ACUTE RENAL FAILURE

Acute renal failure (ARF) is a common and serious problem in clinical medicine. It is
characterised by an abrupt reduction (usually within a 48-h period) in kidney function.
This results in an accumulation of nitrogenous waste products and other toxins (azotemia). Many
patients become oliguric (low urine output) with subsequent salt and water retention. In patients
with pre-existing renal impairment, a rapid decline in renal function is termed ‘acute on chronic
renal failure’.
The nomenclature of ARF is evolving and the term acute kidney injury (AKI) is being
increasingly used in clinical practice. Urine production of less than 400 mL/day is termed
oliguria, and urine production of less than 50 mL/day is termed anuria.
Classification
The diagnostic criteria for AKI is based on an increase in serum creatinine or the presence of
oliguria. Criteria have recently been introduced for the definition and staging of the condition;
the acronym RIFLE is used (Risk, Injury, Failure, Loss and End-stage renal disease (ESRD)),
which is now becoming established in clinical practice.
The first consensus definition/classification for AKI was the RIFLE classification system, which
categorizes patients into groups based on their change in serum creatinine or GFR from baseline,
or decreased urine output.3 The categories of kidney dysfunction in the RIFLE classification
include patients at risk (R), those with kidney injury (I), and those with kidney failure (F). Two
additional categories of clinical outcomes are sustained loss (L), which requires RRT for at least
4 weeks; and end stage (E), which necessitates RRT for at least 3 months.

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Figure. 1
Pathogenesis
The production and elimination of urine requires three basic physiologic events:
 Blood flow to the glomeruli
 The formation and processing of ultrafiltrate by the glomeruli and tubular cells
 Urine excretion through the ureters, bladder, and urethra
Many conditions can alter these physiologic events leading to AKI. These are classified as
prerenal azotemia, and functional, intrinsic, and postrenal AKI (Table). It is possible for more
than one of these categories to coexist.
Normal renal function depends on adequate renal perfusion.
The kidneys receive up to 25% of cardiac output, which is greater than 1 L/minute of blood flow.
Prerenal azotemia occurs when blood flow to the kidneys is reduced.
 Major causes include decreased intravascular volume (e.g., hemorrhage or dehydration
[including overdiuresis]), decreased effective circulating volume states (e.g., cirrhosis or
heart failure [HF]), hypotensive events (e.g., shock or medication-related hypotension),
and renovascular occlusion or vasoconstriction.
 Because no structural damage occurs to the kidney parenchyma per se, correcting the
underlying cause rapidly restores GFR. Sustained prerenal conditions can result,
however, in glomerular ischemia causing acute tubular necrosis (ATN).

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Functional AKI results when medical conditions or drugs impair glomerular ultrafiltrate
production or intraglomerular hydrostatic pressure.
 Blood travels through the afferent arteriole and enters the glomerulus, where it is filtered,
and exits through the efferent arteriole (Fig.). The afferent and efferent arterioles work in
concert to maintain adequate glomerular capillary hydrostatic pressure to form
ultrafiltrate. Many medications can drastically reduce intraglomerular hydrostatic
pressure and GFR by producing afferent arteriolar vasoconstriction or efferent arteriolar
vasodilation (Fig.)
Intrinsic AKI can occur at the microvascular level of the nephron, glomeruli, renal tubules, or
interstitium.
 Vasculitic diseases (e.g., Wegener granulomatosis, cryoglobulinemic vasculitis) involve
the small vessels of the kidney.
 Glomerulonephritis and systemic lupus erythematosus, although relatively uncommon,
result in glomerular damage. ATN is by far the most common cause of intrinsic AKI. In
fact, the term acute tubular necrosis is often used interchangeably with AKI.
 ATN occurs in part because the renal tubules require high oxygen delivery to maintain
their metabolic activity. Consequently, any condition that causes ischemia to the tubules
(e.g., hypotension, decreased blood flow) can induce ATN.
 Moreover, the tubules may be exposed to exceedingly high concentrations of nephrotoxic
drugs (e.g., aminoglycosides). Interstitial nephritis or inflammation within the renal
parenchyma is most often associated with drug administration (e.g., penicillins).
Postrenal AKI occurs when there is an outflow obstruction in the upper or lower urinary tract.
 Lower tract obstruction is most common and can be caused by prostatic hypertrophy,
prostate or cervical cancer, anticholinergic drugs that cause bladder sphincter spasm, or
renal calculi.
 Upper tract obstruction is less common and occurs when both ureters are obstructed or
when one is obstructed in a patient with a single functioning kidney. Postrenal AKI
usually resolves rapidly after the obstruction has been removed. Post obstructive diuresis
can be dramatic (e.g., 3–5 L/day).

