PPF 532: RENAL DISORDERS

DR. GITAU CHEGE

Gitau S. Chege ( PhD)

Acute renal Failure
 KEY CONCEPTS
▪ A common complication in the hospitalized patient and is
associated with a high mortality rate

▪ Categorized based on the anatomic area of injury or malfunction:

▪ Prerenal - decreased renal blood flow

▪ Intrinsic - a structure within the kidney is damaged

▪ Postrenal - an obstruction is present within the urine collection system

▪Risk factors include advanced age, acute infection, preexisting

chronic respiratory or cardiovascular disease, dehydration, and
CKD
 KEY CONCEPTS
▪ ACF lacks a specific & sensitive sign to herald its onset
▪ hence a thorough patient history, physical examination, &
laboratory assessment of serum & urine are necessary

▪ Prevention is key; there are very few therapeutic options for the
therapeutic management of established ARF

▪ Supportive management remains the primary approach to prevent or

reduce the complications
▪ Renal replacement therapies (RRTs), nutritional support,
avoidance of nephrotoxins, blood pressure & fluid
management
 KEY CONCEPTS

▪ Patients with prolonged or severe ARF, RRTs are the cornerstone of

support
▪ Facilitate an aggressive approach to fluid, electrolyte & & waste
management

▪ Diuretic resistance is a common phenomenon in the patient with

ARF

▪ Aggressive sodium restriction, combination diuretic therapy, or

a continuous infusion of a loop diuretic
 KEY CONCEPTS

▪ Drug-dosing regimens for ARF patients receiving intermittent

hemodialysis (IHD) are predominantly extrapolated from data
derived from CKD patients

▪ Drug dosing guidelines for ARF patients receiving continuous renal

replacement therapies (CRRTs) are poorly characterized

▪ Individualized doses may need to be determined by estimating the

clearance of medications associated with a high risk of toxicity by the
patient and the CRRT procedure
 INTRODUCTION

▪ Development of ARF presents a difficult challenge to the

clinician because there are many possible etiology & the
onset is often asymptomatic

▪ Ambulatory setting, patients may not notice ARF symptoms for

days to weeks

▪The mortality rates of ARF of up to 60% have been reported in

hospitalized patients
 DEFINITION

▪ A Sudden & dramatic decrease in GFR (occurs over hours/days,

sometimes over weeks)，resulting in an increase in the plasma
concentration of waste products urea (BUN) & creatinine, uric
acid, phosphate, sulfates.

▪ This relatively abrupt decline in renal function is in contrast to

CKD, which is defined by the presence of proteinuria/
albuminuria for at least 3 months, in combination with a GFR of <
90 mL/min/1.73 m2
RIFLE
 DEFINITION

▪ A decrease in urine output is often observed, but is not

required for ARF to be present

▪ Compared to a normal urine output of ≥1,200 mL/day, patients

with ARF are often categorized as being
i. Anuric (urine output < 50 mL/day)

ii. Oliguric (urine output < 500mL/day)

iii. Non-oliguric (urine output > 500 mL/day)

 Etiology and Classification
①Prerenal（Results from
hypoperfusion of the renal parenchyma,
with or without systemic arterial
hypotension ( see table)
Blood Kidney
② Intrinsic (Direct damage to the kidneys), e.g.
flow
kidney diseases (Glomerulonephritis,
pyelonephritis ), interstitium, acute tubular necrosis,
ATN ( ischemia and reperfusion injury, renal
Ureter Ureter
poisons, or reduced blood supply).

