To “Pee” or not to “Pee”—the
KIDNEY in health and disease
“It is no exaggeration to say that the
composition of the blood is determined not by
what the mouth takes in but by what the
kidneys keep.” Homer W. Smith (1895-1962)
Some numbers…
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Renal diseases are responsible for a great
deal of morbidity but are not major causes
of mortality.
Approximately 45,000 deaths are attributed
to renal disease per year (as compared to
650,000 deaths due to heart disease,
560,000 due to cancer, and 145,000 due to
stroke) (National Center for Health Statistics,
2002)
Some numbers…
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Millions of persons are affected annually by
nonfatal kidney diseases, most notably infections
of the kidney or lower urinary tract, kidney stones,
and renal obstruction.
Twenty percent of all women have a urinary tract
infection or kidney infection at some time in their
lives
20% of all women and 10% of all men 65 and older
have bacteriuria; double those #’s in nursing homes
(25-50% of women, and 15%-40%) in men
Some numbers…
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10% of men and 5 % of women will have a
kidney stone by the age of 70; about one
million Americans are treated each year for a
kidney stone
BPH is a major cause of bladder outlet
obstruction
Kidney cancer, bladder cancer, prostate
cancer are major urologic cancers (especially
as the population ages)
Some numbers…
• Urinary incontinence is estimated to affect
between 15% and 30% of independent adults
ages 65 and older
• Costs the US about $20 billion per year to be
incontinent
Kidney failure
• Bones can break, muscles can atrophy, glands
can loaf, even the brain can go to sleep,
without immediately endangering our
survival; but should the kidneys fail…neither
bone, muscle, gland nor brain could carry on.
--Idem
CKD and renal failure…
• From 1988 to 2004 the rates of chronic kidney disease
climbed from 10 percent to 13 percent of the US
population
• Contributing factors? Diabetes, hypertension, obesity,
and the aging U.S. population (JAMA 2007; 298:2038)
• Chronic kidney disease affects 16.8% of the U.S.
population over 20
• Only about 1 in 8 men and 1 in 16 women with
moderate (stage 3) kidney disease know they have it—
YIKES! If we can pick it up, we can slow it down or
reverse it!
Renal failure and renal dialysis
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If renal failure is left untreated it will cause
death within two to three weeks
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Dialysis—from the Greek word for “separation”—
Willem Kolff, M.D. devoted his entire medical career
to the treatment of renal failure after watching the
death of a 22-year old patient die from the disease.
He invented the first dialysis machine in 1941 (using
materials from a local factory) and in 1945 he
successfully treated the first patient, a 67 year-old
woman who lived another 7 years on dialysis
Renal failure and renal dialysis
• 1960—Scribner and colleagues at the University of
Washington developed a blood-access device using
Teflon-coated plastic tubes, which facilitated the use
of repeated hemodialysis as a life-sustaining
treatment for patients with uremia
• It was called the Scribner shunt…led to the
development of AV fistulas and grafts and to longterm renal replacement therapy and the era of the
“artificial kidney”
A little more history…
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Gustav Simon, in 1869, performed the first
successful removal of a human kidney, the
patient survived and the remaining kidney
“picked up the slack” so to speak
FACT: The healthy kidney can grow enough
to handle 80% of the load that 2 kidneys
used to handle
Dr. Joseph Murray, Boston
• During WWII Murray treated burn patients and
wondered why skin rejection occurred when
grafts were donated by other people. He and
another colleague surmised that the closer the
genetic relationship the longer the graft would
last
• December 23, 1954 the first transplanted kidney
from a 23 year-old man to his identical twin; the
recipient lived another 8 years; Murray won the
Nobel Prize in 1990
Looking for a kidney somewhere else because the
waiting list in the U.S. is too long?
• India for $15,000; China? $62,000
• U.S.? $262,900
• Organ harvesting rings around the world; latest one
from Kosovo (2008)
• China—convicts on death row are routinely tested,
typed, and held for on-demand “donations”
• Pakistan, India, and Indonesia—slum dwellers sell
their body parts (Scott C, The Red Market, Wired,
2011)
• ARE YOU AT RISK FOR CKD?
The SCORED questionnaire—to identify
patients at high risk for kidney disease
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I am between 50 and 59 years of age—2
I am between 60 and 69 years of age—3
I am 70 years or older – 4
I am a woman – 1
I had or have anemia – 1
I have high blood pressure – 1
I am diabetic – 1
I have a history or heart attack or stroke--1
The SCORED questionnaire—to identify
patients at high risk for kidney disease
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I have a history of CHF or HF – 1
I have circulation disease in my legs – 1
I have protein in my urine – 1
If you score 4 or higher on the test you have a
1 in 5 risk of chance of having chronic kidney
disease
• Get it checked out! (88-95% accuracy in
identifying kidney disease)
• Arch of Intern Med 2008 (Feb 29)
Let’s start at the very beginning…
• How much embryology did you get in nursing
school?
• The sperm meets the egg and then…
Embryologic development
• Kidneys appear during the 3rd week of fetal
development; Three sets of kidneys develop;
first two are discarded and the third time is
the charm
• By the 3rd month the fetus is excreting urine
into the amniotic fluid; urine becomes the
main component of amniotic fluid
Embryology—the development of the
kidney
• The kidneys and the ears from the same
mesenchymal tissse
• The otorenal axis
• Nephrotoxic drugs and ototoxc drugs
Location, location, location…
• Kidneys located in the retroperitoneal space
between T12 and L3
• Right lower than the left
Kidney size is NOT affected by body build
• The kidneys grow at the same rate that the
entire body grows, until ~25-26. This is the age
that internal organs reach their final
dimensions.
• The mean dimensions of the kidneys upon
maturation are: length~12cm (~4.7 inches),
width~6 cm (~2.4 inches) and thickness~ 3 cm
(~1.2 inches).
• The weight of one kidney averages about 120150 g (4.5-5 oz).
PEARL:
• The kidney makes up less than 0.5% of the
body’s weight, yet takes in 20-25% of the
resting body’s cardiac output and uses 20-25%
of the body’s oxygen
• It’s busy…
Kidney size
• Any decrease in size (atrophy) is not normal. An
enlarged kidney is normal only in cases when one
kidney is removed and the remaining kidney
enlarges to compensate for the functional
absence of the first.
• THE MOST IMPORTANT NON-INVASIVE TEST FOR
RENAL DISEASE is a renal ULTRASOUND to
determine renal size
The kidney…retroperitoneal space
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CVA tenderness
Acute pyelonephritis
Glomerulonephritis
Palpation? Can you palpate the kidney in an
adult?
