Presentation is loading. Please wait.

Presentation is loading. Please wait.

Aminoglycoside-Induced Acute Tubular Necrosis PHCL 442 Lab Discussion 2 Raniah Al-Jaizani M.Sc.

Similar presentations

Presentation on theme: "Aminoglycoside-Induced Acute Tubular Necrosis PHCL 442 Lab Discussion 2 Raniah Al-Jaizani M.Sc."— Presentation transcript:

1 Aminoglycoside-Induced Acute Tubular Necrosis PHCL 442 Lab Discussion 2 Raniah Al-Jaizani M.Sc

2 Classification of ARF New rise in SrCrPrerenalIntrarenal Glomerular Disease Acute Tubular Necrosis Interstitial Nephritis Post-renal

3 Classification of ARF Kidney

4 Glomerular & Tubular Functions

5 Aminoglycoside-Induced ATN Risk factors:  Patient related:  Elderly  Underlying renal disease  Dehydration  Hypotension/Shock syndrome  Hepatorenal synderome  Aminoglycoside related:  AGs choice: geniamicin> toberamycin> amikacin  Therapy > 3 days  Multiple daily dosing  Serum trough>2 mg/l

6 Aminoglycoside-Induced ATN Risk factors (cont.):  Concomitant therapy:  Furosemide, Ampho B, Vancomycin, and Cyclosporine.

7 Aminoglycoside-Induced ATN Mechanism 5% AGs actively reabsorbed by the proximal tubule cells bind to brush-border cells (tubule lumen) pinocytosis & enter interacellular space formation of myeloid bodies releasing large conc. Of AGs & lysosomal enzymes in to tubule lumen tubular destruction. Rank order of nephrotoxicity: Neomycin> gentamicin> toberamycin>amikacin>netilmicin> streptomycin

8 Aminoglycoside-Induced ATN Extended interval dosing vs. Regular dosing  One large daily AGs dose  Concentration-dependant killing activity  High peak conc. improve efficacy & undetectable trough conc. before next dose reduce toxicity  Less costly

9 To prevent aminoglycoside-induced nephrotoxicity inclinical practice:  Use aminoglycosides as an once daily dose rather than divided dose especially in high-riskindividuals.  Serial monitoring of renal function (serum creatinine) should be carried-out for early detection of nephrotoxicity.  Avoid combination of aminoglycosides with other potential nephrotoxins (amphotericin, cisplatin, diuretics, contrastmaterial, etc.).  During aminoglycoside therapy, ensure adequate hydration especially in the elderly.  Modify the dose according to GFR.  Avoid aminoglycosides in a patient with liver disease. 9

10 Amphotericin B-Induced Nephrotoxicity What is the mechanism of toxicity and how to overcome it? Assignments: Word processing Reference (s) Answered by


12 Diabetic nephropathy  Microvascular complication of diabetes resulting in albuminuria and progressive decline in kidney function.  The leading cause of ESRD ESRD = End Stage Renal Disease

13 DM & Kidney Disease 50% within 10 years >75% within 20 years ESRD in type I DM DM = Diabetes Mellitus ESRD = End Stage Renal Disease 13

14 DM & Diabetic Nephropathy Mechanisms leading to diabetic nephropathy BPGlucoseMale Protein intake AgeSmokingCholes. Hgb A1C BP = Blood Pressure 14

15 Natural History of Diabetic Nephropathy Onset of DM 02-5715>20 Hyperfiltration (functional changes) Stage 1 Silent phase (structural changes) Stage 2 Incipient nephropathy Stage 3 Overt nephropathy Stage 4 Onset of proteinuria ESRD Stage 5 Dialysis/ Transplant Time(yrs) 15

16 Diabetic Nephropathy & Albuminuria 16

17 Diabetic Nephropathy & Albuminuria Albuminuria is the earliest sign of kidney involvement in patients with DM It correlates with the rate of progression of kidney disease Type I DM >5 years test for albuminuria annually Type II DM test for albuminuria annually starting from time of diagnosis The presence of albuminuria indicates irreversible kidney damage 17

18 Management Goals Delay the need for dialysis therapy as long as possible Manage 2ry complications 18

19 Management Strategies Intensive glucose control Antihypertensive therapy Dietary protein restriction 19

20 Intensive Glucose Control  Glycemic control is indicated to reduce proteinuria & slow the rate of decline in GFR  The ADA recommended goals:  Pre-prandial plasma glucose = 90 – 130 mg/dl  Peak post-prandial plasma glucose < 180 mg/dl  Hgb A1C < 7% GFR = Glomerular Filtration Rate ADA = American Diabetes Association’s 20

21 Antihypertensive Therapy  Untreated HTN is associated with reduction in GFR  The control of BP has been shown to slow the progression of kidney disease and increase life expectancy in DM patients HTN = HyperTeNsion BP = Blood Pressure 21

22 Antihypertensive Therapy  To control BP ACEIs or ARBs are the preferred agents  They have been shown to reduce proteinuria & decrease rate of decline in GFR  They are used an all diabetic patients & microalbuminuria even if their BP is normal  BP goal in patients with DM & kidney disease is < 130/80 mm Hg ACEIs= Angiotensin Converting Enzyme Inhibitors ARBs = Angiotensin Receptor Blockers 22

23 Antihypertensive Therapy  At initiation of therapy ACEIs & ARBs can increase SrCr by up to 30% which is acceptable  They are not used in patients with bilateral renal artery stenosis  Monitor for hyperkalemia 23

24 Antihypertensive Therapy Non-dihydropyridine calcium channel blocker (diltiazem & verapamil) could be used in combination with ACEIs Diuretics can be used to control edema Other antihypertensive agents may be considered to control BP 24

25 Dietary Protein Restriction High protein intake can increase intraglomerular pressure thereby accelerating the progression of diabetic nephropathy Restrict protein intake to 0.6 – 0.8 g/kg/day 25

26 Patient Case M.R. is a 32 y.o African American female (Wt 63 kg; Ht 5’8”) with a 15 years history of type I Dm who present to the diabetes clinic with 1 week history of nausea, vomiting and general malaise. She has been noncompliant with regular appointments and her blood glucose>200mg/dl on prior evaluations, with Hg A1C 8% 2 month ago. Laboratory values: Na 143 mEq/l; K 5.3 mEq/l; Cl 106 mEq/l; SrCr2.9 mg/dl; BUN 63 mg/dl; and RBG 220 mg/dl; urinary albumin 700 mg/24 hr PE: Bp 155/102 mm Hg 26

27 Patient Case 1. What is the cause of M.R.’s advanced kidney disease? 2. How should M.R.’s kidney disease be managed? 27

28 Patient Case K 5.3 mEq/l; Cl 106 mEq/l; SrCr2.9 mg/dl; BUN 63 mg/dl; and RBG 220 mg/dl; Hg A1C 8% 28

Download ppt "Aminoglycoside-Induced Acute Tubular Necrosis PHCL 442 Lab Discussion 2 Raniah Al-Jaizani M.Sc."

Similar presentations

Ads by Google