Transcript ACUTE VS. CHRONIC KIDNEY FAILURE

ACUTE & CHRONIC KIDNEY
FAILURE
By Maritza I. Garcia-Duran & Joao Mc-O’neil
Internal Medicine
06/21/2010
ACUTE KINEY FAILURE A.K.A. ACUTE
KIDNEY INJURY (AKI)
rapid loss of kidney function
REVERSIBLE
CAUSES
OTHER SIGNS AND SYMPTOMS OF AKI
•f/b generalized swelling, d/t waste products build
in the blood.
•Met. Acidosis
•Arrhythmias d/t hyperkalemia. Including v-tach
and v-fib
•Encephalopathy = altered thinking and
pericarditis d/t uremia and low serum calcium
•Anemia d/t decreased EPO production
•Hypertension d/t inc fluid deposited in lung causing
CHF
•Tachypnea
DIAGNOSIS
1. Rapid time course (less than 48 hours)
2. Reduction of kidney function
a. Rise in serum creatinine
Absolute increase in serum
creatinine of ≥0.3 mg/dl
Percentage increase in serum
creatinine of ≥50%
b. Reduction in urine output,
defined as <0.5 ml/kg/hr for more
than 6 hours (about 210mL in 6
hours)
HUMAN REFERENCE RANGE OF
SERUM CREATININE
0.5 to 1.0 mg/dL (about 45-90 μmol/L)
for women
0.7 to 1.2 mg/dL (60-110 μmol/L) for
men.
 While a baseline serum creatinine of
2.0 mg/dL (150 μmol/L) may indicate
normal kidney function in a male body
builder, a serum creatinine of 1.2 mg/dL
(110 μmol/L) can indicate significant
renal disease in an elderly female
MANAGEMENT
1.treatment of the underlying cause
2.avoid nephrotoxins (antibiotics,
chemotherapeautics, contrast dye, PCN,
Aminoglycosides, ACEI, NSAIDS, etc.)
3.Monitoring of renal function, by serial
serum creatinine measurements and
4. monitoring of urine output
5.urinary catheter: helps monitor urine
output and relieves possible bladder
outlet obstruction, such as with an
enlarged prostate
Specific therapies
a) intravenous fluids is typically the first step to improve
renal function.
b) Volume status may be monitored with the use of a
central venous catheter to avoid over- or underreplacement of fluid.
c) inotropes such as norepinephrine and dobutamine to
improve cardiac output and renal perfusion.
d) Dopamine may be harmful.
e) Diuretic agents like furosemide
f) Renal replacement therapy: like hemodialysis
COMPLICATIONS
•Metabolic acidosis
•Hyperkalemia
•pulmonary edema
•end-stage renal failure
requiring lifelong dialysis or a
kidney transplant.
QUESTION
For each of the following questions, choose the
pathophysiologic mechanism of reduced
glomerular filtration rate (GFR).
A. Acute tubular necrosis
B. Decreased relaxation of afferent arterioles
C. Glomerulonephritis
D. Hypovolemia
E. Increased relaxation of efferent arterioles

QUESTION 1

A 55 yo male has a history of HTN and MI. He is
seen in the clinic to follow up on his blood
pressure. There are no sxs. The patient’s
current medical regimen includes amlodipine,
hydrochlorothiazide, and atenolol. Blood
pressure is measured at 165/83 in both arms.
The remainder of the physical examination is
notable for an abdominal bruit. Lisinopril is
added to the regimen. One week later blood work
shows a creatinine that has risen from 1.3mg/dL
to 5.0 mg/KL
ANSWER E: INCREASED RELAXATION
OF THE EFFERENT ARTERIOLES
Decreased renal perfusion, or pre-renal failure, is
a common cause of renal failure and is often
rapidly reversible. GFR is manteined at a
constant state by PG → relax Afferent arteriole,
and Ang II → contract Efferent arteriole (EA).
 An ACEI (Lisinopril) → decrease Ang II →
increase relaxation of EA → decrease GFR →
increase creatinine.

QUESTION 2

An 88-year-old female is admitted to the hospital
after being found in her apartment with altered
mental status by family members. Physical
examination is notable for delirium, poor skin
turgor and dry MM. BUN is 63mg/dL, and
creatinine is 1.3 mg/dL.
ANSWER: D , HYPOVOLEMIA

