ACUTE & CHRONIC

KIDNEY FAILURE
By Randall Feather and Brett Burtenshaw
Internal Medicine
09/20/2010
ACUTE KINEY FAILURE or
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
b. Absolute increase in serum
creatinine of ≥0.3 mg/dl
Percentage increase in serum
creatinine of ≥50%
c. 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
 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
 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 under-replacement 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
1. Vascular-renal artery stenosis
-ischemic nephropathy, hemolytic-
uremic syndrome and vasculitis
2.Glomerular-focal segmental
glomerulosclerosis and IgA nephritis
3.Diabetic nephropathy and lupus
nephritis
4.Tubulointerstitial including
polycystic kidney disease, drug and
toxin-induced chronic
tubulointerstitial nephritis and
reflux nephropathy
5.Obstructive such as with bilateral
kidney stones and diseases of the
prostate
 Signs and symptoms
•Increase in serum creatinine
or protein in the urine
•Hypertension and/or
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
•Hyperkalemia : symptoms malaise and
potentially fatal cardiac arrhythmias
•Erythropoietin decreased = anemia,
which causes fatigue
•Fluid volume overload - mild edema to
life-threatening 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
 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
PCKD-
CKD
 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
 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 year old 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. Tetracycline.
B. Gentamicin
C. Erythromycin
D. Nafcillin
E. 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 amino-glycosides,
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).