• Not unless the kidney is HUGE…(tumor)
• Polycystic kidney disease (PKD)
The kidney…retroperitoneal space
• Palpation? Can you palpate the kidney in an
adult?
• Not unless the kidney is HUGE…(tumor)
• Polycystic kidney disease (PKD)
Polycystic kidney disease
• Autosomal dominant polycystic kidney disease (ADPKD)
• 1/1000; C>AA; 4-10% of patients w/ kidney failure on dialysis
or needing transplant
• 50% by age 50 have renal failure
• Kidneys can be the size of a football
Associated structures
• Ureters
• Bladder
• Urethra
Ureters
• 10 – 12 inches (25 – 30 cm) and about 0.04 to 0.4 inches
(1 – 10 cm) in diameter
• When the bladder fills, the distal end of the ureter closes
to prevent urine from backing up into the kidney
• If this mechanism is not working properly bacteria can
reflux into the ureters and up to the kidneys—
vesicoureteral reflux
• Muscularis layer of the ureter propels urine via
peristalsis to bladder—1 to 5 contractions per minute
Ureters
• Pregnancy--progesterone slows down peristalsis
• Kidney stones—the pain?? On a scale from 1 to
1,000?
• The incidence of kidney stones increases with age
and it’s higher in Caucasians than African-Americans.
There is a significant regional variation in kidney
stone formation with the highest prevalence in the
Southeastern part of the United States.
Digression…kidney stones
• Does fluid intake make a difference? YES
• This approach increases urine flow rate and decreases
the urine solute concentration—both mechanisms
prevent kidney stones. In warmer climates,
inadequate fluid intake causes dehydration, which
increases the acidity of urine and stone formation.
(Southeastern U.S.= hot=increased kidney stones)
• This time-honored recommendation for reducing the
risk of kidney stones is to take two or more liters of
fluids per day. And, not just any fluids…
Fluids and kidney stones…
• Certain fluids have been associated with a
high risk of kidney stones—these include soft
drinks and tea. (Southeastern U.S.=lots of tea)
Grapefruit juice has also been linked to an
increased risk of kidney stones but the
mechanism is unknown.
The good news…
• Alcohol, especially wine, and coffee
consumption have been negatively
associated with kidney stones. YES!!
there is a God.
Kidney stones
• Foods that are high in potassium decrease
urinary calcium and increase urinary citrate
excretion.
• Some vegetables, such as spinach and
rhubarb, as well as peanuts, cashews, and
almonds, have high oxalate content and
should be avoided.
Bladder
• Medium-full bladder holds about 1 pint (500
mL) of urine and measures 5 inches (12.5 cm) in
length
• Fully expanded, the bladder can hold 1 quart (1
L) or more and YES, it can burst
• Newborns void 5-to 40 times a day
• At 2 months a baby voids 400 mL (14 fl oz) per
day
• Adolscents and adults—1.5 quarts (1500 ml)
per day
Urination
• Awareness of urination starts at about 15
months
• Control of nighttime urination sometimes
takes until age four
• Girls vs. boys and potty training
Urethra
• 1.5 inches (4 cm) in women
• MEN? Depends on who you ask…hahaha…
• 6-8 inches (15-20 cm)
Cystitis
• Lower urinary tract infections
• Lots of reasons—back to front wiping (E. coli
and the rectum), pH changes, lack of estrogen,
vesicoureteral reflux
• Young girls? Old girls?
The importance of estrogen and the
maintenance of urinary tract health
• Estrogen receptors and the urethra
• Prepuberty , perimenopause, and
postmenopause
• E.Coli and the rectum
Treatment of urinary tract infections
• TMP-SFX—Bactrim/Septra—watch out for K+ levels
in patients on ACE inhibitors or patients with CKD
and ESRD
• Fluoroquinolones – the “floxacins” – used when
greater than 20% resistance to TMP-SFX
• Side effects: C. difficile, tendonitis with acute
ruptured Achilles’ tendons in high-risk patients
(elderly and patients on Prednisone)
The antibiotics—the fluoroquinolones, the
“floxacins”…
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Ciprofloxacin (Cipro)*(2) (↑ INR)
Lomefloxacin (Maxaquin)(2)
Norfloxacin (Noroxin)*(2)
Ofloxacin (Floxin)(2)*
*uncomplicated UTI if resistance to TMP/SMX is ≥20%
• Levofloxacin (Levaquin) (3)—too broad spectrum for UTI
Gross anatomy
• Renal capsule
• Renal cortex (glomeruli—
80-85% of nephrons lie in
cortex)
• Renal medulla (collecting
ducts and some Loops of
Henle)
• renal papillae
• the renal interstitium
(columns)
• renal pelvis (pyelo)/calyces
The anatomy of a nephron—greater detail
• The basic functioning unit of the kidney
• The nephron—1.5 million per kidney in
normal birth weight individuals**
Premature babies/LBW babies
• LBW babies are much more likely to develop
hypertension later on in life and it may be due
to the fact that they have less nephrons to
start with
• Autopsies on patients between 35-59
• 10 kidneys w/ known hypertension; 10 w/
normal BP
• Average number of nephrons in people w/
HBP was fewer than ½ that of people w/
normal BP
Premature babies/LBW babies
• Couldn’t find damaged nephrons or nephrons that
had dropped out—suggesting inherited # of
nephrons
• Good prenatal nutrition and the # of nephrons—
restricting proteins ↓ # of developing nephrons
• (N Engl J Med 9 Jan 2003)
Premature babies/LBW babies
• Another implication
• Screening kidney donors for LBW may be important
when deciding who might be a candidate as an
appropriate donor
• The donor loses 50% of nephrons—if remaining
kidney has fewer #’s due to LBW, this increases the
risk of hypertension in the donor—overworked and
underpaid triggering the release of reninangiotensin-aldosterone
The anatomy of a nephron—greater detail
• Afferent arteriole → glomerulus → basement
membrane → Bowman’s capsule → tubular
system (proximal convoluted tubule (PCT),
Loop of Henle, distal convoluted tubule (DCT),
collecting duct)
• Peritubular capillaries (the vasa recta)
The nephron and the filtration
membrane
• The filtration membrane—3 layers
1) the endothelial cells of the glomerulus
2) the basement membrane between the
glomerulus and the,
3) epithelial cells of Bowman’s capsule
• Diseases—1) Lupus nephritis 2) “sugar” diabetes 3)
nephrotic syndrome
The glomerular filtration membrane
Glom
1.The glomerular capillary wall (lined
with endothelial cells)
2. The basement membrane (a
glycoprotein layer)
3. The fenestrated wall (epithelial)
cells of Bowman’s capsule into