③Postrenal
Acute obstruction that affects the normal flow
of urine out of both kidneys enlarged prostate, Bladder
kidney stones, bladder tumor or injury.
Drugs & AKI
 Risk Factors For The Development Of AKI
6. Underlying cardiovascular
1. Older age
disease
2. Higher baseline SCr
7. Prior heart surgery
3. Underlying CKD
8. Dehydration resulting in
4. Diabetes
oliguria
5. Chronic respiratory illness
9. Acute infection

10. Exposure to nephrotoxins.

 DIAGNOSTIC WORK UP

Approach to a patient with AKI

 CAREFUL HISTORY IS ESSENTIAL
▪Exposure to nephrotoxins & drugs
▪Anuria may indicate post-renal causes
▪ Skin rashes may indicate allergic nephritis
▪ Evidences of volume depletion: diarrhea, bleeding
▪ Pelvic & per-rectal examination: look for evidence of abortion
▪ Ischemia or trauma to the legs or arms may indicate rhabdomyolysis
▪A history of prostatic disease, nephrolithiasis
▪ Recent surgical or radiologic procedures
▪ Past & present use of medications
▪ Family history of renal diseases
 CLINICAL
PRESENTATION
▪ Highly variable, depending on the
etiology (see the table)

▪ 1st step is to determine if the renal

complication is acute, chronic, or
the result of an acute change in a
patient with known CKD
Patient Assessment
An exhaustive review
convectional,
complementary, &
alternative medications,
should be completed.
Special attention:
diuretics, NSAIDs,
antihypertensives,
recent contrast dye
exposure
Patient Assessment
 Blood Tests
▪ Blood urea nitrogen (BUN) & Serum createnine concen
▪ BUN:SCr ratio can delineate prerenal causes from intrinsic
& postrenal causes
▪Urea reabsorption is inversely proportional to the urine flow
rate
▪Thus normal steady-state BUN:SCr ratio is ≈ 10:1.
▪ In prerenal conditions, the BUN:SCr ratio is greater than 20:1
because sodium & water are actively reabsorbed in the renal
tubules to expand the effective circulating volume
 Blood Tests
✓ Urea, an ineffective osmole, is reabsorbed as a result of increased
water reabsorption, whereas creatinine is not reabsorbed
• Presence of hypercalcemia or hyperuricemia can indicate a hematologic
malignancy.
• Tumor lysis syndrome is a condition that occurs in patients with leukemia
after chemotherapy induction
• Increased level of creatine kinase or myoglobin in the face of AKI usually
indicates rhabdomyolysis.
• Eosinophilia may suggest acute allergic interstitial nephritis from drug
exposure.
• High levels of circulating immune complexes in the presence of AKI
suggest glomerulopathies
 Urinalysis
• Presence of highly concentrated urine, as determined by elevated
urine osmolality & specific gravity, suggests prerenal azotemia
• Presence of proteinuria or hematuria can indicate glomerular
damage
• Nephrotic syndrome is characterized by urinary protein losses
greater than 3.5 g/1.73 m2/day
• Proteinuria can also result from tubular damage; that protein loss is
rarely over 2 g/day, however
• Microscopic examination of the urine provides helpful clues for
determining the source of AKI (see table next slide)
1. URINALYSIS: MICROSCOPIC EVALUATION OF
URINARY SEDIMENT
 Urinalysis: Microscopic Evaluation
of Urinary Sediment
• Presence of few formed elements or hyaline casts is
suggestive of prerenal or postrenal azotemia.
• Many RBCs may suggest calculi, trauma, infection or tumor
• Eosinophilia : Occurs in 95% of patients with acute allergic
nephritis
• Brownish pigmented cellular casts & many renal epithelia cells
are seen in patients with acute tubular necrosis (ATN)
• Pigmented casts without erythrocytes in the sediment from
urine but with positive dipstick for occult blood indicates
hemoglobinuria or myoglobinuria
 Urinalysis: Microscopic Evaluation
of Urinary Sediment
Dipstick test:
 Trace or no proteinuria with pre-renal and post-renal AKI;

 Mild to moderate proteinuria with ATN

 Moderate to severe proteinuria with glomerular diseases.

 RBCs & RBC casts in glomerular diseases

 Crystals, RBCs & WBCs in post-renal ARF.

 Radiography/Imaging

Ultrasonography: Helps to see..

 the presence of two kidneys, for evaluating kidney size &
shape, & for detecting hydronephrosis or hydroureter.

 renal calculi, & renal vein thrombosis.