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Figure. 2
Schematic of renal blood flow. Blood enters the glomerulus via the afferent arteriole. The intraglomerular
hydrostatic pressure leads to ultrafiltration across the glomerular into the proximal tubule. The unfiltered
blood leaves the glomerulus via the efferent arteriole. In conditions of decreased renal perfusion, efferent
arteriolar vasoconstriction occurs to increase intraglomerular hydrostatic pressure and maintain ultrafiltrate
production. Afferent arteriolar vasodilation also occurs to improve blood flow into the glomerulus.

Figure. 3

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Drugs that alter renal hemodynamics by causing afferent arteriole vasoconstriction or efferent arteriole
vasodilation. ACEIs, angiotensin-converting enzyme inhibitors; ARBs, angiotensin II receptor blockers; CCBs,
calcium-channel blockers; COX-2, cyclo-oxygenase-2; NSAIDs, nonsteroidal anti-inflammatory drugs.

Clinical evaluation
History and Physical Examination

A thorough physical examination, when used in conjunction with the history, can be invaluable
in confirming the cause of AKI.
1. The patient’s volume status should be evaluated first. Evidence of dehydration (e.g.,
syncope, weight loss, orthostatic hypotension) or decreased effective circulating volume
(e.g., ascites, pulmonary edema, peripheral edema, jugular venous distension) usually
indicates prerenal azotemia. The presence of edema in a patient with normal cardiac
function can, however, signal the early signs of nephrotic syndrome.
2. Concurrent rash and AKI associated with recent antibiotic exposure suggest drug-induced
allergic interstitial nephritis.
3. The clinician should suspect rhabdomyolysis in a patient with trauma or crush injuries
and AKI.
4. An enlarged prostate, painful urination, or wide deviations in urine volume can suggest
obstructive AKI causes.
5. Flank and lower abdominal pain suggest upper obstruction, whereas urinary frequency,
hesitancy, dribbling, and abdominal fullness indicate lower obstruction.

Laboratory evaluation
Common renal function tests
Blood Tests
A. Introduction
1. Renal function may be assessed by measuring blood urea nitrogen (BUN) and serum
creatinine. Renal function decreases with age, which must be taken into account when
interpreting test values.
a. These tests primarily evaluate glomerular function by assessing the glomerular
filtration rate (GFR).

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b. In many renal diseases, urea and creatinine accumulate in the blood because they are
not excreted properly.
c. These tests also aid in determining drug dosage for drugs excreted through the
kidneys.
2. Azotemia describes excessive retention of nitrogenous waste products (BUN and creatinine)
in the blood. The clinical syndrome resulting from decreased renal function and azotemia is
called uremia.
a. Renal azotemia results from renal disease, such as glomerulonephritis and chronic
pyelonephritis.
b. Prerenal azotemia results from such conditions as severe dehydration, hemorrhagic
shock, and excessive protein intake.
c. Postrenal azotemia results from such conditions as ureteral or urethral stones or
tumors and prostatic obstructions.
3. Clearance: a theoretical concept defined as the volume of plasma from which a measured
amount of substance can be completely eliminated, or cleared, into the urine per unit time—can
be used to estimate glomerular function.
B. BUN
1. Urea, an end product of protein metabolism, is produced in the liver. From there, it travels
through the blood and is excreted by the kidneys. Urea is filtered at the glomerulus, where the
tubules reabsorb approximately 40%. Thus, under normal conditions, urea clearance is about
60% of the true GFR.
2. Normal values for BUN range from 8 mg/dL to 18 mg/dL (3.0 to 6.5 mmol/L).
a. Decreased BUN levels occur with significant liver disease.
b. Increased BUN levels may indicate renal disease. However, factors other than
glomerular function (e.g., protein intake, reduced renal blood flow, blood in the
gastrointestinal tract) readily affect BUN levels, sometimes making interpretation of
results difficult.
C. Serum creatinine
1. Creatinine (CR), the metabolic breakdown product of muscle creatine phosphate, has a
relatively constant level of daily production. Blood levels vary little in a given individual.