the first part of the tubule (the
proximal tubule)(epithelial
cells)
1) Lupus nephritis 2) diabetic
nephropathy 3) nephrotic
syndrome
1
BM
2
BC
PCT
3
3
A note on the tubules of the kidney…
• The tubules of Bowman’s capsule and the
PCT—proximal convoluted tubule) are lined
with epithelial cells
• The epithelial cells are extremely vulnerable to
hypoxia
• Without oxygen, the epithelial cells become
necrotic and slough into the tubule; clogging
the works resulting in
• Acute tubular necrosis (ATN)
Ethylene glycol nephrosis results in
acute tubular necrosis
• Dogs and cats love the sweet taste of
antifreeze
• Crystals precipitate in the tubular lumen
resulting in intrarenal obstruction,
degeneration and necrosis of the lining of the
tubular epithelium
• Irreversible renal failure
Kidney disease
• Traditional approach is to divide the kidney
into 4 basic morphologic components
• 1) Glomeruli--glomerulonephritis
• 2 + 3) Tubules—tubulointerstitial diseases
including pyelonephritis)
• 3) Interstitium
• 4) Blood vessels
Kidney disease
• Early manifestations of each component tend to be
distinct and some components seem to be more
vulnerable to specific forms of renal injury
• Most glomerular diseases are immunologically
mediated
• Most tubular and interstitial disorders are frequently
caused by toxins (drugs) or infectious agents
(pyelonephritis)
• Blood vessel disease—atherosclerosis or HTN, blood
flow problems (hypovolemic shock, septic shock, HF)
The kidney as an innocent bystander…
• In addition to primary kidney disease, the kidney is
involved in many systemic diseases and conditions
• Hypertension
• Diabetes mellitus
• The deadly duo--“Sugar” diabetes and hypertension
• HF (Heart failure)
• Septic shock, hypovolemic shock
• DIC (Disseminated intravascular coagulation)
• HUS (Hemolytic uremic syndrome)
The kidney as an innocent bystander…
• Autoimmune diseases—lupus, autoimmune
glomerulonephritis, Goodpasture’s disease,
Wegener’s granulomatosis, sarcoidosis,
amyloidosis (? Autoimmune)
The kidney as an innocent bystander…
• Toxic effects of drugs—aminoglycosides,
radiocontrast agents, amphotericin,
cisplatinum, acetaminophen, NSAIDS,
methicillin, ampicillin, rifampin, allopurinol,
cimetidine (Tagamet)
• Cancer—malignant infiltration, multiple
myeloma
• Others—rhabdomyolysis, gout
Blood supply of the kidney
• Aorta→renal artery→branches into
arcuate→interlobular artery to the afferent
arteriole …
What can go wrong? atherosclerosis
• Fatty plaques in the renal artery--chronic
decreased blood flow to the kidney
• Renal artery stenosis
• Renal atrophy
Who’s at risk for atherosclerosis and
kidney disease?
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Family History
Diabetics
Coronary artery disease
Peripheral arterial disease
Erectile dysfunction
Hypertension
Smoking
Geriatric patients
Can we reduce atherosclerosis and kidney
disease? Say yes to drugs
The statin “sisters”…
• lovastatin (Mevacor)
• simvastatin (Zocor)
• atorvastatin (Lipitor)
• fluvastatin (Lescol)
• pravastatin (Pravachol)
• pitavastatin (Livalo)
• rosuvastatin (Crestor)—( boosts HDLs by 1214% vs. ~6% for the other statins) **
The “Statins”—what do they do?
• Reduce total cholesterol levels
• Decrease LDL levels--LDL is the most atherogenic
of the cholesterols and puts fat right smack dab
into all of the arterial walls; therefore, statins
decrease plaque formation
• Statins also stabilize plaques and prevent plaque
rupture, and…
• Statins shrink plaques in all arteries improving
blood flow to all vital organs such as the brain,
the heart, and the kidneys…
• And as mentioned, Crestor (rosuvastatin) in
particular, increases HDLs
Why are HDLs good for you?
1) HDL’s clear excess cholesterol from the blood; HDL’s
are also potent “anti-oxidants” and prevent LDL
from oxidizing; the HDLs are also potent “antiinflammatory” lipoproteins; keep levels above 40
mg/dL (1.04 mmol/L) and above 60 mg/dL (≥ 1.55
mmol/L) would be ideal
2) For every 5 mg/dL (0.13 mmol/L) decrease in HDL
below the mean, the risk of heart disease increases
by 25%
3) For every 21-mg/dL (0.5 mmol/L) increase in HDL,
patients are 50% less likely to develop albuminuria
(Diabetes Care January 06)
Drugs your patients might be on that INCREASE the
risk of atherosclerosis
• Progestins, androgens, cyclosporines, tacrolimus,
thiazide diuretics, setraline (Zoloft), and the atypical
antipsychotics (clozepine/Clozaril,
risperidone/Risperdal, olanzapine/Zyprexa)) increase
LDLs
• New ones—Block D2 receptors and 5-HT2C
• Blocking 5-HT2c serotonin receptor increases weight
gain; increased susceptibility to insulin resistance and
type 2 diabetes AND heart disease
What else can go wrong with the blood supply
into and out of the kidney?
• Hypertension with decreased blood flow
(treat with PRILS or ARBS)
• Diabetes with hypertension and
atherosclerosis (STATINS, PRILS or ARBS)
• Clamping the aorta above the renal artery
(AAA surgery)
• Sudden cessation of blood flow with a renal
artery embolus
What can go wrong with the blood supply
to and from the kidney?
• Decreased blood pressure with acute blood loss and
hypovolemic shock, heart failure, dehydration, septic
shock
• Afferent arteriole vasoconstriction with NSAIDs;
efferent arteriole vasodilation with ACE inhibitors in
a patient with renal insufficiency
• Microthrombosis of glomeruli—DIC (disseminated
intravascular coagulation)
• Immune complex deposition in the glomerulus
triggering the inflammatory response (lupus
nephritis)
How about blood flow OUT of the
kidney?
• renal vein → inferior vena cava → right atrium
• Patient presented with atrial fibrillation.
• Checked all of the usual causes; c/o flank pain,
hematuria
• Renal cell carcinoma growing into the renal
vein, IVC, right atrium
Major functions of the kidney
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Fluid and electrolyte balance
Acid-base balance
Vitamin D and calcium metabolism
RBC production via the hormone
erythropoietin
• Maintain blood pressure via ReninAngiotensin-Aldosterone System (RAAS)
Secretes renin from the juxtaglomerular
apparatus—RAAS system
• Baroreceptors in the afferent arteriole sense pressure and
volume…low pressure? Low volume? I CAN HELP by releasing
renin (a messenger)
• Angiotensinogen to angiotensin I (liver);
ACE (angioconverting enzyme) converts I to….
