Chapter 133: Renal Function Evaluation and the Approach to the Patient with Acute Renal Failure

1
Chapter 133 Renal Function Evaluation and the
Approach to the Patient with Acute Renal
Failure

• ?????? ??????

2
INTRODUCTION(1)

• The kidneys for the excretion of end-products
  of metabolism ( urea, creatinine, and uric acid)
  and for control of the concentration of many body
  fluid constituents ( Na, K, Cl-, and H).
• The glomerular filtrate contains virtually no
  RBCs, and its composition is similar to that of
  interstitial fluid except that it has a protein
  concentration only one two-hundredth that of
  plasma.

3
INTRODUCTION(2)

• More than 99 of the filtrate containing water,
  elec-trolytes, and small molecules (e.g., glucose
  and uric acid) is reabsorbed by the tubules.
• glomerular filtration rate (GFR), averages
  125ml/min in adult men.

4
EMERGENCY DEPARTMENT DIAGNOSTICS

5
Urine Volume

• Urine volume is a poor indicator of renal
  dysfunction.
• Oliguria, defined as a urine volume of 100 to 400
  ml/24 hr.
• Alternating oliguria and anuria is a classic
  indicator of intermittent obstruction that occurs
  as urine collects behind an obstructing stone or
  tumor and then is allowed to flow past as the
  obstructing material shifts position.

6
Urinalysis

• dipstick screening for heme pigment, protein,
  glucose, ketones, and pH (and in some
  laboratories leukocyte esterase or nitrite
  reduction).
• microscopic examination of a spun specimen of
  freshly voided urine.

7
Urinalysis

• Heme
• Heme pigment catalyzes the oxidation of
  ortho-tolidine by peroxidase.
• detects both free hemoglobin or myoglobin(more
  sensitive) and hemoglobin contained in RBCs.
• false-negative vitamin C, dilute urine and in
  urine containing large amounts of protein.
• A positive dipstick result should prompt
  micro-scopic examination of the urine.

8
Urinalysis

• Protein(1)
• The dipstick test using the color change of
  tetra-bromophenol blue, can reliably yield
  positive re-sults when the concentration is
  greater than 30 mg/dl.
• 3 to 5 times more sensitive to albumin than to
  globulins and immunoglobulin light chains.
• False-positive alkaline urine, hematuria, or
  pro-longed immersion of the dipstick in the
  urine.
• False-negative dilute urine.

9
Urinalysis

• Protein(2)
• The sulfosalicylic acid (SSA) test is more
  sensitive to proteinuria (detecting 5 mg/dl of
  nonalbumin or albumin protein).
• False-positive radiographic contrast agents,
  PCN, or sulfonylurea drugs.
• False-negative alkaline urine.
• If the SSA result is significantly more positive
  than the dipstick, a urine electrophoresis should
  be performed to detect nonalbumin proteins( the
  light chains associated with multiple myeloma).

10
Urinalysis

• Microscopic Examination(1)
• 5 RBC/hpf is the threshold of abnormality.
• Large numbers of polymorphonuclear leukocytes
  interstitial nephritis, papillary necrosis, and
  pyelo-nephritis.
• Uric acid crystals uric acid nephropathy.
• Oxalic acid or hippuric acid crystals ethylene
  glycol ingestion.

11
Urinalysis

• Microscopic Examination(2)
• Casts are formed from urinary Tamm-Horsfall
  protein, a product of the tubular epithelial
  cells mixed with albumin, red cells, tubular
  cells, or cellular debris.
• Hyaline casts(devoid of contents) dehydration,
  after exercise, or glomerular proteinuria?
  pre-renal azotemia or obstruction.
• Red-cell casts glomerular hematuria?
  glomerulo-nephritis or vasculitis.
• White-cell casts renal parenchymal inflammation.

