurrence of 1° disease; usual w/u + immunosupp levels, BK virus load, U/S, then bx if no other cause

•  ↑ risk of infxn (incl opportunistic such CMV, JC, BK viruses) & malignancy (incl PTLD)

•  ↑ CVD risk due to HTN (calcineurin inhib, RAS), DM & dyslipidemia (immunosupp meds)