• angiotensin II (tissues, primarily lung)—”angie” zips to the
adrenal cortex…can “al” come out to play?
• aldosterone (primarily from the adrenal cortex; some tissue
aldosterone production as well)
• Angiotensin II is a potent vasoconstrictor and aldosterone
reabsorbs water and sodium (excretes potassium)
Bottom line
• Vasoconstriction via angiotensin II—blood
pressure goes up
• Sodium and water retention (with K+
excretion) via aldosterone—blood pressure
goes up…
Essential hypertension and the kidney
• It’s estimated that ~70% of all patients with
“essential hypertension” have an upregulation of the RAAS – too much “angie”
resulting in vasoconstriction and too much
“al” resulting in sodium and water retention
and potassium excretion
The RAAS
• Too much RAAS?
• Too much “angie” and too
much “AL”
• Too much vasoconstriction
and too much sodium and
water retention
• The ACE inhibitors to the
rescue!!
RENIN
ANGIOTENSIN 1
ANGIOTENSIN 2
The ACE inhibitors
• Block the conversion of
angiotensin I to angiotensin
II
• No ANGIE?
• No AL-dosterone
• Vasodilate and blood
pressure drops
• Inhibit aldosterone and
sodium and water are
excreted and potassium is
retained
RENIN
ANGIOTENSIN 1
ACE--
ANGIOTENSIN 2
“Prils”—The ACE inhibitors
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Captopril (Capoten)
Enalapril (Vasotec)
Lisinopril (Prinivil, Zestril)
Fosinopril (Monopril)
Perindopril-- (Aceon)
Moxepril (Univasc)
Benazepril (Lotensin)
Quinapril (Accupril)
Trandolapril (Mavik)
Ramipril (Altace)
“Sartans”--ARBs
• Angiotensin receptor blockers (bypass ACE) and work by
blocking the angiotensin-II receptors on tissues
• Who are they? The “Sartan Sisters”…
• losartan—Cozaar
• valsartan—Diovan
• candesartan—Atacand
• irbesartan—Avapro
• telmisartan—Micardis
• olmesartan—Benicar
• eprosartan—Tevetan
• azilsartan -- Edarbi
Normal function: Angiotensin II helps maintain
glomerular filtration pressure in the nephron
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Afferent arteriole
(vasodilated via
(prostaglandins)
Blood entering
glomerulus
Glomerulus→filter
Efferent arteriole
(vasoconstricted via
(angiotensin II)
Blood exiting
glomerulus
Prostaglandins
filter
Angiotensin II
Toilet
The Diabetic Kidney…hyperglycemia/HTN (the deadly
duo)
• Hyperglycemia
and/or hypertension
boost prostaglandins and
vasodilate the afferent
arteriole
• Hyperglycemia and
hypertension increase
angiotensin II and vasoconstrict the efferent
arteriole
• Intraglomerular hypertension
causes microalbuminuria
Microalbuminuria --10fold > risk of RD & CKD)
Why is microalbuminuria a “bad” thing?
• The presence of microalbuminuria suggests that large vessel
walls are more permeable to lipoproteins (causing
atherosclerosis) and/or damage from the local release of
growth factors
• There is a 4-fold increase in acute coronary syndromes in Type
1 DM greater than 35 years old;
• When microalbuminuria is present the risk is increased by a
factor of 140!
• Aggressive treatment demonstrates beneficial effects not
only on macrovascular disease but on microvascular disease
as well (retinopathy and nephropathy)
SO, what is “aggressive treatment”?
• Reduce the albumin in the urine with the
PRILS (ACE inhibitors) or ARBs by reducing
intraglomerular hypertension
• Decrease the cardiovascular risk and fat
deposition in the renal arteries with the
STATINS (to lower LDL-cholesterol)(more
later)
Other drugs and the RAAS
• Direct renin inhibitor (DRI)--anti-hypertensive
drug known as aliskirin/ Tekturna
• spironolactone/Aldactone and eplerenone
(Inspra)—aldosterone antagonists
SO, PICK A PRIL, any PRIL or, if they can’t tolerate the side
effects, pick an ARB (angiotensin receptor blocker)
PRILS
ARBs
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Captopril (Capoten)
Enalapril (Vasotec)
Lisinopril (Prinivil, Zestril)
Fosinopril (Monopril)
Perindopril (Aceon)
Moxepril (Univasc)
Benazepril (Lotensin)
Quinapril (Accupril)
Trandolapril (Mavik)
Ramipril (Altace)
losartan (Cozaar),
valsartan (Diovan),
candesartan (Atacand)
telmisartan (Micardis)
irbesartan—Avapro
olmesartan—(Benicar)
eprosartan—Tevetan
azilsartan -- Edarbi
The Diabetic Kidney…hyperglycemia/HTN (the deadly
duo)
• Any drug that blocks
angiotensin II is going to
“open” up the efferent
arteriole and reduce
pressure in the glomerulus
• For each 1 gm decrease in
proteinuria, kidney disease
progression is slowed by 1
mL/min/year—PRILS and
SARTANS can decrease the
decline by 50% or MORE
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Major functions of the kidney
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Fluid and electrolyte balance
Acid-base balance
Vitamin D and calcium metabolism
RBC production via the hormone
erythropoietin
Maintain blood pressure via ReninAngiotensin-Aldosterone System (RAAS)
RBC production and erythropoietin
• Secretes erythropoietin to stimulate the bone marrow to
produce RBCs—the failing kidney does not secrete
erythropoietin therefore one of the earliest signs of
declining renal function is the presence of anemia
• Anemia has been independently associated with an
increased risk of left ventricular dilation, left ventricular
hypertrophy, coronary artery disease, heart failure
• Each 1 gm ↓ causes  LV dilation by 42%)(50% lower
survival rates with LVH)
• Almost half of all stage 3 CKD, are anemic (Stage 3—is
characterized by a GFR of 30-60 mL/min/1.73 m²)
Anemia and CKD
• The link between heart failure, CKD, and renal failure
is known as cardiorenal anemia syndrome
• In the “old” days renal patients had to receive packed
RBCs frequently to give them adequate RBCs
• Synthetic erythropoietin known as the ESAs
(erythropoiesis stimulating agents) have been
available since 1989
• Epoetin alfa (1989) and darbopoetin alfa (2001)
Anemia and CKD
• BUT…fully restoring hemoglobin (to greater
than 13 g/dL) in patients with CKD increases
their risk of all-cause mortality, poorly
controlled BP, and AV access thrombosis…so
partial restoration of Hb is advised.