12
Urinalysis

• Microscopic Examination(3)
• Granular casts(cellular remnants and debris) and
  renal tubular epithelial cells ? ATN.
• Fatty casts(like oval fat bodies)heavy
  proteinuria and the nephrotic syndrome?glomerular
  disease.
• Eosinophil-containing casts (after staining the
  sediment) ? allergic interstitial nephritis.
• telescoped sediment(a combination of cellular
  casts and broad and waxy casts) ? ongoing damage
  of the remaining nephrons.

13
Serum and Urine Chemical Analysis

• Creatinine and BUN(1)
• Creatinine clearance, parallels GFR closely, can
  be determined from a 24-hour urine collection,
  Clcr (ml/min) urine Cr(mg/dl)volume(ml)/serum
  Cr(mg/dl)time(min).
• The normal range of the serum creatinine level
  extends from 0.5 mg/dl to 1.5 mg/dl. Clcr
  (ml/min)(140- age)IBW (kg) / 72serum
  Cr(mg/dl)(0.85 for women)

14
Serum and Urine Chemical Analysis

• Creatinine and BUN(2)
• Spurious elevations can be caused by
  acetoace-tate (which cross-reacts in the commonly
  used assays) and by certain medications.
• Abrupt cessation of glomerular filtration causes
  the serum creatinine to rise by 1 to 2mg/dl/day.
• ?lt1 mg/dl/day?? some renal function preserved.
• ? gt 2 mg/dl/day ? rhabdomyolysis

15
Serum and Urine Chemical Analysis

• Creatinine and BUN(3)
• ?BUN Increased protein intake, GI bleeding, and
  catabolic effects of fever, trauma, infection, or
  drugs such as tetracycline and corticosteroids.
• ?BUN liver failure or protein malnutrition.
• Once glomerular filtrate has been formed, renal
  urea clearance is largely a function of flow
  rate. Urea clearance is thus decreased in
  patients with prerenal azotemia or acute
  obstruction, despite preservation of tubular
  function ? the ratio of the BUN to the serum
  creatininegt 101.

16
Serum and Urine Chemical Analysis

• Urine Sodium and Fractional Excretion of Sodium
• Normally, urine Na (UNa) concentration parallels
  Na intake. Low urine Na concentration thus
  indicates not only intact reabsorptive function
  but also the presence of a stimulus to conserve
  Na
• The FENa, defined as (UNa/PNa)/(UCr/PCr) 100,
  reflects the fraction of filtered sodium that
  escapes reabsorption and is excreted in the
  urine.

17
Serum and Urine Chemical Analysis

• Urine Sodium and Fractional Excretion of Sodium

18
Serum and Urine Chemical Analysis

• Urine Sodium and Fractional Excretion of Sodium
• Causes of High or Low FENa and UNa in Patients
  with ARF
• UNa lt20 mEq/L, FENa lt1
• Prerenal azotemia
• Acute glomerulonephritis
• Acute obstruction
• Contrast-induced ATN (Some cases)
• Rhabdomyolysis-associated ATN (some cases)
• Early sepsis
• Nonoliguric ATN (10 of cases)
• UNa gt40 mEq/L, FENa gt1
• ATN (90 of cases)
• Chronic obstruction
• Diuretic drugs
• Osmotic diuresis
• Underlying chronic renal failure

19
Imaging Studies

• Intravenous pyelography (IVP)
• The classic findings of obstruction
• kidneys that are normal to large in size
• nephrograms that become increasingly dense (for
  up to 24 hours after contrast injection)
• delayed opacification of dilated collecting
  systems.
• further significant decrease in renal function
  (serum Crgt 2.5 mg/dl 33 VS a normal Cr 2)
• The newer nonionic contrast agents have the same
  potential for nephrotoxicity.

20
Imaging Studies

• Ultrasonography
• Dilatation of the collecting system is generally
  apparent within 24 to 36 hours of the onset of
  obstruction.
• Detecting intrarenal and ureteral calculi.