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2. Creatinine is excreted by glomerular filtration and tubular secretion. Creatinine clearance

parallels the GFR within a range of _ 10% and is a more sensitive indicator of renal damage
than BUN levels because renal impairment is almost the only cause of an increase in the serum
creatinine level.
3. Normal values for serum creatinine range from 0.6 to 1.2 mg/dL (50 to 110 mmol/L).
a. Values vary with the amount of muscle mass—a value of 1.2 mg/dL in a muscular
athlete may represent normal renal function, whereas the same value in a small, sedentary
person with little muscle mass may indicate significant renal impairment.
b. Generally, the serum creatinine value doubles with each 50% decrease in GFR.
For example, if a patient’s normal serum creatinine is 1 mg/dL, 1 mg/dL represents 100%
renal function,
2 mg/dL represents 50% function, and 4 mg/dL represents 25% function.
D. Creatinine clearance
1. Creatinine clearance, which represents the rate at which creatinine is removed from the
blood by the kidneys, roughly approximates the GFR.
a. The value is given in units of milliliters per minute, representing the volume of blood
cleared of creatinine by the kidney per minute.
b. Normal values for men range from 75 to 125 mL/min.
2. Calculation requires knowledge of urinary creatinine excretion (usually over 24 hrs) and
concurrent serum creatinine levels. Creatinine clearance is calculated as follows:

Where ClCR is the creatinine clearance in milliliters per minute, CU is the concentration of
creatinine in the urine, V is the volume of urine (in milliliters per minute of urine formed over the
collection period), and CCR is the serum creatinine concentration.
3. Suppose the serum creatinine concentration is 1 mg/dL, and 1440 mL of urine was collected in
24 hrs (1440 mins) for a urine volume of 1 mL/min. The urine contains 100 mg/dL of creatinine.
Creatinine clearance is calculated as:

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Incomplete bladder emptying and other problems may interfere with obtaining an accurate timed
urine specimen. Thus, estimations of creatinine clearance may be necessary. These estimations
require only a serum creatinine value. One estimation uses the method of Cockcroft and Gault,
which is based on body weight, age, and gender.
a. This formula provides an estimated value, calculated for males as:

b. For females, use 0.85 of the value calculated for males.

c. Example: A 20-year-old man weighing 72 kg has a CCR of 1.0 mg/dL; thus

5. Determination of GFR. The modified diet in renal disease (MDRD) equation is considered a
more accurate measurement of GFR than other equations used to estimate renal function
(e.g., Cockcroft –Gault) in patients with reduced GFR and is used in staging renal disease.
Patients must have a serum creatinine concentration.
a. The MDRD equation for males is as follows:

Where Pcr is serum creatinine. For females, multiply the result by 0.742; for African
Americans, multiply by 1.210.
b. The MDRD has been validated in Caucasians, patients with diabetic kidney disease,
kidney transplant recipients, and African Americans and Asians with nondiabetic kidney
disease.
c. The MDRD equation has not been validated in patients _ 18 years of age, pregnant
women, patients _ 70 years of age, other ethnic groups, patients with normal kidney
function who are at an increased risk for chronic kidney disease, and patients with normal
renal function.

