1 / 153

NEPHROLOGY

NEPHROLOGY. ACUTE RENAL FAILURE. A cute renal failure (ARF) C ommunity-acquired Acute renal failure H ospital-acquired Acute renal failure ICU - acquired Acute renal failure M ultifocal insult to kidney. 2007 American college of clinical pharmacy (ACCP) . ACUTE RENAL FAILURE.

herve
Download Presentation

NEPHROLOGY

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. NEPHROLOGY

  2. ACUTE RENAL FAILURE Acute renal failure (ARF) Community-acquired Acute renal failure Hospital-acquired Acute renal failure ICU-acquired Acute renal failure Multifocal insult to kidney 2007 American college of clinical pharmacy (ACCP)

  3. ACUTE RENAL FAILURE Acute renal failure (ARF) Polycystic kidney disease 2007 American college of clinical pharmacy (ACCP)

  4. Acute renal failure (ARF) • ARF or AKI is an acute decrease in kidney function (GFR) over hours associated with an accumulation of nitrogen waste products and (usually) volume. 2007 American college of clinical pharmacy (ACCP)

  5. ARF • Dec. of ≥ 25% in GFR • Inc. in SCr ≥ 0.5 mg/dl (in patient with normal renal function ) • Inc. in SCr ≥ 1 mg/dl (in patient with chronic kidney disease) • Urine output less than 0.5 mL/kg/hour for more than 6 hours. *Fluid overload * Acid-base abnormalities • Inc. in BUN out of proportion to increases in the SCr.

  6. Urine output Classification:

  7. ACUTE RENAL FAILURE Community-acquired Acute renal failure Hospital-acquired Acute renal failure 2007 American college of clinical pharmacy (ACCP)

  8. 2- Community-acquired Acute renal failure • Low incidence (<1%) and high survival rate of 70%-95%. • Single insult to the kidney • Reversible 3- hospital-acquired Acute renal failure • Moderate incidence(2%-5%) • Moderate survival rate 30%-50%. • Single or multifocal insults to the kidney. • Reversible. 2007 American college of clinical pharmacy (ACCP)

  9. ACUTE RENAL FAILURE ICU-acquired Acute renal failure Multifocal insult to kidney 2007 American college of clinical pharmacy (ACCP)

  10. 4- ICU-acquired Acute renal failure • High incidence (6%-23%) • Low survival (10%-30%) 5-Multifocal insult to kidney Poorly reversible 2007 American college of clinical pharmacy (ACCP)

  11. Estimating glomerular filtration rate Formula for the Cockcroft-Gault equation: Estimated creatinine clearance, or GFR = [(140-Age) * Mass (in kg)] / [72 * Serum creatinine (in mg/dL)] x 0.85 if female

  12. Cockcroft-Gault equation • Difficult because commonly used equations (Cockcroft-Gault and MDRD) are not appropriate • Use in stable SCr • Brater and Jeliffeare probably more accurate than the Cockcroft-Gault in ARF

  13. Estimating glomerular filtration rate in ARF-cont’d GFR Calculator for Children Schwartz Formula GFR (mL/min/1.73 m2) = k (Height) / Serum Creatinine k = Constant o k = 0.33 in Preemie Infants o k = 0.45 in Term infants to 1 year old o k = 0.55 in Children to 13 years o k = 0.65 in Adolescent males (Not females because of the presumed increase in male muscle mass. The constant remains .55 for females.) Height in cm Serum Creatinine in mg/dl LOINC® Technical Brief

  14. Estimating glomerular filtration rate in ARF-cont’d Brater and Jeliffe equations more accurate than Cockroft-Gault equations but have not been vigorously validated in the literature. MDRD is not appropriate in ARF. 2007 American college of clinical pharmacy (ACCP)

  15. B-Jelliffe (mL/min/1.73 m 2) • Ess (males) = IBW x (29.3 -[0.203 x (age)])Ess (females) = IBW x (25.1 -[0.175 x (age)])Esscorr = Ess x [1.035 - 0.0377(Scr)] Scr  = If serum creatinine values are RISING, enter the most RECENT SCR.  If SCR values are declining enter the AVERAGE VALUE between the two SCR values. E = Esscorr - [4 x IBW x (Scr2-Scr1)] /  (Time difference in days) Scr2= latest serum creatinine.   Scr1= earlier serum creatinine.CrCl (ml/min/1.73 M2) = E / (14.4 x Scr)