21
Imaging Studies

• Computed tomography (CT scan)
• Hydronephrosis and dilated ureters can be seen
  with-out contrast enhancement.
• The cause of obstruction (e.g., lymphoma,
  retroperi-toneal hemorrhage, metastatic cancer,
  or retroperi-toneal fibrosis) can be delineated.
• Visualizing ureteral obstruction at the level of
  the bony pelvis.
• Bilateral ureteral obstruction produced by
  malignancy or retroperitoneal fibrosis is the
  most important cause of the nondilated
  obstructive uropathy.
• When noninvasive studies produce negative
  results, the diagnosis must be made by RP or by
  AP via a percuta-neous nephrostomy.

22
APPROACH TO HEMATURIA

23
APROACH TO HEMATURIA

• Painless hematuria is estimated to occur in the
  general population at an incidence of 3 to 4.
• The causes of hematuria can be divided into
  hematologic, renal (glomerular or nonglomerular),
  and postrenal causes(Box 133-2).
• The most common causes of hematuria
• 1. kidney stones
• 2. carcinoma of the kidney or bladder
• 3. urethritis
• 4. urinary tract infection
• 5. benign prostatic hypertrophy (BPH)
• 6. glomerulonephritis.

24
APROACH TO HEMATURIA
25
APROACH TO HEMATURIA

• the Pattern and Character of the Hematuria
• on initiation of voiding ? a urethral source.
• in the last few drops of urine ? a prostatic or
  bladder neck source.
• Total hematuria ? a source in the bladder,
  ureter, or kidney.
• Brown or smoky-colored urine ? a renal source.
• Blood clots ? a nonglomerular renal or lower
  urinary tract source of bleeding.
• cyclic or associated with menses ? endometriosis
  of the ureter or bladder.

26
APROACH TO HEMATURIA

• History
• A recently sore throat ? PSGN.
• A history of foreign travel or residence abroad ?
  schistosomiasis or tuberculosis.
• Medication ? AIN , papillary necrosis, or
  hemorrhagic cystitis.
• Anticoagulant use
• Family history ? polycystic or other familial
  kidney disease, sickle cell disease, or renal
  calculi.
• A history of strenuous exercise

27
APROACH TO HEMATURIA

• Symptoms
• Flank pain ? calculus, neoplasm, renal
  infarction, obstruction, or infection.
• Frequency, dysuria, or suprapubic pain ? cystitis
  or urethritis.
• In adult men, perineal pain, dysuria,and terminal
  hematuria ? prostatitis.
• Symptoms suggestive of a multisystem disorder
  (e.g., systemic lupus erythematosus) should also
  be sought.

28
APROACH TO HEMATURIA

• Sign(PE)
• Endocarditis (new heart murmur) or atrial
  fibrillation (irregular rhythm) ? renal embolism.
  
• CV angle tenderness ? pyelonephritis or stone
  disease.
• A palpably enlarged kidney ? polycystic kidney
  disease or renal malignancy.
• The prostatic examination ? prostatitis, BPH, or
  cancer.
• Examination of the external genitalia ? a
  urethral meatal lesion.
• PV examination ? vulvovaginal sources.

29
APROACH TO HEMATURIA

• Urinalysis
• Red urine ( dipstick-negative and free of RBCs) ?
  ingestion of beets, red berries, or food
  coloring by urate crystals or by drugs such as
  phenazo-pyridine (Pyridium) and rifampin.
• Red-cell casts, other casts, or lipiduria or
  significant proteinuria hematuria ? intrinsic
  renal diseases.
• Hematuria pyuria or bacteriuria ? UTI
• Even if WBC(-) or organisms(-) ?do U/C to rule
  out hemorrhagic cystitis, esp. with lower tract
  symptoms.
• Eosinophiluria (on Wrights stain or Hansels
  stain) ? AIN.