• Target Hb of 11-12 g/dL; Monitor Hb at least
monthly when on ESAs
Major functions of the kidney
• Fluid and electrolyte balance
• Acid-base balance
• Vitamin D and calcium metabolism
RBC production via the hormone
erythropoietin
Maintain blood pressure via ReninAngiotensin-Aldosterone System (RAAS)
Vitamin D metabolism
• The kidney converts the vitamin D from the skin and
diet to the active form of vitamin D (calcitriol)
• Vitamin D is necessary for the absorption of calcium
from the GI tract
• Calcium and phosphorus must always be “in
balance” in the blood
• If the kidneys fail, phosphate is retained and results
in hyperphosphatemia
Aids in Vitamin D metabolism
• With increased phosphate retention due to kidney failure
or decreased calcium absorption due to lack of vitamin D,
the parathyroids increase their production of Parathyroid
Hormone (PTH)
• PTH breaks down bone to replace the calcium to balance
the hyperphosphatemia—known as secondary
hyperparathyroidism and it wreaks havoc with bones
causing the osteomalacia of chronic renal failure
• Phosphate binders in patients with renal failure
• Decrease foods that contain phosphates (a registered
dietician is your best friend)
Treatment of hyperphosphatemia
• Phosphate binders
• Sevelamer carbonate (Renvela) a buffered
form of the anion-exchange resin sevelamer
hydrochloride (Renagel) has been approved
for use by hemodialysis patients. Renvela will
replace Renagel, which has been shown to
induce or exacerbate metabolic acidosis in
patients on dialysis.
• Medical Letter, February 25, 2008, Vol. 50 (1280): 13.
Some notes on Vitamin D
• 10-15 minutes of exposure to sunlight on face,
hands, and arms 2-3 days per week is required to
synthesize sufficient amounts of vitamin D (in shorts
and a t-shirt, people can soak up enough UV-B rays
to produce 12,000 U of vitamin D within 20 minutes)
• Sunscreen? SPF-8?
• Food—fatty fish, cod liver oil, and egg yolks
• Fortified foods—milk, breakfast cereals, margarine,
butter, certain brands of OJ and yogurt
Major functions of the kidney
Fluid and electrolyte balance and acid base
balance
Vitamin D and calcium metabolism
RBC production via the hormone
erythropoietin
Maintain blood pressure via ReninAngiotensin-Aldosterone System (RAAS)
Fluid and electrolyte and acid-base balance
• Regulation of water,
• Electrolytes: Sodium, chloride, potassium, and phosphorus
• Excretion of excess urea and creatinine
•
Excretion of excess hydrogen ions
If the kidney fails…
• Retention of water—edema, weight gain, HBP
• Retention of urea (BUN) and creatinine (as measured
by serum creatinine and creatinine clearance)
• Retention of Na+ resulting in hypertension
• Retention of K+ resulting in hyperkalemia and
potentially life-threatening cardiac arrythmias
• Retention of phosphorus resulting in
hyperphosphatemia
• Retention of H+ ions—metabolic acidosis
Free water is regulated by ADH (antidiuretic hormone)
• Conservation of free water
• Diurnal rhythm—kicks in around midnight
with water conservation and reduced
urination at night
• NO ADH at night? Clinical sign of NOCTURIA
Anti-diuretic hormone
• ADH is produced by the hypothalamus and
released from the posterior pituitary in
response to osmoreceptors located in the
hypothalamus
• ADH receptors on the distal tubule and
collecting duct
Free water is regulated by ADH
(antidiuretic hormone)
• Early a.m. specimen is concentrated (as
measured by the specific gravity)—1.025
• One of the earliest signs of renal insufficiency
is the inability to concentrate urine at night—
early a.m. specimen, 1.010; mid-day
specimen, 1.010, evening specimen,
1.010…GET IT? 
Anti-diuretic hormone
• OR…beer and ETOH inhibit ADH—a 6-pack of
beer before bedtime? urinating all night
• And morphine increases ADH as well as
tightens the urinary sphincter (urinary
retention—problem after surgery in patients
on PCA pumps or anyone receiving morphine)
Other causes of nocturia?
• Inability of the kidney to respond to ADH—immaturity?
Enuresis in kids? (DDAVP--desmopressin);
• Nephrogenic diabetes insipidus—genetic lack of receptors
• “sugar” diabetes—glucose is an osmotic diuretic
• Enlarged “prostrate”
• UTI
• CHF (“funny things happen in the middle of the night”)
• Pregnancy
• Diuretics at bedtime—lasix, HCTZ
• Drugs can cause the Syndrome of Inappropriate ADH
Aldosterone
• Aldosterone (part of the RAA system) is
produced by the adrenal gland primarily in
response to angiotensin II
• Low sodium, high potassium, low BP or low
volume and the RAAS kicks into action
• Aldosterone interacts with receptors on the
distal tubules to conserve water AND sodium;
the sodium is exchanged for potassium;
potassium is secreted into the distal tubules
and excreted
Too much sodium and water?
• Aldosterone antagonists (blockers)—
spironolactone (Aldactone) and eprelrenone
(Inspra)
Now that you know what the kidney is
supposed to do…
What do YOU do?
• Accurate intake and output
• Daily weights
• Check for signs of fluid retention—peripheral
edema, jugular vein distention, S3
• Blood pressure
• Interpretation of lab tests
Doin’ the double-dub—S3 (also listen for an S4
with LVH; Apical impulse is displaced laterally)
Lab tests
• BUN
• Serum creatinine
• Estimated glomerular filtration rate (GFR) as
measured by the MDRD formula or the
Cockcroft-Gault equation
Blood urea nitrogen (BUN)
•
•
Urea is a commonly used marker for the diagnosis
of renal failure/kidney injury; by-product of protein
metabolism (not produced at a constant rate
BUN (8-18 mg/dL)—three reasons for an elevated
BUN
–
–
–
decreased GFR
Increased tissue metabolism (burns, crush injuries,
rhabdomyolysis)
increased load of urea for excretion from the diet
(protein)
What about the Atkin’s diet?
• High content of valine and lysine increases
intraglomerular pressure and can accelerate
kidney damage in impaired kidneys
• Should a diabetic go on the Atkin’s diet?
• How about an 80-year old?