  16. A-Brater(mL/min/70 kg) • CrCl =[293-2.03(age)] x [1.35-0.01685(SCr1+SCr2)] + 49(SCr1+SCr2) * 0.86 if F • (SCr1+SCr2) (SCr1+SCr2) ∆t day

  17. RISK FACTORS • Preexisting CKD (eGFR less than 60 mL/minute/1 .73m2) • Volume depletion—Vomiting, diarrhea, poor fluid intake, fever, diuretic use • Effective volume depletion – CHF, liver disease with ascites • Obstruction of the urinary tract

  18. RISK FACTORS • Use of nephrotoxic medications • Intravenous radiographic contrast • Aminoglycosides, amphotericin • NSAIDs and COX-2 inhibitors • ACEIs and ARBs • Cyclosporine and tacrolimus

  19. RISK FACTORS 2007 American college of clinical pharmacy (ACCP)

  20. CLASSIFCATION OF ARF 2007 American college of clinical pharmacy (ACCP)

  21. CLASSIFCATION OF ARF • Pre-renal (functional) • Renal (structural) • Post-renal (obstruction) 2007 American college of clinical pharmacy (ACCP)

  22. Pre-renal (functional) • Prerenal AKI • Initially, the kidney is undamaged • Characterized by hypoperfusion to the kidney • Systemic hypoperfusion: Hemorrhage, volume depletion, drugs, CHF • Isolated kidney hypoperfusion: Renal artery stenosis, emboli • Urinalysis will initially be normal (no sediment) but concentrated. • Physical examination: Hypotension, volume depletion

  23. Renal (structural) • Kidney is damaged. Damage can be linked to structure involved: Small blood vessels, glomeruli, renal tubules, and interstitium • Most common cause is ATN and others AIN, vasculitis, and acute glomerulonephritis • Urinalysis will reflect damage • Urine generally not concentrated • Physical examination: Normotensive, euvolemic, or hypervolemic; check for signs of allergic reactions or embolic phenomenon • History: Identifiable insult, drug use, infections

  24. Post-renal (obstruction) • Kidney is initially undamaged • Bladder outlet obstruction is the most common • Lower urinary tract obstruction may be caused by calculi • Ureteric obstructions cause by clots or intraluminal obstructions • Extrarenal compression cause postrenal disease • Increased intraluminal pressure upstream of the obstruction will result in damage if obstruction is not relieved • PE: Distended bladder, enlarged prostate • History: Trauma, benign prostatic hypertrophy, cancers

  25. Prevention of AKI • Avoid nephrotoxic drugs when possible. • Ensure adequate hydration. • Patient education

  26. Treatment and Management of Established AKIPrerenalazotemia: • Correct primary hemodynamics • Normal saline if volume depleted • Pressure management if needed • Blood products if needed

  27. Postrenalazotemia • Relieve obstruction. Early diagnosis is important. Consult urology and/or radiology

  28. Intrinsic: • No specific therapy universally effective • Eliminate the causative hemodynamic abnormality or toxin. • Avoid additional insults. • Fluid and electrolyte management. Prevent volume depletion or overload and electrolyte imbalance

  29. Medications used in AKI • Fenoldopam and Atrialnatriuretic peptide : May reduce need for renal replacement therapy (RRT) and in-hospital mortality • Loop diuretics: Consider loop diuretics for patients who are • Oliguric , euvolemic or hypervolemic. • Diuretic does not reduce mortality or improve renal recovery but may assist in fluid/ electrolyte management. • Given intravenously at relatively high doses • Low-dose dopamine. Ineffective. Avoid

  30. Dialysis (RRT) • Renal replacement therapy—Indications • BUN greater than 100 • Volume overload unresponsive to diuretics • Uremia or encephalopathy • Life-threatening electrolyte imbalance e. Refractory acidosis

  31. Prevention of ARF • Avoid nephrotoxic drugs. • Hydration : 0.9% NACL. • Pt. education • *Tight glycemic control 80-110 mg/dl using insulin (reduce ARF by 41%) Also reduce infection, days on mechanical ventilation and ICU length of stay. 2007 American college of clinical pharmacy (ACCP)

