Acute Kidney Disease

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a sudden and rapid decrease in renal function leading to electrolyte imbalances and accumulation of nitrogenous wastes

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acute kidney injury

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definition of acute kidney injury

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--abrupt increase of SCr of more than 50% over24-48 hrs
--increase of 1mg/dL in patient with pre-existing renal disease

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a classification prediction model for kidney injury using SCr/GFR and urine output

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RIFLE

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R in rifle

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RISK
increase SCr x1.5 or GFR decreases >25%

OU: <0.5ml/kg/hr x 6hrs

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I in rifle

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INJURY
increase SCr x 2 or GFR decreases >50%
OU: <.5ml x12hrs

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increase SCr x 3 or GFR decrease >75%
OU: < 0.3 x24hrs or anuria in 12hrs

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FAILURE (rifle)

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persistent AKI = complete kidney function loss >4weeks

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LOSS (rifle)

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end stage kidney disease

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ESKD (rifle)

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general risk factors for AKI

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-over 60 years old
-acute infection
-pre-existing Resp or Cardio disease
-chronic kidney disease
-dehydration, hypotension
-nephrotoxins(IV dyes, aminoglycosides, NSAIDS)

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3categories of AKI

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1. pre-renal
2. intrinsic
3. post-renal

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causes of Pre-renal AKI

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1. intravascular volume depletion (most common)
2. decrease cardiac output
3. decreased systemic vascular resistance
4. other hemodynamic changes

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what lab values are elevated in pre-renal AKI

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1. BUN
2. SCr
3. BUN: SCr (20:1)

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what is present in an urinalysis during pre-renal AKI

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1. dark color
2. elevated specific gravity
3. elevated urine osmolality
4. hyaline casts

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what kind of care is needed in pre- renal AKI

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supportive care

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3 drugs that cause drug-induced pre-renal AKI

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1. ACE inhibitors
2. angiotensin receptor blockers
3. NSAIDS

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mechanism of ACEinh and ARBs in drug induced prerenal aki

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1. dilate efferent--decrease glomerular perfusion pressure
2. decreases GFR

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mechanism of nsaids in drug induced prerenal aki

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1. inhibit prostaglandin dilation of afferent--decrease perfusion
2. decreases GFR

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types of kidney damage in intrinsic AKI (within the kidney)

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1. renal tubules (ATN)
2. glomerulus ( glomerulonephropathies)
3. interstitium (acute interstitial nephritis)
4. blood vessels (vascular damage)

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one of the most common causes of acute renal failure that is caused by cell death of the proximal tubule

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Acute Tubular Necrosis (ATN)

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what are the major causes of ATN?

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1. ischemia
2. nephrotoxins

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exogenous nephrotoxins that cause ischemia for ATN

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aminoglycosides, amphotericinB, vanco, acyclovir, cephalosporins

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endogenous nephrotoxin that cause ischemia for ATN

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uric acid, myoglobin, hemoglobin

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is ATN symptomatic or asymptomatic

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often asymptomatic

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what does the urinalysis show for acute tubular necrosis

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1. brown-dark color
2. brown, granular casts
3. renal tubule epithelial cells

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4 drugs that cause drug induced ATN

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1. aminoglycosides
2. amphotericin B
3. cisplatin
4. contrast media

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mechanism of aminoglycosides in drug induced ATN

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lysosomes burst and release drug into nephron

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mechanism of amphotericin B in drug induced ATN

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alters cell permeability and creates pores

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this is directly toxic to proximal tubule cells or vasoconstricts to reduce intrarenal perfusion causing drug induced ATN

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contrast media

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ways to manage drug induced acute tubular necrosis

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1. hydrate pre and.post admin
2. sodium bicarb
3. N-acetylcysteine (mucomyst)
4. renal vasodilators

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glomerulus is damaged an allows large proteins, blood, and charged molecules to pass

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glomerulonephritis

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causes for glomerulonephritis

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autoimmune disease, post-strep disease, diabetes, sickle cell, lithium

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what antibodies are tested in glomerulonephritis

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ANCA and complement

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nephrOtic syndrome

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systemic and non-inflammatory

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nephrItic syndrome

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inflammatory

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signs and lab findings for nephrotic syndrome

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edema, weight gain, fatigue, proeinuria >3.5g/day

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signs and lab findings for nephritic syndrome

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1. hematuria, HTN, proteinuria >1.5 to ~3g/day
2. pus in urine
3. cell and granular casts

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management approach to glomerulonephritis

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1. supportive
2. immunosuppressives

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interstitial tissue and surrounding tubules become inflamed due to hypersensitivity

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interstitial nephritis

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symptoms of interstitial nephritis

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fever, rash, arthralgias

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most common drugs that cause drug induced interstitial nephritis

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methicillin, penicillin, rifampin, cipro, sulfonamides, nsaids, valproic acid, PPI

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Blood smear showing eosinophils and urinalysis showing WBC, casts, and eosinophils

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Interstitial Nephritis

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Obstruction of urinary outflow, can lead to fluid accumulation and increased glomerular pressures

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Post-Renal AKI

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Causes of Post-Renal AKI

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BPH, kidney stones, urethral obstruction, cancer(bladder, pelvic, cervical), neurogenic bladder

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Medications that can cause Drug-Induced Postrenal Azotemia

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Anticholinergics, sulfonamides, allopurinol, foscarnet, acyclovir, methotrexate

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Poor hydration, higher doses, and longer treatment are risk factors for

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nephrolithiasis (kidney stones)

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Urinalysis has little to no proteinuria, high osmolality, low urine Na, and BUN:SCr >20:1

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Post renal AKI

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Post renal AKI can lead to intrinsic injury which can be seen in what lab values

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increase urine Na, FeNa5 increases

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This must be done to confirm an obstruction

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ultrasound

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most common measure of overall kidney function

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GFR

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FENa% =

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[(UNa/SNa) / (UCr/SCr)] x100

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FENa% >2%

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renal tubule damage; decreased reabsorption of Na

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FENa% <1%

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pre-renal dysfunction; increased Na reabsorption

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If patient is on Lasix, what must be done instead of FENa%

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FeUrea% =
[(UUN/BUN) / (UCr/SCr)] x 100

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Normal urine pH

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4.5-7.8

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Protein or albumin in urine

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protein: trace to none
Albumin: <30mg/day

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As GFR decreases, SCr

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increases

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Gold standard for measurement of renal function

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Golumerular Filtration Rate (GFR)

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Normal range of GFR

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90-140 mL/min

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What is the guide for drug dose adjustments in the presence of renal impairment

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Creatnine Clearance (CrCl)

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Factors affecting Serum Creatnine Concentration

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females(d), blacks(I), diet(vegetarian(d) or meat eater(I)), muscle, malnutrition, amputation, muscle wasting

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CrCl=(140-age)xBW) / SCrx72
(x0.85 if women)

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Cockcroft-Gault Equation

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Ideal Body Weight for men =

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50kg + or - 2.3

every inch above/below 60

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Ideal Body Weight for women =

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45.5kg + or - 2.3

every inch above/below 60

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Use Total Body Weight if:

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TBW < IBW

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Adjusted Body Weight =

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(0.4 x (TBW-IBW)) + IBW

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If patient is over 65 years old and has a SCr less than 1mg/dL

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use SCr of 0.8mg/dL

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some monitory parameters for patients with established AKI are:

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1. Fluid ins/outs, weight, vitals, electrolytes, drugs/regimens, nutrition, glucose