Classic presentation of dehydration with poor
skin turgor and dry MM. In light of her advance
age, a creatinine of 1.3 mg/dL reflects very poor
renal functon.
CHRONIC KIDNEY
DISEASE (CKD), ALSO
KNOWN AS CHRONIC
RENAL DISEASE
progressive loss
of renal function
over a period of
months or years.
IRREVERSIBLE
Causes
•diabetic nephropathy,
• hypertension
• glomerulonephritis.
•HIV nephropathy.
•PCKD
CLASSIFICATION
Vascular-renal artery stenosis -ischemic
nephropathy, hemolytic-uremic syndrome and
vasculitis
2. Glomerular-focal segmental glomerulosclerosis
and IgA nephritis
diabetic nephropathy and lupus nephritis
3. Tubulointerstitial including polycystic kidney
disease, drug and toxin-induced chronic
tubulointerstitial nephritis and reflux
nephropathy
4. Obstructive such as with bilateral kidney stones
and diseases of the prostate
5. On rare cases, pin worms infecting the kidney can
also cause idiopathic nephropathy.
1.
Signs and symptoms
•increase in serum creatinine or
protein in the urine
•hypertension and/or suffering from
congestive heart failure
•Urea accumulates, leading to
azotemia and ultimately uremia
(symptoms ranging from lethargy to
pericarditis and encephalopathy).
•Urea is excreted by sweating and
crystallizes on skin ("uremic frost").
•Hyperkalemia : symptoms malaise and
potentially fatal cardiac arrhythmias
•Erythropoietin decreased = anemia, which
causes fatigue
•Fluid volume overload - mild edema to lifethreatening pulmonary edema
•Hyperphosphatemia - due to reduced
phosphate excretion
•hypocalcemia (due to vitamin D3 deficiency)tetany.--progresses to tertiary
hyperparathyroidism, with hypercalcaemia,
renal osteodystrophy and vascular
calcification that further impairs cardiac
function.
•Metabolic acidosis, due to accumulation
of sulfates, phosphates, uric acid etc. This
may cause altered enzyme activity by
excess acid acting on enzymes and also
increased excitability of cardiac and
neuronal membranes by the promotion of
hyperkalemia due to excess acid
(acidemia)
•accelerated atherosclerosis
•Cardiovascular disease-worse prognosis
DIAGNOSIS
•It is important to differentiate CKD from acute
renal failure (ARF) because ARF can be reversible.
•gradual rise in serum creatinine (over several
months or years) as opposed to a sudden increase in
the serum creatinine (several days to weeks).
•Abdominal ultrasound CKD KIDNEYS ARE
SMALLER THAN NL (LESS THAN 9CM), except in
DM nephropathy or PCKD
•nuclear medicine MAG3 scan to confirm blood flows
and establish the differential function between the
two kidneys. DMSA scans are also used in renal
imaging; with both MAG3 and DMSA being used
chelated with the radioactive element Technetium99.
PCKDCKD
TREATMENT
There is no specific treatment
unequivocally shown to slow the worsening of
chronic kidney disease.
If there is an underlying cause to CKD, such
as vasculitis, this may be treated directly with
treatments aimed to slow the damage.
 In more advanced stages, treatments may be
required for anemia and bone disease.
 Severe CKD requires one of the forms of
renal replacement therapy; this may be a form
of dialysis, but ideally constitutes a
 kidney transplant.[1]
TREATMENT
•The goal of therapy is to slow down or halt the
otherwise relentless progression of CKD to stage
5.
•Control of blood pressure (ACEIS, OR ARBs) as
they have been found to slow the progression of
CKD to stage 5
•erythropoietin and vitamin D3, calcium.
•Phosphate
•stage 5 CKD, renal replacement therapy is
required, in the form of either dialysis or a
transplant.
•dietary modifications includes limiting protein
intake.
QUESTION #1
A 57 yearold man is on maintenance
hemodialysis for chronic renal failure. Which
of the following metabolic derangement can be
anticipated
A.Hypercalcemia
B.Hypophosphatemia
C.Osteomalacia
D.Vitamin D excess
E.Hypoparathyroidism
ANSWER
C. Osteomalacia
Chronic renal failure treated with hemodialysis results
in predictable metabolic abnormalities. The kidneys fail
to excrete phosphate, leading to hyperphosphatemia
and fail to excrete phosphate, leading to
hyperphosphatemia, and fail to syntehsize 1,25
(OH)2D3. Vitamin D deficiency causes impaired
interstitial calcium absorption. Phosphate retention,
defective intestinal absorption, and skeletal resistance
to parathyroid hormone all results in hypocalcemia.
Hypocalcemia causes secondary hyperparathyroidism,
and the excess PTH production worsens the
hyperphosphatemia by increasing phosphorus release
from bone. These derangements impair collagen
synthesis and maturation, resulting in skeletal
abnormalities collectively reffered to as renal
osteodystrophy. Osteomalacia, osteosclerosis, and
osteitis fribrosa cystica may all be seen. (Kasper et al.,
2005, pp. 1656-1657).
QUESTION #2
A 60 year old patient with long-standing diabestes
has a creatinine of 3.6 which has been stable for
several years. Which of the following antibiotics
requires the most dosage modification in chronic
renal failure?
A.
B.
C.
D.
E.
Tetracycline.
Gentamicin
Erythromycin
Nafcillin
Choramphenicol.
ANSWER
B. Gentamicin
Many drug require dosage modifications in chronic
renal insufficiency. Bioavailability, distribution, action,
and elimination of drugs all may altered. Drug that are
nephrotoxic may be contraindicated or used only with
extreme care in renal insuficiency. The aminoglycosides, vancomycin, ampicillin, most cephalosporins,
methicillin, penicillin G, sulfonamides, and
trimethoprim all should be given in reduced dosage to
patients with chronic renal failure. The aminoglycosides
and vancomycin can be nephrotoxic and should be used
with caution in renal insufficiency. The small group of
antibiotics not needing dosage modification includes
chloramphenicol, erythromycin, the isoxazolyl
penicillins (nafcilllin and oxacillin) and moxifloxacin.
(Kasper et al., 2005, p. 1662, 19).
“What is man but an ingenious
machine designed to turn with
‘infinite artfulness’, the red
wine of shiraz into urine” …!
Isak Denison