• No harmful effect in young people with
normal kidneys
• Renal disease and dietary restrictions
Serum creatinine
• Creatinine is released from skeletal muscle at a
relatively constant state, is freely filtered at the
glomerulus, and is not reabsorbed or metabolized by
the kidneys
• Hence, it’s popularity for measuring the ability of the
kidneys to filter; if the kidneys are not filtering
properly creatinine will be retained and the serum
creatinine will be increased
• Normal reference range is 0.5 to 1.0 mg/dL* (to
convert to micromoles per liter, multiply by 88.4)
• See Caveats
A few caveats--serum creatinine
• Can be influenced by age, gender, muscle
mass, diet, concomitant diseases, circadian
rhythm, and stability of renal function, tubular
secretion, & drugs (cimetidine/Tagamet
increases creat cl)
Serum creatinine (varies with sex and age)
newborn (0.3-1.0)
infant (0.2-0.4)
child (0.3-0.7)
Adolescent (0.5-1.0)
Adult Male (0.6-1.3)
Adult Female (0.5-1.2) (women have 15% less muscle
mass than men, hence serum creatinine is lower)
Elderly patients—less muscle mass, decreased filtration
due to aging kidney
Critically ill patients and serum
creatinine
• Patients are not in a steady state and an
increase in creatinine lags behind renal injury
by as much as 12 hours to 2 days
Important notes…
– The NIH Consensus conference of 1993
recommends that patients with chronic kidney
disease be referred to a renal team when the
serum creatinine has increased to 1.5 mg/dL in
the female and 2.0 mg/dL in the male
– Most nephrologists report that patients are
usually referred to a renal healthcare team when
their serum creatinine level is 3-4 mg/dL or
greater…earlier is better!
serum creatinine and the estimated GFR
– What is the glomerular filtration rate? A determination of
how much the glomerulus filters; can be determined by
how much creatinine is CLEARED into the toilet (also
known as creatinine clearance)
Calculating the eGFR—2 equations
• MDRD (modification of diet in renal disease)
formula
• ml/min/1.73m2 = 170 x (SCr)-0.999x (age)-0.176
x (BUN)-0.170 x (alb)0.318 x (0.762 if female) x
(1.180 if black)
• Cockcroft-Gault equation
• OMG! GET A CALCULATOR or
• GFR calculators are available at:
• http://kidney.org
• http://nephron.com/cgi-bin/MDRD.cgi
Estimated GFR
– normal estimated GFR in young adults is 105130 mL/min/1.73 m² (women 105 mL/min, guys
125 mL/min)
– a GFR of less than 60 mL/min/1.73 m²
represents a loss of more than half of normal
kidney function
– GFR decreases with age—the 1% rule
Stages of chronic kidney disease based on
the GFR
– CKD-1 = GFR>90 mL/min or higher
– CKD-2 = GFR 60-89 mL/min=mild renal
insufficiency
– CKD-3 = GFR 30-59 mL/min=moderate renal
insufficiency* (refer to nephrologist)
– CKD-4 = 16-29 mL/min =severe renal
insufficiency
– CKD-5 = 0-15=failure or ESRD (end-stage renal
disease) (dialysis or transplant)
Major causes of end-state renal
disease (Cooper, et al.NEJM 2010)
•
•
•
•
•
•
•
•
•
•
•
Diabetes – 33.9%
Glomerulonephritis – 16.1%
Polycystic kidney disease – 10.1%
Hypertension – 7.9%
Analgesic nephropathy – 4.7%
Reflux nephropathy – 4.7%
Renovascular disease – 3.7%
Interstitial nephritis – 2.2%
Obstructive nephropathy –1.2%
Failing kidney transplant – 3.2%
Other – 15.3%
Co-existing conditions
•
•
•
•
•
•
•
Diabetes – 42.6%
Hyperlipidemia – 60.9%
Cardiovascular disease – 39.6%
Ischemic heart disease – 29.5%
Peripheral vascular disease – 17.1%
CHF – 4.5%
Stroke – 2.7
Smoking status
• Current smoker – 11.4%
• Former smoker – 50.7%
• Never smoked – 37.9%
The GFR and the geriatric patient
• 75-year-old = 1.2 mL/min x 45 years = 53 mL/min;
120-53=67 mL/min in a HEALTHY 75-year-old (not
taking into account weight, ethnicity, or gender)
The pitfalls of relying on serum creatinine
to evaluate renal function
• 85-year-old, 50-kg Caucasian female vs. 55year-old, 70-kg African American Male
• SCr 1.5 in each of the patients
• CrCl as measured by the MDRD (using age,
sex, color and serum creatinine)
• 35 mL/min/173m2 in the C female (CKD-3)
• 63 mL/min/1.73m2 in the AA male (CKD-2)
Urinalysis
• In addition to ultrasound, the urinalysis is the
second part of the ‘non-invasive’
measurement of renal function
• Checking for protein in the urine (and other
components) is an essential part of the renal
work-up
Urinalysis
• Can tell you all sorts of interesting information
• Glucose—transport maximum 180 mg/dL;
over that amount and you’ll have glucosuria
(geriatric patients the Tm is 140 mg/dL)
• Proteinuria—trace, 1+, 2+, 3+, 4+ (glomerular
injury with higher numbers)
Urinalysis
• Pink or brownish tinge—blood, bile salts, red
beets
• Bright yellow—riboflavin in multivitamins
• Frothy—bile salts (blocked bile duct, liver
disease); protein (large amounts, glomerular
disease)
• Ketones—fruity odor; diabetes, low carb diet,
fasting or starvation
Asparagus
• Why does your urine smell when you eat
asparagus?
• Or does it?