Retrograde pyelography: is done when obstructive uropathy is

suspected
 Complications of AKI
Intravascular overload:
Weight gain, hypertension, elevated central venous pressure
(raise JVP), Pulmonary edema
Electrolyte disturbance
 Hyperkalemia: (serum K+ > 5.5 mEq/L): decreased renal
excretion combined with tissue necrosis or hemolysis.
 Hyponatremia : (serum Na+ concentration < 135 mEq/L ):
excessive water intake in the face of excretory failure
 Complications of AKI
Electrolyte Disturbance
 Hyperphosphatemia : (serum Phosphate concentration of >
5.5 mg /dl ) failure of excretion or tissue necrosis

 Hypocalcemia : (serum Ca++ < 8.5 mg/dl ) results from

decreased active Vit-D, hyperphosphatemia, or
hypoalbuminemia

 Hypercalcemia: (serum Ca++ > 10.5 mg /dl) may occur during

the recovery phase following rhabdomyolysis induced acute
renal failure.
 Complications of AKI
Metabolic acidosis :(arterial blood PH < 7.35 ) is associated
with sepsis or severe heart failure

Hyperuricemia: due to decreased uric acid excretion

Bleeding tendency : may occur due to platelet dysfunction &

coagulopathy associated with sepsis

Seizure: may occur related to uremia

 Clinical Example 2
A 52-year-old woman has been referred to Cancer care center for staging and
treatment of newly diagnosed cancer of the bladder. Her past health has been
good and she is taking no medications. Her initial physical examination is
entirely normal except for the presence of a fungating lesion of the bladder.
Laboratory studies reveal a BUN of 25 mg/dl and a serum creatinine level of 1.4
mg/dl.

Her family bring her into the emergency room because of weakness, nausea,
vomiting and a decrease in mental alertness. BP 152/88, 1+edema in the lower
legs；50 cc urine/day；Urine creatinine 133mg/dl; serum creatinine 10.6mg.dl;
BUN 142 mg/dl; the electrocardiogram shows tall peaked T-waves.
Ultrasonography reveals two kidneys and a suggestion of hydronephrosis
bilaterally.
• What is the diagnosis of the disease?
• Point out the manifestations.
• Explain the mechanism of manifestations.
PREVENTION AND
TREATMENT
Acute Renal Failure
 INTRODUCTION
▪ Outcome of established ARF is dismal, prevention is critical
▪ ARF due to decreased perfusion secondary to abdominal
surgery, coronary bypass surgery, acute blood loss in trauma,
and uric acid nephropathy
▪ Goals of treatment
▪ Prevent ARF
▪ Avoid or minimize further renal insults that would worsen the
existing injury or delay recovery
▪ Provide supportive measures until kidney function returns.
 GENERAL APPROACH TO PREVENTION
▪ Dependent on the setting the patient is in

▪ Guidance regarding their optimal daily fluid intake ≈ 2 L/day)

to avoid dehydration

▪ Evaluate fluid balance

▪( e.g., acute changes in weight) in patient on chemotherapy or uric acid
nephropathy,

▪ Dietary restrictions in nephrolithiasis patients.

▪ Proper care and monitoring patient with a Foley catheter, to

ensure that post-obstructive ARF does not develop
 NONPHARMACOLOGIC THERAPIES

▪ Hydration

▪ Many situations in which administration of a nephrotoxin can’t

be avoided

▪ Radiocontrast dye

▪ Antibiotics & other drugs

▪Adequate hydration and sodium loading (normal saline was

superior in preventing ARF) .

▪Dose: 1 mL/kg per hour beginning the morning that the

radiocontrast dye was going to be given
 NONPHARMACOLOGIC THERAPIES
Preventive Dialysis
▪ Novel approach to reducing the incidence of radiocontrast
dye nephrotoxicity

▪ Patient at high risk of ARF provided with RRT

prophylactically.