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E. Cystatin C
 Although SCr has long been the primary marker for renal function, cystatin C is a
relatively new biomarker being investigated as a more precise measure of GFR.
 Cystatin C is cleared predominantly through the kidneys, and elevated levels are
observed in patients with declining renal function. Reference ranges for cystatin C are
similar to SCr (≤1.0 mg/L).
 In contrast to SCr, which is produced from muscle cells, cystatin C is produced by the
blood cells and is not significantly influenced by factors such as muscle mass, diet, age,
sex, and race.
 In addition, increases in serum cystatin C levels tend to occur earlier than increases in
SCr, making it possible to detect renal insufficiency in patients at an earlier stage. This is
particularly desirable in patients with diabetes, hypertension, or cardiovascular disease
who may be at higher risk for the development of renal disease.
 Cystatin C is also being evaluated as a potential predictor of cardiovascular disease, and
preliminary research has also been directed at the role of cystatin C in Alzheimer disease
and demyelinating conditions like multiple sclerosis.
Urinalysis
1. The urinalysis is an important diagnostic tool for differentiating AKI into prerenal
azotemia, intrinsic AKI, or obstructive AKI (Table 30-2). The presence of highly
concentrated urine, as determined by elevated urine osmolality and specific gravity,
suggests prerenal azotemia. During dehydrated states, vasopressin (antidiuretic hormone)
is secreted, and the renin-angiotensinaldosterone system (RAAS) is activated. These
mechanisms promote the reabsorption of water and sodium at the collecting duct of the
nephron, which serves to expand the effective circulating volume in an attempt to restore
renal perfusion. As a result of diminished urine volume, the urine osmolality and specific
gravity increase dramatically. Patients with prerenal azotemia and oliguria often have a
urine osmolality greater than 500mOsm/kg. The maximal urine osmolality can exceed
1,200 mOsm/kg.
2. The presence of proteinuria or hematuria can indicate glomerular damage. Nephrotic
syndrome is characterized by urinary protein losses greater than 3.5 g/1.73m2/day.
Proteinuria can also result from tubular damage; that protein loss is rarely over 2 g/day,

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however. The protein content can be used to differentiate glomerular versus tubular
damage. The low-molecular-weight protein, β2-microglobulin, is freely filtered at the
glomerulus and reabsorbed at the proximal tubule. Therefore, the presence of excessive
β2-microglobulin in the urine suggests a tubular source of AKI, such as ATN.
Conversely, albumin is not readily filtered at the glomerulus; hence, the presence of
heavy albuminuria suggests a glomerular source of AKI.
3. White blood cells (WBCs) and WBC casts can indicate an inflammatory process in the
glomerulus, such as acute interstitial nephritis (AIN) or pyelonephritis. Red blood cells
(RBCs) and RBC casts can result from strenuous exercise or can indicate
glomerulonephritis. Allergic interstitial nephritis can be detected by the presence of
urinary eosinophils. Obstructive AKI causes, such as nephrolithiasis, can be identified by
the presence of crystals in the urine.
Urinary chemistries
 The fractional excretion of sodium (FENa) is a measurement of how actively the kidney
is reabsorbing sodium, and it is calculated as the fraction of filtered sodium excreted in
the urine using creatinine as a measure of GFR.
 In prerenal azotemia, the functional ability of the proximal renal tubule remains intact. In
fact, its sodium-reabsorbing abilities are markedly enhanced because of the effects of
circulating vasopressin and activation of the RAAS. Both the FENa and urine sodium
concentration become markedly low (<1% and <20 mEq/L, respectively) in prerenal
conditions.
 In contrast, these indices are elevated in ATN because the renal tubules lose their ability
to reabsorb sodium; the FENa is greater than 2%, and the urine sodium is greater than 40
mEq/L. FENa values between 1% and 2% are generally inconclusive.
Management
 Early preventive and supportive strategies
 Identification of patients at risk
Optimisation of renal perfusion
A diagnosis of acute deterioration of renal function caused by renal underperfusion implies that
restoration of renal perfusion would reverse impairment by improving renal blood flow, reducing
renal vasoconstriction and flushing nephrotoxins from the kidney. The use of crystalloids in the