Urinalysis
• Specific gravity—1.001-1.035; tests the ability
of the kidneys to concentrate urine
• ADH and the urine; first morning specimen
• If you drink nothing for a full day, your kidneys
continue producing urine at a specifc gravity
of 1.025
• Lose the ability to concentrate urine and the
specific gravity will be 1.010 at any time of day
Urinalysis
•
•
•
•
•
•
•
•
Marijuana
Cocaine
Alcohol
Steroids
RBCs
RBC casts
WBCs
WBC casts
Acute Kidney Injury (AKI)
• Today the term acute kidney injury has replaced ARF,
with an understanding that such an injury is a
common clinical problem in critically ill patients and
is predictive of an increase in morbidity and mortality
• Acute renal failure is still used but there was no
uniform standard for diagnosing and classifying acute
renal failure; more than 35 different definitions used
in clinical practice
ARF
• Comprises a family of syndromes that are characterized by an
abrupt (over hours or days) decrease in the GFR
• May occur in the absence of prior renal dysfunction, or it may
represent an acute exacerbation in a patient with known
stable chronic kidney disease
• Oliguria (less than 400 to 500 mL/24 h) may be a presenting
manifestation, although the urine volume may be variable,
ranging from less than 100 mL to greater than 3 L per day
• Primary manifestation is the accumulation of nitrogenous
waste products—primarily creatinine and BUN
AKI
• Refers to a sudden decline in kidney function that
causes disturbances in fluid and electrolyte, and
acid-base balance because of a loss of clearance of
small solutes and a decreased GFR
• AKI has a broad spectrum and encompasses the
entire renal failure syndrome in all patients—not just
those that require renal replacement therapy but
also in patients with minor changes in renal function
Criteria for AKI includes assessment of 3
grades of severity
• Risk of acute renal failure— serum creatinine
increased 1.5 times normal or GFR decreased > 25%;
urine output < 0.5 mL/kg x 6 hours
• Injury to the kidney-- serum creatinine increased 2
times normal or GFR decreased > 50%; urine output
< 0.5 mL/kg x 12 hours
• Failure of renal function-- serum creatinine increased
3 times normal or GFR decreased > 75% ; urine
output < 0.5 mL/kg for 12 hours or anuria for 12
hours
Two outcome classifications for AKI
• Loss—complete loss of renal function for > 4
weeks
• End-stage renal disease—need for renal
replacement therapy for > 3 months
• KNOWN AS THE RIFLE classification
• Risk, Injury, Failure, Loss, End-stage kidney
disease
Classification of ARF syndromes (in tertiary
care centers)
• Prerenal—insult occurs prior to the kidneys
(21%)
• Renal—within the kidnesy (intrinsic)(45% with
ATN)
• Postrenal—after (10%)(obstructive uropathy)
Causes of prerenal ARF
•
•
•
•
•
•
•
Intravascular volume depletion—
GI losses
Renal—diuretics, osmotic diuresis
Cutaneous (burns)
Hemorrhage (hypovolemic shock)
3rd spacing (pancreatitis)
Decreased effective blood volume—CHF, cirrhosis, nephrotic
syndrome, sepsis, anesthesia
Causes of prerenal ARF
• Altered intrarenal hemodynamics—such as preglomerular
(afferent) vasoconstriction (NSAIDS—COX1, COX
2)(prescription NSAID use increases risk of ARF in elderly by
58%)
• Cyclosporine, tacrolimus, hypercalcemia
• postglomerular (efferent) vasodilation (ACE inhibitors,
angiotensin receptor blockers)(older age, NSAIDS + ACE
inhibitors, diuretic RX and diabetics highest risk)
• Abdominal compartment syndrome—increased intraabdominal pressure with increased renal venous pressure
(trauma patients requiring massive volumes of fluids; fluid
sequestration, pancreatitis, peritonitis)
Intrinsic ARF
• Associated with renal parenchymal injury
• Most commonly results from ischemic or toxic injury
to renal tubular epithelial cells
• Also includes glomerular diseases (autoimmune) and
vascular and interstitial inflammatory processes
(allergic) that are associated with rapid loss of renal
function
Intrinsic ARF
• Acute glomerulonephritis— postinfectious GN (ex.
Acute poststreptococcal {Group A beta hemolytic
strep} GN), endocarditis-associated GN, Hemolytic
Uremic Syndrome*, Thrombotic Thrombocytopenic
Purpura, rapidly progressive glomerulonephritis
(RPGN)
• Acute vascular syndromes—renal artery
thromboembolism, renal artery dissection, renal vein
thrombosis, atheroembolic disease
• DIC—disseminated intravascular coagulation
Hemolytic uremic syndrome and E.
Coli O157:H7
• Mid-70’s, mutation in Venezuela; Shigella + E. coli
• Moved up through Central America into Southern Texas in the
early ’80’s (1982 first identified)
• 3rd most deadly toxin in the world; 10-100 pathogens to make
you ill or kill you
• Produces a toxin that kills the kidneys
• The leading culprit in 2006 for food-borne illness
• Cook burgers to 160° F
• Produce – bagged spinach and lettuce
E. Coli O157:H7
• Very young, very old, very immunocompromised
• Acute Renal Failure in Kids
• 1993 Jack-in-the-Box in Seattle/Tacoma (500/4
deaths)
• Mickey D’s—30 outbreaks per year
• Supportive Treatment
Meningococcemia and DIC
• DIC is characterized by microthrombi in the
small vessels
• Decreased urinary output is one of the first
signs
• Check the platelet counts and coagulation
studies (fibrinogen, thrombin time, D-dimers
or fibrin split products)
Causes of intrinsic ARF
• Acute Tubular Necrosis
• Ischemic—hypotension, hypovolemic shock, sepsis,
cardiopulmonary arrest, cardiopulmonary bypass
• Nephrotoxic—drug-induced such as the aminoglycosides,
radiocontrast agents, amphotericin, cisplatinum,
acetaminophen
• Pigment nephropathy—intravascular hemolysis and
rhabdomyolysis (massive muscle damage—trauma, statin
drugs (rare)
Causes of intrinsic ARF
• Acute interstitial nephritis—drug-induced (penicillins,
cephalosporins, sulfonamides, rifampin, dilantin, furosemide,
NSAIDS)
• Infection-related—bacterial infections, viral, rickettsial
disease, TB
• Systemic diseases—SLE, Wegener granulomatosis
(granulomatous inflammation involving the respiratory tract
and necrotizing vasculitis of the small and medium sized
vessels; necrotizing glomerulonephritis is common)
• Malignancy—malignant infiltration, multiple myeloma (BenceJone’s proteins—what are these?)