▪ Hemofiltration initiated prior to and continued for 24 hours

PHARMACOLOGIC THERAPIES
Dopamine and Diuretics
 Low doses of dopamine (≤2 mcg/kg/min) increase renal blood
flow & might be expected to increase GFR. This might flush
out nephrotoxins from the tubules

 loop diuretics may decrease tubular oxygen consumption by

reducing solute reabsorption

 A blinded controlled trial of (dopamine + Furosemide at 0.5

mcg/kg/min+ 0.9% NaCl ) proved beneficial
PHARMACOLOGIC THERAPIES
Fenoldopam mesylate

 A selective dopamine A1 receptor agonist that increases

blood flow to the renal cortex

 Prevent the development of ARF in many settings including

contrast dye induced nephropathy (CIN)

 Originally approved for use as an IV antihypertensive agent

 Later randomized controlled trials (RCT) showed that it’s a

viable in prevention of ARF in some clinical settings.
PHARMACOLOGIC THERAPIES
N-Acetylcysteine

 Thiol-containing antioxidant that reduce the risk of developing

CIN in patients with pre-existing kidney disease

 Should be given to all patients at risk for CIN

 600 mg P.O. 12 hourly for 4 doses with the 1st dose

administered prior to contrast exposure

Theophylline

 Reduce the incidence of CIN (comparable to NAC)

PHARMACOLOGIC THERAPIES
Glycemic Control

▪Tight blood glucose resulted in significant improvements in

mortality ( 41%)

▪standard control (<200 mg/dL) or intensive glucose control

measures (goal blood glucose concentrations of 80 to 110
mg/dL)
 MANAGEMENT

Established Acute Renal Failure

GENERAL APPROACH TO TREATMENT
▪ Short-term goals : minimizing the degree of insult to the
kidney, reduce extrarenal complications, & expedite the
patient’s recovery of renal function.
▪ Ultimate goal: Restore the patient’s renal function to their
pre-ARF baseline.
▪ Prerenal sources of ARF should be managed with
hemodynamic support and volume replacement.
▪ Immune related etiology (interstitial nephritis or
glomerulonephritis) : immunosuppressive therapy
▪ ARF with other clinical conditions (cardiac & liver failure)
are associated with higher mortality
▪ NB: Supportive care is the mainstay of ARF management
regardless of etiology
 NONPHARMACOLOGIC
▪ Removal of medications associated with diminished renal blood
flow or the physical removal of a prerenal obstruction
▪ Fluid replacement therapy
▪ Moderately volume-depleted ( oral rehydration)
▪ IV therapy: 250 - 500 mL of normal saline over 15 - 30 min.
▪ 1 - 2 L is usually adequate, unless diabetic keto acidosis
(DKA) or hyperosmolar hyperglycemic states patients who
have 10% -15% total-body water deficit

▪ Monitor patient for pulmonary edema, peripheral edema, adequate BP

(diastolic blood pressure > 60 mm Hg), normoglycemia & electrolyte
balance

▪ Septic patient may require up to 10 L due to vascular capacitance and

fluid leakage
 NONPHARMACOLOGIC
▪ Urine output:
▪ Patients with ARF on top of preexisting CKD should not be expected to
produce urine beyond their preexisting baseline

▪ Anuria or oliguria patient need a lower rehydration, such as 250-mL

boluses or 100 mL/h infusions of normal saline

▪ Prerenal ARF due to blood loss/symptomatic anemia

▪ Red blood cell (hematocrit no higher than 30% )transfusion is Rx of
choice.

▪ Albumin (sometimes in patient resistant to crystalloid therapy): severe

hypoalbuminemia (e.g., liver disease, nephritic syndrome)

▪ Intrinsic or post-obstructive ARF involve fluid and electrolyte management.

RENAL REPLACEMENT THERAPIES
▪ Administered either intermittently or continuously
 INTERMITTENT HEMODIALYSIS (IHD)
▪ Last 3 to 4 hours with blood flow rates to the dialyzer typically
ranging from 200 to 400 mL/min

▪ Most frequently used & has several advantages

1. Machines are readily available

2. Rapid removal of volume and solute

3. Rapid correction of most of the electrolyte abnormalities

associated with ARF.
 INTERMITTENT HEMODIALYSIS (IHD)
▪ Stage 5 CKD patient achieve adequate solute & volume
control with thrice-weekly dialysis
▪ but hypercatabolic, fluid-overloaded patients with ARF
may require daily hemodialysis treatments

▪Primary disadvantage
1. hypotension, due to rapid removal of intravascular
volume over a short period of time.