30
APROACH TO HEMATURIA

• Gross hematuria ? cystoscopy.
• R/O renal colic or other disorders of the upper
  urinary tract (e.g., polycystic kidney disease,
  tumor, or obstruction) ? IVP or US ?no upper
  tract lesions ? cystoscopy.
• Most patients above the age of 40 should undergo
  a thorough evaluation after even a single episode
  of hematuria.
• In 5 to 10 of cases no cause can be determined.

31
APPROACH TO PROTEINURIA

32
APPROACH TO PROTEINURIA

• Definition
• Abnormal proteinuria is as excretion of more
  than 150 mg/24 hr in adults.
• more than 140 mg/m2/24 hr in children.

33
APPROACH TO PROTEINURIA

• Classification
• Glomerular proteinuria
• The more common type.
• Results from increased permeability of the
  glomerular capillaries to plasma proteins.
• Protein losses of 10 g or more per day are not
  uncommon

34
APPROACH TO PROTEINURIA

• Classification
• Tubular proteinuria
• Normal glomeruli.
• Smaller proteins that are normally filtered at
  the glomerulus and then reabsorbed in the tubule
  appear in the urine because of tubular or
  interstitial abnormality.
• E.g. urinary tract obstruction, sickle cell
  disease, and other causes of acute or chronic
  interstitial nephritis.
• Daily urinary protein losses rarely exceed 2 g.

35
APPROACH TO PROTEINURIA

• Classification
• Overflow proteinuria
• Urinary loss of small proteins that are present
  in the blood in excessive concentrations and
  appear in the glomerular filtrate in amounts
  exceeding the normal tubular reabsorptive
  capacity (e.g., the light chains produced in
  multiple myeloma).

36
APPROACH TO PROTEINURIA

• Classification
• Transient proteinuria
• Exertion.
• Stress.
• Fever.
• pregnancy (excretion of up to 300 mg protein/day
  can occur).

37
APPROACH TO PROTEINURIA

• Classification
• Orthostatic proteinuria
• During periods when the patient is upright but
  not during recumbency
• Usually transient and benign.
• Excretion of more than 2 g protein/24 hr is
  likely to be caused by a glomerular process,
  whereas less than 2 g is typical of tubular,
  overflow, or orthostatic proteinuria

38
APPROACH TO PROTEINURIA

• Nephrotic syndrome
• Hypoalbuminemia
• Edema
• Nephrotic range proteinuria Greater than 3.5
  g/24 hr.
• Hyperlipidemia.
• Risk for thromboembolic events, including DVT,
  RVT, and pulmonary embolism (hypercoagulable
  state that may be related in part to urinary loss
  and decreased plasma levels of antithrombin III
  and fibrinolytic factors)

39
APPROACH TO PROTEINURIA

• In young female patients, the possibility of
  pregnancy should be kept in mind, since pregnancy
  can exacerbate previously inapparent renal
  disease in late pregnancy, proteinuria may be
  the first sign of preeclampsia.
• Proteinuria RBCs and red-cell casts ? GN.
• Proteinuria pyuria ? AIN.
• Proteinuria glycosuria ? diabetic nephropathy.

40
ACUTE RENAL FAILURE

41
ACUTE RENAL FAILURE

• Acute renal failure (ARF) is a generic term used
  to describe a precipitous decline in kidney
  function.
• Its hallmark is progressive azotemia.
• These include metabolic derangements (e.g.,
  metabolic acidosis and hyperkalemia),
  disturbances of body fluid balance (particularly
  volume overload), and a variety of effects on
  almost every organ system (Box 133-4).

42
ACUTE RENAL FAILURE
43
Prerenal Azotemia

• Characterized by
• 1. increased urine specific gravity
• 2. BUN/Cr ratio gt101
• 3. urine sodium concentration lt20 mEq/dl
• 4. FENa lt1.
• The condition can generally be corrected readily
  by 1. expanding ECF volume,
• 2. augmenting cardiac output, or
• 3. discontinuing vasodilating
  antihypertensive drugs.

