NEPHROLOGY
Fluid and electrolyte
problems in renal
dysfunction
Jennifer Oldridge
Swati Karmarkar
Abstract
The primary function of the kidney is to maintain fluid and electrolyte ho-
meostasis. Each day the kidney must excrete 1500 ml of water and any
excess ingested sodium, potassium, magnesium and phosphate. The kid-
ney also plays a key role in calcium homeostasis. Of the total number of
patients in intensive care 3e25% will develop acute kidney injury and pa-
tients with chronic renal disease will frequently present for surgery. The
treatments for renal dysfunction may themselves cause disturbance in
fluid and electrolyte homeostasis, particularly the use of diuretics and
renal replacement therapy. Loss of normal renal function may lead to
major changes in fluid and sodium balance. Volume status assessment
will be required in patients with renal dysfunction because they are at
risk of both hypovolaemia and hypervolaemia. Loss of renal function
will lead to retention of potassium and magnesium with serious systemic
and cardiovascular consequences including cardiorespiratory compromise
and collapse and cardiac dysrhythmias. Hypocalcaemia will result from
reduced renal calcitriol production and phosphate retention. The identifi-
cation of fluid and electrolyte imbalances and the management of clini-
cally significant changes are required when treating patients with renal
dysfunction on an intensive care unit or who present for anaesthesia.
Keywords Calcium; electrolyte; magnesium; potassium; renal; sodium
Royal College of Anaesthetists CPD matrix: 1A02, 1A01, 2A05, 3A03
Renal dysfunction: prevalence and morbidity
Renal dysfunction results in the loss of fluid and electrolyte ho-
meostasis and the accumulation of potentially toxic products of
metabolism. Problems may arise as a result of chronic renal
dysfunction or as a result of acute renal failure.
Acute kidney injury (AKI) occurs rarely in the community
with an incidence of between 140 and 288 per million. It occurs
in up to 15% of adults admitted to hospital with the elderly being
particularly at risk. The incidence in intensive care patients is
much higher and is quoted as 3e25%. Occurrence is quoted at 5
e7% of all hospitalized patients to varying degrees. An NHS
study has shown severe kidney injury to have a mortality of 30
e40%. Many definitions have been applied to AKI but the RIFLE
Jennifer Oldridge MBBS FRCA is an Anaesthetic ST7 Trainee at the Royal
Preston Hospital, Preston, UK. Conflicts of interest: none declared.
Swati Karmarkar MD (Vrach) DA MD (Anaesthesia) FRCA is a Consultant
Anaesthetist at the Manchester Royal Infirmary, UK. Conflicts of
interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 16:6
Learning objectives
After reading this article, you should be able to:
C
C
explain albumin:creatinine ratio
describe how to treat hyponatraemia of renal disease
C list six treatments of hyperkalaemia
criteria proposed by Bellomo et al.1,2 have now gained general
acceptance.
Chronic renal disease (CRD) has been defined as either a
glomerular filtration rate of less than 60 ml/minute/1.73 m2 for
3 months or more, irrespective of cause, or evidence of kidney
damage for more than 3 months based on abnormalities. The
incidence of CRD is increasing and more than 550 people/
million receive renal replacement therapy (RRT) in the UK
which accounts for over 2% of the NHS budget. NICE has
suggested that chronic renal disease should be classified to
include patients with kidney damage who are at risk of pro-
gressing to failure (Table 1). In 2013, the Kidney Disease:
Improving Global Outcomes (KDIGO) guidance on the evalua-
tion and management of chronic kidney disease adopted the
subdivision of glomerular filtration rate (GFR) categories sug-
gested by the NICE guideline, but also included three albu-
min:creatinine ratios (ACRs) for each GFR category in an
updated classification3 (Table 2).
Early recognition and treatment of patients at risk of devel-
oping AKI on a background of chronic kidney disease (CKD) is
extremely important. AKI in CKD patients can lead to a higher
mortality than AKI in non-CKD patients and it can also alter the
progression of the underlying disease process. Progression to
end-stage renal failure has been found to be higher in patients
who develop AKI in CKD compared to non-CKD.4
Renal dysfunction in the postoperative period
Renal dysfunction and AKI in the postoperative period con-
tinues to be a problem. Historically aneurysm repair and car-
diac surgery requiring cardiopulmonary bypass have
represented a significant risk. Endovascular techniques such as
endovascular repair of the aorta and transcutaneous insertion
of aortic valves are associated with substantial contrast ne-
phropathy. They are also at risk of micro- and macro-
embolization and changes in renal blood flow patterns. The
creatinine rise after these insults can be slow and is defined as
AKI if there is a 25% relative rise 48 hours after administration
of contrast. Prevention measures that have been suggested
include hydration, use of statins, antioxidants such as n-acetyl
cysteine (orally or as infusions), ascorbic acid and alkalinizing
the urine with sodium bicarbonate.
Other high-risk patients are those with existing CKD, patients
undergoing emergency surgery who have a degree of AKI at the
time of presentation and sepsis.5
The most prominent response to anaesthesia and surgery
is water and sodium retention which is directly related
to the magnitude of surgery. During surgery ADH levels increase
50e100-fold and start decreasing towards the end of surgery or
262 Ó 2015 Published by Elsevier Ltd.
 NEPHROLOGY

