ACUTE

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ACUTE CHRONIC KIDNEY FAILURE

• By Maritza I. Garcia-Duran Joao Mc-Oneil
• Internal Medicine
• 06/21/2010

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ACUTE KINEY FAILURE a.k.a. Acute Kidney Injury
(AKI)

• rapid loss of kidney function
• REVERSIBLE

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CAUSES
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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

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DIAGNOSIS

• Rapid time course (less than 48 hours)
• Reduction of kidney function
• Rise in serum creatinine
• Absolute increase in serum creatinine of
  0.3 mg/dl
• Percentage increase in serum creatinine of 50
• Reduction in urine output, defined as lt0.5
  ml/kg/hr for more than 6 hours (about 210mL in 6
  hours)

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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

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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

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• Specific therapies
• intravenous fluids is typically the first step to
  improve renal function.
• Volume status may be monitored with the use of a
  central venous catheter to avoid over- or
  under-replacement of fluid.
• inotropes such as norepinephrine and dobutamine
  to improve cardiac output and renal perfusion.
• Dopamine may be harmful.
• Diuretic agents like furosemide
• Renal replacement therapy like hemodialysis

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COMPLICATIONS

• Metabolic acidosis
• Hyperkalemia
• pulmonary edema
• end-stage renal failure requiring lifelong
  dialysis or a kidney transplant.

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QUESTION

• For each of the following questions, choose the
  pathophysiologic mechanism of reduced glomerular
  filtration rate (GFR).
• Acute tubular necrosis
• Decreased relaxation of afferent arterioles
• Glomerulonephritis
• Hypovolemia
• Increased relaxation of efferent arterioles

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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 patients
  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

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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.

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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.

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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.

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Chronic kidney disease (CKD), also known as
chronic renal disease
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progressive loss of renal function over a period
of months or years. IRREVERSIBLE
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• Causes
• diabetic nephropathy,
• hypertension
• glomerulonephritis.
• HIV nephropathy.
• PCKD

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CLASSIFICATION

• Vascular-renal artery stenosis -ischemic
  nephropathy, hemolytic-uremic syndrome and
  vasculitis
• Glomerular-focal segmental glomerulosclerosis and
  IgA nephritis
• diabetic nephropathy and lupus nephritis
• Tubulointerstitial including polycystic kidney
  disease, drug and toxin-induced chronic
  tubulointerstitial nephritis and reflux
  nephropathy
• Obstructive such as with bilateral kidney stones
  and diseases of the prostate
• On rare cases, pin worms infecting the kidney can
  also cause idiopathic nephropathy.

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• 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").

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• 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.

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• 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

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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
  Technetium-99.

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PCKD-CKD
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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

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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.

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QUESTION 1
A 57 yearold man is on maintenance hemodialysis
for chronic renal failure. Which of the following
metabolic derangement can be anticipated

1. Hypercalcemia
2. Hypophosphatemia
3. Osteomalacia
4. Vitamin D excess
5. Hypoparathyroidism

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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).

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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?
• Tetracycline.
• Gentamicin
• Erythromycin
• Nafcillin
• Choramphenicol.

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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).

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• What is man but an ingenious machine designed to
  turn with infinite artfulness, the red wine of
  shiraz into urine !
• Isak Denison