44
Prerenal Azotemia

• severe prolonged prerenal azotemia can eventuate
  in ATN.
• Patients who have CHF or cirrhosis form an
  important subset of those with prerenal azotemia.
  These individuals are often salt- and
  water-overloaded, yet their effective
  intraarterial volume is decreased. Administration
  of diuretics has the potential to decrease
  intravascular volume further, with decreased
  glomerular filtration and prerenal azotemia the
  result. For some patients with advanced CHF or
  hepatic disease, a state of chronic stable
  prerenal azotemia may be the best achievable
  compromise between symptomatic volume overload
  and severe renal hypoperfusion.

45
Prerenal Azotemia

• Glomerular perfusion may also be decreased in
  patients with normal intravascular volume and
  normal renal blood flow who take ACEI or, more
  commonly, prostaglandin inhibitors (e.g. NSAIDs).
  Renal vasodilator prostaglandins are critical in
  maintaining glomerular perfusion in patients with
  conditions such as CHF, chronic renal
  insufficiency, and cirrhosis, in which elevated
  circulating levels of renin and angiotensin II
  act to diminish renal blood flow and GFR. Other
  risk factors include advanced age, diuretic use,
  renovascular disease, and diabetes. Renal
  insufficiency secondary to NSAIDs, is generally
  reversible after cessation of the causative
  agent.

46
Postrenal (Obstructive) ARF

• Obstruction is an reversible cause ARF.
• Most commonly produced by BPH or by functional
  bladder neck obstruction (medication side effects
  or neurogenic bladder).
• Intrarenal obstruction may result from
  intratubular precipitation of uric acid crystals
  (tumor lysis), oxalic acid (ethylene glycol
  ingestion), myeloma proteins, methotrexate, or
  acyclovir.
• Bilateral ureteral obstruction may be caused by
  retroperitoneal fibrosis,tumor, surgical
  misadventure, stones, or blood clots.
• A sudden deterioration of renal function in DM,
  analgesic nephropathy, or sickle cell disease
  suggest papillary necrosis.

47
Intrinsic Acute Renal Failure

• These entities are responsible for only 5 to 10
  of cases of ARF in adult inpatients the vast
  majority are due to ATN.
• There is a much greater incidence of glomerular,
  interstitial, and small vessel disease in adults
  who develop ARF outside the hospital.
• In children these entities account for about one
  half of cases of ARF

48
Intrinsic Acute Renal Failure

• Glomerular Disease
• Hematuria, proteinuria (500 mg to 3 g/day, is not
  uncommon), or red cell casts are very suggestive
  of GN in fact, red cell casts are essentially
  diagnostic of active glomerular disease but
  rarely seen with other types of renal disease.
• Conversely, the absence of RBC casts,
  proteinuria, and hematuria essentially excludes
  AGN as the cause of ARF.
• The specific diagnosis of AGN caused by primary
  renal disease is often ultimately made by renal
  biopsy.

49
Intrinsic Acute Renal Failure

• Interstitial Disease
• AIN is most commonly precipitated by drug
  exposure(penicillins, diuretics, anticoagulants,
  and NSAIDs) or by infection(bacterial, fungal,
  proto-zoan, and rickettsial infections).
• classically presents with rash,fever,eosinophilia,
  and eosinophiluria.
• Pyuria, gross or microscopic hematuria, and mild
  proteinuria are observed in some cases.
• A definite diagnosis can be made only on renal
  biopsy. Treatment of AIN is directed at removing
  the presumed cause Renal function generally
  returns to baseline over several weeks, although
  chronic renal failure has been reported to occur.
  