2. Venous access difficult in hypotensive patient (reduce

effectiveness)
 Continuous Renal
Replacement Therapies
 INTRODUCTION

▪ Several CRRT variants;

i. continuous venovenous hemofiltration (CVVH)
ii. continuous venovenous hemodialysis (CVVHD)
iii. continuous venovenous hemodiafiltration (CVVHDF)
▪ Differ in the degree of solute & fluid clearance that can be
clinically achieved as a result of the use of diffusion,
convection, or both
▪ Although solute removal is slower, a greater amount can
be removed over a 24-hour period compared to IHD
▪ The ultrafiltration rate is an important determinant of the
effectiveness of all three forms of CRRT
CONTINUOUS VENOVENOUS
HEMOFILTRATION (CVVH)

• Excess body water and accumulated

endogenous waste products are
removed solely by convection
(passive diffusion)
• Blood =in red
• Hemofilter/ dialyzer membrane = yellow
• ultrafiltration/dialysate compartment = brown.
CONTINUOUS VENOVENOUS
HEMODIALYSIS (CVVHD)

• Waste removal is via passive

diffusion from the blood where
they are in high concentration
to the dialysate
 CONTINUOUS VENOVENOUS
HEMODIALYSIS (CVVHD)
▪ Provides extensive solute removal primarily by diffusion,
where solute molecules at a higher concentration (plasma)
pass through the dialysis membrane to a lower
concentration (dialysate)
▪ Since dialysate flows in a countercurrent direction to the
plasma flow, concentration gradient is maximized
▪ Advantages
▪ lower incidence of clotting than CVVH because of reduced
hemo-concentration as there is less fluid removal during
the process.
CONTINUOUS VENOVENOUS
HEMODIAFILTRATION (CVVHD

• Combines both hemofiltration &

hemodialysis, achieving even higher
solute and fluid removal rates
• Associated with the highest
clearance of drugs and waste
products
EXTENDED DURATION HEMODIALYSIS
“SLEDD

• employs lower blood and dialysate flow

rates that IHD, but due to its extended
duration it is a gentler means of
achieving adequate waste product and
fluid removal.
 CRRT
Ultrafiltration rate
▪ Important determinant of the effectiveness of all three
forms of CRRT
▪ Removal rate of 35 mL/kg/h is associated with improved
survival.
Replacement fluids:
▪ Infused either just before or after the dialyzer/hemofilter
Thrombosis
▪ Significant concern with CRRT due to reduced blood flow
rates ( compared to IHD)
▪ Thus anticoagulation therapy indicated
▪ unfractionated heparin or low-molecular-weight heparin
( direct thrombin inhibitor,) or citrate solution
 CRRT
Thrombosis
▪ Infusing fluids after the hemofilter can result in
hemoconcentration within the filter ( ↑thrombosis)
▪ Replacing fluids before the filter reduces thrombosis risk,
but also reduces solute clearance
Disadvantages
▪ Hospitals lack special equipment necessary
▪ intensive nursing care around the clock ( more expensive)
▪ very little known about drug-dosing
 IHD COMPARED TO CRRT
CRRT IHD
??????
CVVH : drug removed by
convection//ultrafiltration.
Effiicent for small agents
(<15,000 daltons) &
unbound in the plasma.
clearance of a drug is
function of the membrane
permeability( sieving
coefficient)
CVVHDF: clearance is a
combination of both diffusion
& convection.
 PHARMACOLOGIC
NB: NO pharmacologic approach to reverse the decline or
accelerate the recovery of renal function has been proven to
be clinically useful, e.g., thyroxine, dopamine or loop diuretics
loop diuretics
▪ Furosemide, bumetanide & torsemide.
▪ Ethacrynic acid in patient allergic to sulphur
▪ Only indication is fluid-overloaded patients who make
adequate urine in response to diuretics
▪ or in prevention of pulmonary edema rather than invasive
RRT
▪ Furosemide 40 - 80 mg IV is most commonly used due
lower cost, availability in oral and parenteral forms, and
reasonable safety and efficacy profiles
 PHARMACOLOGIC
▪ Torsemide and bumetanide have better oral bioavailability
than furosemide
Mannitol (20%) 12.5 - 25 g IV
▪ an alternative to diuretics, however, in anuric or oliguric
patients, it may lead to hyperosmolar state
Diuretic Resistance
▪ Inability to respond to administered diuretics
▪ Common in ARF and is associated with a poor patient
outcome
DIURETIC
RESISTANCE
 DIALYSIS
½ of patients with CRF eventually require dialysis