Postrenal ARF
• Acute obstruction to the urinary tract from the renal pelvis to
the urethra
• However, for obstruction proximal to the urinary bladder to
result in ARF, it must be bilateral or occur in the setting of a
single functional kidney
Causes of postrenal ARF
• Intrinsic—stones, papillary necrosis, blood clot,
transitional cell carcinoma
• Extrinsic—aortic aneurysm, retroperitoneal or pelvic
malignancy
• Lower tract obstruction—urethral stricture, BPH,
prostatic cancer, transitional cell carcinoma of the
bladder, bladder stones, neurogenic bladder
Feline urologic syndrome
• Obstructive disease of the urethra—especially
in the male feline
• Pathogenesis includes the maintenance of a
constant alkaline urinary pH, increased
intervals between urination, exclusive use of
dog food, and maybe a virus thrown in
• Renal failure
Rx of acute renal failure…the obvious
• Treat the underlying cause…
• Measure electrolytes daily, K+ restriction, diuretics and renal
replacement therapy (RRT) as necessary
• Acidosis—RRT
• Volume—I & O of course; CVP; insensible losses
• Daily weights, volume replacement
• Pulmonary edema—loop diuretics if ANY renal function is left;
if not, RRT
• Nitrates and opiates provide vasodilation in patients with
acute pulmonary edema; oxygen
• Maintain hemoglobin above 10 g/dL
Specific syndromes of ATN
• RCN—radiocontrast nephropathy is one of the most frequent
etiologies of nephrotoxic ATN accounting for 10% of all cases
of hospital-acquired ARF
• Risk factors—baseline renal insufficiency (baseline serum
creatinine greater than 2.0 mg/dl), DM, CHF, large volumes of
contrast media, volume depletion, concurrent use of NSAIDS
or ACE inhibitors
• Risk with normal kidney function=negligible
• Mild to mod renal insufficiency with DM=10-40% risk
• Advanced renal insufficiency=50% risk
• Due to renal vasoconstriction and direct renal tubular
epithelial cell toxicity
RCN (radiocontrast nephropathy)
• Acute rise in serum creatinine 24-48 hours after contrast study
• Peaks 3-5 days after onset of renal failure and returns to baseline in 7-10
days
• Usually non-oliguric
• Prevention—use other imaging techniques in high-risk patients, if
possible; correct hypovolemia, discontinue NSAIDs and ACEI
• Administer saline (1 ml/kg/h from 8 a.m. on the day of the procedure to 8
a.m. the following day—reduces RCN by 50%; especially in women,
diabetics, and patients receiving more than 250 ml of contrast dye
• Use low-osmolality contrast media
• N-acetylcysteine (NAC) (Mucomyst)—potential therapeutic benefit
Aminoglycoside nephrotoxicity
• Develops in 10-15% of patients treated for more than several
days
• Taken up by PCT where they accumulate in high
concentrations and produce cytotoxicity
• Onset of nephrotoxicity usually occurs after 7-10 days of
therapy
• Shedding of epithelial cells into urine (tubular cell casts)
• Complete recovery is possible—high risk groups are patients
with volume depletion, the elderly, cardiac surgery,
preexistent renal disease, and hepatobiliary disease
• Once daily dosing will reduce the nephrotoxicity
Rhabdomyolysis
• Release of muscle cell constituents as the result of
traumatic or nontraumatic injury is the principal
cause of hemepigment associated ARF (myoglobin)
• Increased CK, AST, LDH
• Severe cases result in profound hypovolemia,
metabolic acidosis, electrolyte disturbances
• Treat with aggressive volume replacement with
saline
• Renal replacement therapy may be necessary
Postoperative Acute Renal Failure
• Most commonly associated with vascular, cardiac
and major abdominal surgery, including visceral
organ transplants
• Multifactorial in origin
• Cardiogenic shock, history of renal disease with CC
less than 60 ml/min), emergency surgery, LVEDP
greater than 25 mmHg, age greater than 70, leftmain coronary stenosis greater than 70%, and a
history of PVD
• Decreased incidence in patients undergoing offpump bypass vs. grafting vs. bypass grafting with
cardiopulmonary bypass
Pharmacologic management of ARF
• Prevention—optimizing vascular
hemodynamics to ensure adequate renal
perfusion with saline loading
• Discontinue drugs that increase
vasoconstriction
• Avoid nephrotoxic drugs when possible
• If unavoidable, use dosing schedules and new
preparations
Pharmacologic management of ARF—what
doesn’t work…
• Dopamine infusions—there is NO evidence that
dopamine is of benefit in the prevention or
treatment of ARF; increased risk of arrhythmias,
myocardial ischemia, intestinal ischemia…
• Loop diuretics—clinical studies do NOT support the
use for loop diuretics; outcomes are not improved
• Atrial natriuretic peptide—the literature does not
support the use of ANP
Renal replacement therapy
• Given the lack of effective pharmacologic therapy,
the management of ARF remains primarily
supportive, with RRT the cornerstone of treatment
• Dialysis is more difficult in ARF patients—they are
more hemodynamically unstable, more
hypercatabolic, have greater nutritional
requirements and have a a larger daily fluid intake
(vs. chronic RF patients)
• Multiple modalities to provide RRT
Renal replacement therapy
• When should it start in acute renal failure?
• The gold standard was to initiate RRT when the BUN
hit 100 mg/dl
• 1999 study showed the early RRT with a BUN less
than 60 mg/dl vs. a BUN greater than 60 mg/dl was
associated with a 39% survival as compared to a
20.3% survival
• (Getings, LG, Reynolds HN. Outcome in post-traumatic acute renal failure
when continuous renal replacement therapy is applied early vs. late.
Intensive Care Med 25:805-813, 1999.)
Renal replacement therapy
• Intermittent hemodialysis or,
• Continuous renal replacement therapy (CRRT)?
• Insufficient data to favor intermittent vs. CRRT,
however, in hemodynamically unstable patients,
CRRT can be more safely performed due to a lesser
tendency to exacerbate hypotension
• Peritoneal dialysis (only use if nothing else is
available), or
Historical highlight
• The ancient Chinese, Roman, and German
societies frequently used urine as mouthwash.
Surprisingly, the ammonia in urine is a good
cleanser. Do not try this unless desperate
measures are necessary.
The end.
• Barb Bancroft, RN, MSN, PNP
• CPP Associates, Inc.
• www.barbbancroft.com
• BBancr9271@aol.com
Bibliography
• Bosch X, Poch E, Grau JM. Rhabdomyolysis and Acute
Kidney Injury. N Engl J Med 2009. 361;1:62-72.
• Buhsmer J. Overview of CKD and anemia. The
Director; 13(4)
• Cooper BA et al. A Randomized, Controlled Trial of
Early versus Late Initiation of Dialysis. N Engl J Med
2010; 363;7:609-619.
• Crus DN, Perazella MA. Drug-induced acute
tubulointerstitial nephritis. Hosp Practice 1998 Feb
15; 151-164.
• Friedman JM. Ace Inhibitors and congenital
anomalies. N Engl J Med 2006 Jun 8; 2498-2500.
Bibliography
• Ghanasekaran I, Dimitrov H. Primary care
management of anemia in chronic kidney
disease. Patient Care May 2006
• Guzzo TJ, Drach GW. Major Urologic Problems
in Geriatrics: Assessment and Management.
Med Clin N Am 2011, 95:253-264.
• Himmelfarb J, Ilizler TA. Hemodialysis. N Engl J
Med 2010; 363;19:1833-1845.
• Palevsky P. Acute Renal Failure. Journal of the
American Society of Nephrology. March 2003;
2(2).
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• Robbins and Cotran. Pathologic Basis of Disease 7th
Edition. 2006.
• Wish JB, Coyne DW. Use of Erythropoiesisstimulating agents in patients with anemia of chronic
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pharmacoeconomic limitations of existing therapies.
Mayo Clin Proc. 2007 (Nov);82(11):1371-1380.
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