50
Intrarenal Vascular Disease

• Large vessel
• Renal artery thrombosis or stenosis
• Renal vein thrombosis
• Atheroembolic disease
• Small and medium vessel
• Scleroderma
• Malignant hypertension
• Hemolytic uremic syndrome
• Thrombotic thrombocytopenic purpura

51
Intrarenal Vascular Disease

• The cause of thrombosis is trauma, after
  angio-graphy and to aortic or renal arterial
  dissection.
• Scleroderma renal crisis
• malignant hypertension and rapidly progressive
  renal failure.
• vascular involvement of the medium-sized vessels,
  such as scleroderma, often spares the
  preglomerular vessels and tends not to produce an
  active urine sediment. Extrarenal manifestations
  (rash, fever, arthritis, pulmonary symptoms) are
  usually evident.
• Specific therapy with angiotensin-converting-enzym
  e inhibitors

52
Acute Tubular Necrosis

• Refers to a generally reversible deterioration of
  kidney function associated with any of a variety
  of renal insults.
• Oliguria may or may not be a feature.
• The diagnosis is made after prerenal and
  postrenal causes of ARF and disorders of
  glomeruli, interstitium, and intrarenal
  vasculature have been excluded.
• The most common precipitant of ATN is renal
  ischemia during surgery or after trauma.

53
Acute Tubular Necrosis

• Causes of acute tubular necrosis
• Ischemia
• Shock
• Sepsis
• Third spacing (e.g. 75 of major burns,
  heatstroke )
• All causes of severe prerenal azotemia (e.g.
  HHNK)
• Nephrotoxins
• Antibiotics and NSAIDs
• Radiographic contrast agents
• Pigment (myoglobin, hemoglobin)

54
Causes of Pigment-Induced Acute Renal Failure

• Rhabdomyolysis and myoglobinuria
• Vigorous exercise
• Arterial embolization
• Status epilepticus
• Status asthmaticus
• Coma- and pressure-induced myonecrosis
• Heat stress
• Diabetic ketoacidosis
• Myopathy
• Alcoholism
• Hypokalemia
• Hypophosphatemia

• Hemoglobinuria
• Transfusion reactions
• Snake envenomation
• Malaria
• Mechanical destruction of RBCs by prosthetic
  valves
• G6PD deficiency
• only in the presence of coexisting dehydration,
  acidosis, or decreased renal perfusion.
• ATN may be produced by the hemolysis of as 100
  ml blood

55
ATN associated with rhabdomyolysis

• Often oliguric.
• Characterized by rapid increases in
• Serum creatinine (increments of gt2 mg/dl/day)
• BUN/Crlt101.
• Serum potassium.
• Serum phosphorus.
• Serum uric acid (may accumulate to levels high
  enough to suggest acute uric acid nephropathy.).
• Serum CPK is a much more sensitive test than
  urine dipstick (a positive result for heme in
  only 50).
• No biochemical parameter can be used to predict
  in which patients who have rhabdomyolysis ARF
  will develop. (eg.CPK, myoglobinuria,
  hyperkalemia)

56
Aminoglycosides

• Nephrotoxicity is correlated with higher doses
  and longer duration of therapy, increased age,
  impaired renal function, dehydration, and
  exposure to other nephrotoxins.
• It has been suggested that once-a-day
  administration of a somewhat higher dose is
  associated with less nephrotoxicity
• Clinically significant renal dysfunction usually
  occurs only after several days and often after
  more than a week of therapy. However, renal
  failure can develop as long as 10 days after a
  drug has been discontinued.

57
Radiographic contrast agents

• A common cause of hospital-acquired renal
  insufficiency.
• Renal failure produced by these agents may be
  defined as an increase in serum creatinine level
  of 50 over baseline, with a temporal relation to
  contrast medium administration and in the absence
  of other identifiable causes.
• The highest incidence is that after
  arteriography.
• Typically an increase in the serum Cr is noted
  within 3 d of exposure, with a return to normal
  within 10 to 14 d.