Diffuse harmful waste out of body

Control BP

Keep safe level of chemicals in body

2 types
 Hemodialysis

 Peritoneal dialysis
 HEMODIALYSIS: INDICATIONS
1. Uremia - azotemia with symptoms and/or signs

2. Severe Hyperkalemia

3. Volume Overload - usually with congestive heart failure (pulmonary

edema)

4. Toxin Removal - ethylene glycol poisoning, theophylline overdose,

etc.

An arterio-venous fistula in the arm is created surgically

Catheters are inserted into the fistula for blood flow to dialysis machine
 HEMODIALYSIS
3-4 times a week

Takes 2 - 4 hours

Machine filters blood & returns it to

body
 HEMODIALYSIS: PROCEDURE
1. Procedure for Chronic Hemodialysis

a. Blood is run through a semi-permeable filter membrane bathed in

dialysate

b. Composition of the dialysate is altered to adjust electrolyte parameters

c. Electrolytes and some toxins pass through filter

d. By controlling flow rates (pressures), patient's intravascular volume

can be reduced

e. Most chronic hemodialysis patients receive 3 hours dialysis 3 days per

week
 HEMODIALYSIS: EFFICACY

Some acids, BUN & creatinine are reduced

Phosphate is dialyzed, but quickly released from bone

Very effective at reducing intravascular volume/potassium

Once dialysis is initiated, kidney function is often reduced

Not all uremic toxins are removed & patients generally do not feel "normal"

Response of anemia to erythropoietin is often suboptimal with hemodialysis

 CHRONIC HEMODIALYSIS
MEDICATIONS

Anti-hypertensives - labetolol, CCB, ACE inhibitors

Eythropoietin (Epogen®) for anemia in ~80% dialysis pts

Vitamin D Analogs - calcitriol given intravenously

Calcium carbonate or acetate to decrease phosphate & PTH

RenaGel, a non-adsorbed phosphate binder, is being developed for

hyperphosphatemia

DDAVP may be effective for patients with symptomatic platelet problems

 TYPES OF ACCESS
Temporary site

AV fistula
 Surgeon constructs by combining an artery and a vein

 3 to 6 months to mature

AV graft
 Man-made tube inserted by a surgeon to connect artery and vein

 2 to 6 weeks to mature
TEMPORARY CATHETER
AV FISTULA & GRAFT
 CHRONIC RENAL
FAILURE
Long-Term Management
 Renal Dialysis
 Hemodialysis
 Common complications
WHAT THIS MEANS?

No BP on same arm as fistula

Protect arm from injury

Control obvious hemorrhage

 Bleeding will be arterial

 Maintain direct pressure

No IV on same arm as fistula

A thrill will be felt – this is normal

ACCESS PROBLEMS

AV graft thrombosis

AV fistula or graft bleeding

AV graft infection

Steal Phenomenon
 Early post-op

 Ischemic distally

 Apply small amount of pressure to reverse symptoms

PERITONEAL DIALYSIS
Abdominal lining filters blood
3 types
 Continuous ambulatory
 Continuous cyclical
 Intermittent
CONSIDERATIONS

Make sure the dressing remains intact

Do not push or pull on the catheter

Do not disconnect any of the catheters

Always transport the patient and bags/catheters as one

piece

Never inject anything into catheter

 PHARMACOLOGIC
(DIURETIC RESISTANCE)
Causes
▪ Reduced number of functioning nephrons
▪ Heavy proteinuria ( in glomerulonephritis), diuretic bound
to these proteins
▪ intestinal edema,