  32. Treatment and management of Established ARF A-Fluid management - Maintain renal perfusion & production of urine - Diuretic therapy: (consider of Pt. who are oliguric and euvolemic, or hypervolemic) B. Loop diuretic: bumetanide-furosemide-torsemide –ethacrynic acid Parenteral therapy • Furosemide intermittent therapy:40-80 mg IV q 6-8 hrs • Furosemide continous inf.: 40-80 mg IV bolus, then 10- 20 mg /hr • Other diuretics:Thiazide - Metolazone - Mannitol 2007 American college of clinical pharmacy (ACCP)

  33. Treatment and management of Established ARF Acidosis Restrict dietary protein (< 0.5 g/kg/day of high quality protein Sodium bicarbonate to maintain bicarbonate (HCO3 ) > 15 meq /L and arterial P 7.2 Dialysis Electrolyte and nutrition abnormalities 2007 American college of clinical pharmacy (ACCP)

  34. Renal Damage 2007 American college of clinical pharmacy (ACCP)

  35. DRUG-INDUCED KIDNEY DAMAGE • Drugs are responsible for kidney damage through many mechanisms • Evaluate potential drug-induced nephropathy based on the period of ingestion, patient risk factors, and the propensity of the suspected agent to cause kidney damage

  36. Renal Damage • Idiosyncratic reaction: not predictable • Predictable reactions : High dose • Risk factors • Epidemiology • Kidney at risk • Pseudo drug – induced nephropathy 2007 American college of clinical pharmacy (ACCP)

  37. Renal Damage Cont’d Predictable reactions – based PK and Pt. risk factors • -Hypoperfusion/ischemia • -Inflammation • -Direct cellular damage Risk factors • -Prior history of CKD • -Increased age 2007 American college of clinical pharmacy (ACCP)

  38. Epidemiology • 7% of all drug toxicities • 18%–27% of AKI in hospitals • 1%–5% of NSAID users in community • Most implicated medications: • Aminoglycosides • NSAIDs, ACEIs • Contrast dye • Amphotericin

  39. Why kidney at risk • High exposure to toxin: Kidney receives 20%–25% cardiac output • High intrarenal drug metabolism • Tubular transport processes • Concentration of solutes (i.e., toxins) in tubules • High-energy requirements of tubule epithelial cells • Urine acidification

  40. Pseudo drug- induced nephropathy • Drugs that inhibit Cr tubular secretion: Triamterene; cimetidine • Drugs that increase BUN: Corticosteroids; tetracycline • Drugs that interfere with Cr assay: Cefoxitin and other cephalosporins

  41. Acute Tubular Necrosis • Most common drug-induced kidney disease in the inpatient setting

  42. Acute Tubular Necrosis(ATN) 1-Aminoglycoside nephrotoxicity (1.7 % - 58 % ) 2007 American college of clinical pharmacy (ACCP)

  43. Acute Tubular Necrosis(ATN) 1-Aminoglycoside nephrotoxicity 2007 American college of clinical pharmacy (ACCP)

  44. Acute Tubular Necrosis(ATN) • 2. Radiographic contrast media nephrotoxicity (IV contrast) • 3rd leading cause of inpatient ARF • 2 % - 50 % (incidence) • * Hospital mortality rate 34 % • Radiographic contrast media nephrotoxicity • Consists of • Iso-osmolar (300 mOsm/kg) • low-osmolar (780–800 mOsm/kg) • high-osmolar (more than 1000 mOsm/kg) agents • Also categorized as ionic versus nonionic 2007 American college of clinical pharmacy (ACCP)

  45. Acute Tubular Necrosis(ATN) 2. Radiographic contrast media nephrotoxicity (IV contrast) 2007 American college of clinical pharmacy (ACCP)

  46. Acute Tubular Necrosis(ATN) 2007 American college of clinical pharmacy (ACCP)

  47. Acute Tubular Necrosis(ATN) 2007 American college of clinical pharmacy (ACCP)

  48. Acute Tubular Necrosis(ATN) 2-Radiographic contrast media nephrotoxicity (IV contrast)

More Related