58
Radiographic contrast agents

• The most important risk factors for
  contrast-induced ATN are
• preexisting renal insufficiency (gt2.5 mg/dl or
  gt1.5mg/dl in diabetics)
• multiple myeloma, particular with dehydration
• age greater than 60 years
• volume depletion
• higher doses of contrast material (gt2ml/kg)
• repeated doses of contrast material (lt72hr)

59
APPROACH TO THE PATIENT WITH AZOTEMIA OR ACUTE
RENAL FAILURE

60
ARF VS CRF

• Old records and laboratory results are
  invaluable.
• The finding of small kidneys on abdominal
  radiography or of the bony changes of secondary
  hyperparathyroidism on hand films suggests that
  renal failure is chronic.
• Anemia, hypocalcemia, and hyperphosphatemia, on
  the other hand, should not be relied on to
  identify patients who have CRF since these
  abnormalities can develop rapidly in ARF

61
General Management

• Patients who have oliguric ARF have a
  significantly higher mortality rate and a much
  greater risk of complications than those who are
  not oliguric
• Recovery from oliguric ATN occurs after an
  average of 15-25 days, versus 5-10 days for
  nonoliguric ATN.
• Since nonoliguric patients are easier to manage,
  an attempt to increase urine flow is warranted.
  Such an attempt is successful 30 to 50 of the
  time.

62
General Management

• The of furosemide is 2 to 6 mg/kg IV (maximum 400
  mg), but there is an increased risk of
  ototoxicity at the higher doses, and if the
  patient does not respond with an increase in
  urine output, additional doses are not helpful.
• The recommended dose of mannitol is 12.5 to 25 g
  IV. If urine output does not increase, further
  doses may cause hyperosmolality and clinically
  significant intravascular volume overload in
  patients with impaired renal function.
• Dopamine (1 to 3 mg/kg/min) , with and without
  furosemide, is in an effort to increase urine
  output, but its efficacy has not yet been
  validated in prospective studies.

63
Pigment-induced ATN

• Avoidance of hemolysis and muscle injury.
• Aggressive volume repletion.
• Alkalinization (myoglobin precipitates in an acid
  urine but not in an alkaline urine).
• Mannitol infusion (to reduce the likelihood of
  ARF and to control hyperkalemia).
• Furosemide has not consistently shown a
  beneficial effect.
• Early dialysis may be required to control rapidly
  developing hyperkalemia, hyperphosphatemia, and
  hyperuricemia.

64
Contrast-induced ATN

• Require only supportive therapy but should be
  hospitalized and seen by a nephrologist.
• Volume replete before the study.
• The administered dose of contrast should be kept
  as low as possible.
• Multiple studies should be avoided.
• Concomitant use of other nephrotoxins should be
  avoided.
• Mannitol given before or just after contrast
  administration may be protective

65
Volume and Metabolic Complications

• Hyperkalemia(1)
• The most common metabolic cause of death in
  patients with ARF.
• Although some hyperkalemic patients note muscular
  weakness, the vast majority are generally
  asymptomatic until major manifestations of
  cardiotoxicity supervene.
• If the serum potassium level is greater than 6.5
  mEq/L, and particularly if ECG changes are
  present, urgent intervention is necessary.

66
Volume and Metabolic Complications

• Hyperkalemia(2)
• IV calcium (10 ml 10 calcium gluconate or
  calcium chloride over 2 minutes) for reversing
  cardiotoxicity.
• IV insulin with glucose.
• IV bicarbonate(caution with volume overload and
  hypocalcemic tetany or seizures)
• Inhaled albuterol.
• Using a potassium-binding ion exchange resin
  Kayexalate, by enhancing urinary potassium
  excretion, or by dialysis.

67
Volume and Metabolic Complications

• Hypocalcemia
• Vitamin D-dependent intestinal absorption of
  calcium is decreased in ARF because of decreased
  renal synthesis of 1,25-dihydroxyvitamin D.
• Another factor promoting hypocalcemia is the
  complexing of calcium with retained phosphate
  rhabdomyolysis-associated ARF in particular is
  often associated with the deposition of complexed
  calcium in muscle and other tissues.
• Incipient or frank tetany should be treated with
  intravenous calcium (10 to 20 ml 10 calcium
  gluconate over several minutes).