Management
▪ Overcome resistance is to administer via continuous
infusions instead of intermittent boluses
▪ combinations with diuretics ( loop diuretics + diuretic from
a different pharmacologic class
E.g., oral metolazone + furosemide or mannitol plus intravenous
loop diuretics
 PHARMACOLOGIC
(ELECTROLYTE MANAGEMENT)
▪ Hypernatremia & fluid retention are frequent
complications
▪ sodium intake restricted: No more than 3 g from all sources ( IV &
enteral intake
▪ NB: intravenous antibiotics are major source of sodium
1 L of 0.9% NaCl 154 mEq (3.5 g)
IV metronidazole ( usual dose ) 1.3 g
IV Ampicillin 800 mg
piperacillin 700 mg
Fluconazole 500 mg

▪ In in continuous and intermittent RRTs, hyponatremia

does not develop since isonatremic (135 to 140 mEq/L)
dialysate or ultrafiltrate replacement solution
▪ Should be monitored daily
 PHARMACOLOGIC
(ELECTROLYTE MANAGEMENT)
Hyperkalemia, hyperphosphatemia & hypermagnesemia
(lesser extent) frequently encountered
▪ Hyperkalemia (90% renally eliminated)
▪ Most common electrolyte disorder
▪ > 6 mmol/L : Life-threatening cardiac arrhythmias
▪ K restriction is essential
▪ monitored at least daily & twice daily for those who are
seriously ill
▪ Metabolic acidosis: result in increased ECF K
▪ ubiquitous presence in foods & medication
▪ Medication : alkalinizers (Polycitra
 PHARMACOLOGIC
(ELECTROLYTE MANAGEMENT)
▪ Phosphorous & magnesium also require monitoring
▪ Not removed efficiently by dialysis
▪ Early stages of ARF, hyperphosphatemia might be more
common than hypophosphatemia
▪ Significant amount of P released from tissue destruction
(e.g., trauma, rhabdomyolysis, tumor lysis syndrome)
▪ Treatment of hyperphosphatemic state include CRRT
▪ Calcium-containing antacids should be avoided : precipitate
calcium phosphate in the soft tissues
 PHARMACOLOGIC
(NUTRITIONAL INTERVENTIONS)
▪ Baseline nutritional status is a strong predictor of outcomes
in patients with ARF
✓ provision of enteral nutrition in ARF patient in intensive care units is
associated with an improvement in outcomes
✓ Parenteral nutrition has not demonstrated same benefits
Protein
▪ NB: Since fluid intake is restricted ( due to volume overload)
design and provision of adequate parenteral or enteral
nutrition are problematic
▪ Septic patients with ARF are usually are hypercatabolic
✓ Patient can not tolerate amount of fluid required to replace
the protein
✓ protein intake up to 2.5 g/kg/day required
 PHARMACOLOGIC
(NUTRITIONAL INTERVENTIONS)
Heat
▪ Heat lost during CRRT & room-temperature (RT) IV
ultrafiltrate replacement solutions resulting in an energy loss
of 800 kcal/day (warming solutions)
DRUG-DOSING CONSIDERATIONS
▪ Optimization of drug therapy is difficult
▪ Variables influencing responses include;
i. patient’s residual drug clearance
ii. Accumulation of fluids (alter VD)
iii. Delivery of CRRT or IHD ( alter drug clearance)
▪ TDM esp. renally eliminated drugs (>30% excreted
unchanged in the urine) & narrow therapeutic range drugs
▪ If normal hepatic function: Choose agent eliminated by liver
 EVALUATION
OF
THERAPEUTIC
OUTCOMES
VIGILANT
MONITORING
 EVALUATION OF THERAPEUTIC
OUTCOMES
▪ In established ARF, daily measurements of
1. urine output,
2. Fluid intake,
3. Weight
4. Vital signs
5. electrolytes & BUN
▪ TDM for drugs with narrow index
END