R - Cr <2x or oliguria for 6h; I - Cr >2x or oliguria for 12h; F - Cr >3x or oliguria for 24h or anuria for 12h, L - persistent AKI with loss of kidney function for more than 4w, ESRD is more than 3mo.
Hyaline casts are formed by Tamm Horsfall protein. ATN there is granular casts (tubuloepithelial casts). RBC casts or WBC casts suggests AIN.
Urinary indices only useful before intervention (saline), oliguria, and no CKD.
pre-renal really means "salt-avid physiology"
glomerular injury - NSAIDs, gold, penicillamine, captopril, pamidronate, IFN, ticlopidine, Plavix, OCP, gemcitabine, mitomycin C
tubulointerstitial injury - contrast, aminoglycosides, vancomycin, amphoB, pentamidine, cisplatin, tenofovir, bisphosphates, osmotic, b-lactams, quinolones, sulfa, PPI, allopurinol, diuretics
crystals - MTX, acyclovir, indinavir, atazanavir, sulfadiazine, TMP-SMX, acyclovir, uric acid
post - RP fibrosis from methydopa
HRS1 - acute, fulminant, with precipitating factor (LVP, diuresis, GIB, ETOH, hepatitis, infection)
HRS2 - insidious, smoldering
HRS - Cr > 1.5, GFR < 40, no shock, lack of improvement after stopping diuretics for 2d and with plasma expansion with 1g/kg albumin, no nephrotoxins, no proteinuria, no obstruction. Usually demonstrates Una < 10, olugria, hyponatremia.
HRS tx with liver transplant, vasoconstrictors +/- TIPS, vasoconstrictors (NE, octr, midodrine, vaso and terlipressin, albumin 1.5g/kg d1 and 1g/kg d3)
PICARD study suggested mortality may be worse with diuretics.
filtration is convective clearance of solutes
dialysis is the diffusive clearance of solutes
Less HD instability in patients on continuous modalities with MAP 5mmHg higher. No difference on mortality or renal recovery. Continuous modalities also had better fluid removal after a period of days. CVVH requires anticoagulation, different machines, and special training. SLED/EDD is very comparable to CVVH but also requires anticoagulation.
Vietnam study in NEJM 2002 showed that peritoneal dialysis in acute infection associated renal failure led to mortality rates of 47% compared to 15% with CRRT.
Palevksy NEJM 2008 and Belloma NEJM 2009 did not show a benefit to more dialysis. Schiffl NEJM 2002 showed improved survival in daily dialysis compared to every other day.
Effluent of 35cc/kg/hr is better than 20cc/kg/hr but not better than 45cc/kg/hr.
In small trials ACEi have been shown to be protective.
NS superior to oral hydration and superior to 1/2NS. Lasix is detrimental. However, stopping chronic lasix does not help protect the kidneys. Fenoldopam did not prevent CIN. Prophylactic hemodialysis worsened CIN.
Hypokalemia evaluate with TTKG.
TTKG = (urine K / urine osm) / (plasma K / plasma osm) = (urine K / urine osm) * ( plasma osm / plasma K)
TTKG > 2 then renal wasting AND if hypertensive then aldosterone and renin activity. If both renin AND aldosterone are high (ratio < 10) then suggests renal vascular HTN (diuretic driven, CHF, renin secreting tumors, secondary hyper aldo). Low aldo and low renin suggests exogenous steroids, licorice intake, Liddle/Geller.
JASN 2007 v18 recommends always treating Mg when treating hypoK.
TTKG > 6 then renal driven. ACE, spironolactone, bactrim (amiloride effect), BB, heparin, LMWH
moderate to severe frequently malignant (PTH-rp, bony involvement) or milk-alkali.
Tx is saline. Loop diuretics used sparingly. Steroids can be used in granulomatous disease. Calcitonin works well but rapid tachyphylaxis. Bisphophonates (zoledronic acid).
Calciphylaxis (lower extremity raised, violaceous lesions) and systemic calcinosis (hypoxia, bilateral infiltrates). Do not biopsy because they never heal. Keep CaPhoph product < 70. Corticosteroids and immunosuppressants should be avoided. Mortality is high usually due to sepsis.
Hypocalcemia can be a normal physiological hypoparathyroidism of sepsis. It should be replaced in seizures, tetany, or hemodynamic instability. Correct Mg.
HypoMg can be due to PPIs (depositing Mg into bone), amphB, aminoglycosides. Amiloride, triamterene, amiloride raise Mg levels.
FEMg < 4%
1) renal acid secretion problem (dRTA [1,4])
2) renal loss of HCO3 (pRTA )
3) extra-renal loss of HCO3 (diarrhea, pancreatobiliary fistula, ileal conduits)
4) increased generation of metabolic acid (lactate, ketoacid, cationic and sulfated aminoacids, toxins)
5) increased chloride (NaCl or dilutional)
NAGMA (increased chloride, low albumin, cationic paraproteinemia, hypoPO4, hyperCa, hyperMg, Li, hyperNa)
urine AG measures ammoniagenesis; Na + K - Cl < -30 is normal, <-50 when trying to acidify urine (alkalinize urine).
acidosis with + AG suggests RTA 1 or 4. RTA 4 has hyperkalemia; RTA 1 has hypokalemia and urinary pH > 5.5
RTA 2: proximal tubule has difficulty recovering HCO3; serum HCO3 12-20; can't alkalinize urine and acid secretion limited so urinary pH < 5.5
RTA 4: distal tubule is resistant to aldo or aldo deficiency; decreases Na/K anti-transporter resulting in hyperK and reduced ammoniagenesis resulting in acidosis
AGMA + OG = ethylene glycol (to glycolic oxalic, and hippuric acid), methanol (formic and lactic acid), ethanol, propylene glycol (L and D lactic acid), formaldehyde, and para-aldehyde.
OG but no acidosis = mannitol, glycine, sorbitol, maltone (IgG), isopropyl alcohol, pseudohyponatremia, IV contrast
meds to correct: NaCl, KCl, acetazolamide (worsens hypokalemia), spironolactone, amiloride
Met alkalosis with Ucl > 25 and no diuretic likely has Conn's