68
Volume and Metabolic Complications

• Hyperphosphatemia
• Resulting from decreased renal elimination of
  phosphate.
• Usually ranges from 6 to 8 mg/dl but may be much
  higher with rhabdomyolysis or in catabolic
  states.
• A calcium-phosphate product greater than 70 may
  result in metastatic soft tissue calcification.
• Hyperphosphatemia is often treated with oral
  aluminum-based antacids that bind ingested
  phosphate in the gut.

69
Volume and Metabolic Complications

• Metabolic acidosis
• Compensatory hyperventilation may be mistakenly
  attributed to primary cardiac failure or volume
  overload.
• Treatment is not generally necessary if the serum
  bicarbonate level is greater than 10 mEq/L.
• Overzealous correction may result in hypokalemia,
  hypocalcemia, or volume overload.
• Hypermagnesemia
• Magnesium-containing antacids or laxatives should
  be avoided in the therapy of ARF.

70
Volume and Metabolic Complications

• Hyperuricemia
• Typically in the range of 9 to 12 mg/dl, results
  from decreased renal clearance but may be much
  higher in catabolic patients.
• For reasons that are unclear, gout rarely
  complicates ARF.
• A urinary uric acid/creatinine ratio in excess of
  1 suggests that hyperuricemia is the cause,
  rather than the result, of ARF.
• Diuretics, alkalinization of the urine, and
  dialysis may be necessary.

71
Volume and Metabolic Complications

• Intravascular volume depletion
• Some nonoliguric patients excrete salt and water
  sufficiently well that intravascular volume
  depletion occurs if adequate fluid replacement is
  not provided.
• This prolongs recovery from ARF.
• Volume overload
• Responsible for the hypertension often seen in
  ARF and frequently leads to congestive heart
  failure and pulmonary edema.
• Treated with diuretics or IV nitroglycerin while
  preparations are being made to initiate dialysis.
  

72
Organ System Effects

• Infections
• Uremia impairs host defenses, particularly
  leukocyte function. Infection occurs in 30 to
  70 of patients with ARF and is a significant
  cause of morbidity and mortality.
• Thus, patients with fever require prompt
  investigation and aggressive treatment

73
Organ System Effects

• Pericarditis
• Prevalence of 12 to 20 in dialyzed patients
  with ESRD.
• May also occur in patients with ARF.
• Chest pain that is worse in a recumbent position
  is the most common symptom.
• Pericarditis or pericardial effusion is generally
  an indication for the urgent initiation of
  dialysis in ARF.
• Hemodynamically significant tamponade require
  surgical drainage of the effusion or,
  occasionally, emergency pericardiocentesis.

74
Organ System Effects

• Neurologic abnormalities
• May be precipitated by electrolyte abnormalities,
  medications, or uremia.
• Common symptoms in uremic patients include
  lethargy, confusion, agitation, asterixis,
  myoclonus, and seizures.
• GI abnormalities
• Anorexia, nausea, vomiting, gastritis, and
  pancreatitis are also associated with ARF.
• GI hemorrhage is seen in 10 to 30 of patients
  it results from a combination of stress and
  impaired hemostasis. GI hemorrhage is the second
  leading cause of death in ARF.

75
Organ System Effects

• Normocytic normochromic anemia
• Impaired erythropoiesis, shortened red blood cell
  survival, hemolysis, hemodilution, and
  gastrointestinal blood loss all play a role.
• Bleeding tendency
• Qualitative defect in platelet function
• The prolonged bleeding time can be corrected
  pharmacologically
• Infusion of 10 U cryoprecipitate normalizes the
  bleeding time in 1 to 2 hours, with a return to
  baseline in 24 hours.
• Administration of desmopressin acetate (DDAVP)
  shortens the bleeding time for 4 hours.