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form of 0.9% sodium chloride is an appropriate choice of intravenous fluid since it replaces both
water and sodium ions in a concentration approximately equal to serum. The effect of fluid
replacement on urine flow and intravascular pressures should be carefully monitored. However,
fluid loading with 1–1.5 L saline at <0.5 L/h is unlikely to cause harm in most patients who do
not show signs of fluid overload.
Establishing and maintaining an adequate dieresis
Whilst loop diuretics (most commonly furosemide) may facilitate the management of fluid
overload and hyperkalaemia in early or established AKI, there is no evidence that these agents
are effective for the prevention of, or early recovery from, AKI. It is reasonable to use these
agents whilst the urine output is maintained as this provides space for intravenous drugs and
parenteral feeding including oral supplements.
In experimental settings, loop diuretics decrease renal tubular cell metabolic demands and
increase renal blood flow by stimulating the release of renal prostaglandins, a haemodynamic
effect inhibited by NSAIDs. However, there is no demonstrable impact on clinical outcomes.
Indeed, diuretic therapy should only be initiated in the context of fluid overload. If not, any
diuresis might produce a negative fluid balance and precipitate or exacerbate a pre-renal state.
Doses of up to 100 mg/h of furosemide can be given by continuous intravenous infusion. Higher
infusion rates may cause transient deafness. The use of continuous infusions of loop diuretics has
been shown to produce a more effective dieresis with a lower incidence of side effects than seen
with bolus administration.
Non-dialysis treatment of established acute kidney injury
Uraemia and intravascular volume overload
In AKI (and CKD) the symptoms of uraemia include nausea, vomiting and anorexia, and result
principally from accumulation of toxic products of protein metabolism including urea.
Unfortunately, because uraemia causes anorexia, nausea and vomiting, many severely ill patients
are unable to tolerate any kind of diet. In these patients and those who are catabolic, the use of
enteral or parenteral nutrition should be considered at an early stage.
Intravascular luid overload must be managed by restricting NaCl intake to about 1–2 g/day if the
patient is not hyponatraemic and total luid intake to less than 1 L/day plus the volume of urine
and/or loss from dialysis. Care should be taken with the so-called low-salt products, because
these usually contain KCl, which will exacerbate hyperkalaemia.

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Hyperkalaemia
 Hyperkalaemia is a particular problem in AKI not only because urinary excretion is
reduced but also because intracellular potassium may be released. Rapid rises in
extracellular potassium are to be expected when there is tissue damage, as in burns, crush
injuries and sepsis. Acidosis also aggravates hyperkalaemia by provoking potassium
leakage from healthy cells. The condition may be life-threatening, causing cardiac
arrhythmias, and, if untreated, can result in asystolic cardiac arrest.
 Dietary potassium should be restricted to less than 40 mmol/ day, and potassium
supplements and potassium-sparing diuretics removed from the treatment schedule.
Emergency treatment is necessary if the serum potassium level reaches 7.0 mmol/L
(reference range 3.5–5.5 mmol/L) or if there are the progressive changes in the
electrocardiogram (ECG) associated with hyperkalaemia.
 These include tall, peaked T waves, reduced P waves with increased QRS complexes or
the ‘sine wave’ appearance that often presages cardiac arrest Emergency treatment of
hyperkalaemia consists of the following:
1. 10–30 mL (2.25–6.75 mmol) of calcium gluconate 10% intravenously over 5–10
minutes: This improves myocardial stability but has no effect on the serum potassium
levels. The protective effect begins in minutes but is short-lived (<1 hour), although the
dose can be repeated.
2. 50 mL of 50% glucose together with 8–12 units of soluble insulin over 10 minutes:
Endogenous insulin, stimulated by a glucose load or administered intravenously,
stimulates intracellular potassium uptake, thus removing it from the serum.The effect
becomes apparent after 15–30 minutes, peaks after about 1 hour, and lasts for 2–3 hours
and will decrease serum potassium levels by around 1 mmol/L.
3. Nebulised salbutamol has also been used to lower potassium; however, this is not
effective for all patients and does not permanently lower potassium. If used it is seen as a
temporary emergency measure.
Acidosis
 The inability of the kidney to excrete hydrogen ions may result in a metabolic acidosis.
This may contribute to hyperkalaemia. It may be treated orally with sodium bicarbonate
1–6 g/day in divided doses (although this is not appropriate for acute metabolic acidosis

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seen in AKI), or 50–100 mmol of bicarbonate ions (preferably as isotonic sodium

bicarbonate 1.4% or 1.26%, 250–500 mL over 15–60 minutes) intravenously may be
used. The administration of bicarbonate in acidotic patients will also tend to reduce serum
potassium concentrations. Bicarbonate will cause an increase in intracellular Na+ through
activation of the cell membrane Na+/H+ exchanger, which promotes increased activity of
Na/K ATPase producing increased intracellular sequestration of K+.
 If calcium gluconate is used to treat hyperkalaemia, care should be taken not to mix it
with sodium bicarbonate (by giving this through the same intravenous access site)
because the resulting calcium bicarbonate forms an insoluble precipitate. If elevation of
serum sodium or luid overload precludes the use of sodium bicarbonate, extreme acidosis
(serum bicarbonate of <10 mmol/L) is best treated by dialysis.
Hypocalcaemia
 Calcium malabsorption, probably secondary to disordered vitamin D metabolism, can
occur in AKI. Hypocalcaemia usually remains asymptomatic, as tetany of skeletal
muscles or convulsions does not normally occur until serum concentrations are as low as
1.6–1.7 mmol/L (reference range 2.20–2.55 mmol/L). Should it become necessary, oral
calcium supplementation with calcium carbonate is usually adequate, and although
vitamin D may be used to treat the hypocalcaemia of AKI, it rarely has to be added.
Effervescent calcium tablets should be avoided because they contain a high sodium or
potassium load.
Hyperphosphataemia
Because phosphate is normally excreted by the kidney, hyperphosphataemia can occur in AKI
but rarely requires treatment. Should it become necessary to treat, phosphate-binding agents may
be used to retain phosphate ions in the gut. The most commonly used agents are calcium
containing, such as calcium carbonate or calcium acetate, and are given with food.
Infection
Patients with AKI are prone to infection and septicaemia, which can ultimately cause death.
Bladder catheters, central catheters and even peripheral intravenous lines should be used with
care to reduce the chance of bacterial invasion. Leucocytosis is sometimes seen in AKI and does
not necessarily imply infection. However, pyrexia must be immediately investigated and treated
with appropriate antibiotic therapy if accompanied by toxic symptoms such as disorientation or

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hypotensive episodes. Samples from blood, urine and any other material such as catheter tips
should be sent for culture before antibiotics are started. Antibiotic therapy should be broad
spectrum until a causative organism is identified.
Other problems
Uraemic gastro-intestinal erosions
Uraemic gastro-intestinal erosions are a recognised consequence of AKI, probably as a result of
reduced mucosal cell turnover owing to high circulating levels of uraemic toxins. Proton pump
inhibitors and H2 antagonists are effective. However, proton pump inhibitors should be used
with caution in hospitals where there are signiicant rates of Clostridium dificile diarrhoea,
because they may predispose to the development of this organism. H2 antagonists are an
appropriate alternative. In addition, there is increasing epidemiological evidence linking proton
pump inhibitors with kidney disease
Nutrition
There are two major constraints concerning the nutrition of patients with AKI:
• Patients may be anorexic, vomiting and too ill to eat;
• oliguria associated with renal failure limits the volume of enteral or parenteral nutrition that can
be safely given.
 The basic calorie requirements are similar to those in a non-dialysed patient, although the
need for protein may occasionally be increased in haemodialysis and haemofiltration
because of amino acid loss. In all situations, protein is usually supplied as 12–20 g/day of
an essential amino acid formulation, although individual requirements may vary.
 Electrolyte-free amino acid solutions should be used in parenteral nutrition formulations
for patients with AKI as they allow the addition of electrolytes as appropriate.Potassium
and sodium requirements can be calculated on an individual basis depending on serum
levels. There is usually no need to try to normalise serum calcium and phosphate levels as
they will stabilise with the appropriate therapy, or, if necessary, with haemofiltration or
dialysis.
 Water-soluble vitamins are removed by dialysis and haemofiltration but the standard
daily doses normally included in parenteral nutrition fluids more than compensate for this
loss. Magnesium and zinc supplementation may be required, not only because tissue

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repair often increases requirements but also because they may be lost during dialysis or
haemofiltration.
 It is necessary to monitor the serum urea, creatinine and electrolyte levels daily to make
the appropriate alterations in the required nutritional support. The glucose concentration
should also be checked daily as patients in renal failure sometimes develop insulin
resistance.
 The plasma pH should be checked initially to determine if addition of amino acid
solutions is causing or aggravating metabolic acidosis. It is also valuable to check
calcium, phosphate and albumin levels regularly, and when practical, daily weighing
gives a useful guide to fluid balance.

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