9% of cases. CKD is a stronger predictor of mortality in advanced

Stages of chronic kidney disease (NICE) CHF than left ventricular function.
Stage GFR Description
(ml/minute/1.73 m2) Impacts of treatment of renal dysfunction

1
90 Normal or increased GFR, with

Patients with chronic renal disease are frequently on multiple
other evidence of kidney damage
medications7 to help maintain homeostasis and to treat associ-
2 60e89 Slight decrease in GFR, with
ated conditions such as hypertension, cardiac disease, and dia-
other evidence of kidney damage
betes. While some of these treatments such as bicarbonate and
vitamin D supplementation are aimed at restoring normal ho-
3A 45e59 Moderate decrease in GFR, with
meostasis, these and other medications may cause electrolyte
or without other evidence of kidney
and fluid disturbance. Diuretics in particular may result in sig-
damage
nificant changes in body water, sodium, potassium, and acid/
3B 30e44 Moderate decrease in GFR, with or
base balance. Care must be taken in particular to medications
without other evidence of kidney
damage
controlling blood pressure as these can have a profound effect
4 15e29 Severe decrease in GFR, with or
when combined with anaesthesia in the perioperative period.
without other evidence of kidney
Patients requiring RRT, particularly haemodialysis, may have
damage
profound changes in fluid, electrolyte and acid/base balance at
5 <15 Established renal failure
the time of treatment. In such patients total body water status is
best estimated by body weight changes. These will be recorded
GFR, glomerular filtration rate. regularly in dialysis patients and many patients will know their
own ‘dry weight’. It is important for the anaesthetist to know
Table 1 the normal dry weight and the weight just prior to surgery.
Failure to achieve dry weight is a common problem especially on
within 3e5 days. Other reasons for fluid retention may be effects short-duration dialysis prescriptions.
of anaesthesia on renal blood flow, GFR, effects of hypotension Blood electrolyte levels should be measured regularly in
and hypovolaemia, increased circulating catecholamines and patients who are receiving RRT in critical care or those on
increased plasma cortisol. To determine whether water imbal- long-term RRT who require anaesthesia.
ances are due to deficiency (diabetes insipidus (DI)) or excess of
ADH (syndrome of inappropriate antidiuretic hormone secretion Water
(SIADH)), fluid intake, output, specific gravities and serum Water balance is severely affected by renal dysfunction. Patients
electrolytes should be monitored daily. DI occurs more with CKD are at risk increased risk of fluid overload and this may
frequently than hyponatraemia, and is characterized by large be a stimulus for inflammation and rapid progression of renal
amounts of dilute urine which can lead to hypernatraemia and disease.8 Patients with oliguria and anuria are at risk of water
may require treatment with desmopressin. SIADH peaks on overload as they will lose only about 1000 ml per day from
postoperative day 7 and can present with severe and symptom- insensible and other losses. Daily fluid restriction is frequently
atic hyponatraemia. Management is mainly by fluid restriction. used to control water levels in such patients. Diuretics are often
used to increase fluid excretion in those with some remaining
Fluid management in CKD renal function. Conversely, these patients are at risk of dehy-
dration if other water losses increase such as increased insensible
CKD and congestive heart failure (CHF) are closely associated
loss in sepsis or in patients with diarrhoea. Over-aggressive fluid
(cardio-renal syndrome) and make fluid management difficult in
removal with RRT may also result in dehydration.
these patients with conflicting treatment goals.
Some patients will develop polyuric renal failure (particularly
Preoperative renal dysfunction is a predictor of postoperative
during recovery from AKI). In these patients dehydration may
renal failure.6 A preoperative serum creatinine of more than
develop if intake is not increased to compensate.
176 mmol/litre is an independent predictor of systolic and diastolic
Assessment of hydration status is always required in patients
dysfunction and is associated with major cardiac complications in
with renal failure. If normal body weight (or ‘dry weight’ in
dialysis patients) is known then weighing the patient will give an
Albumin:creatinine ratio (KDIGO) idea of hydration status. Each 1000 ml of water weighs 1 kg.
Daily weights should be conducted on intensive care patients
ACR category ACR (mg/mmol) Terms with renal failure. History of fluid restriction, urine output, RRT,
and fluid balance should be taken. Examination may reveal signs
A1 <3 Normal to mildly increaseda
of fluid overload or dehydration. Attention should be paid to
A2 3e30 Moderately increasedb
hydration of mucus membranes, jugular venous pulse, and
A3 >30 Severely increased
capillary refill, presence of oedema, blood pressure, heart rate
ACR, albumin:creatinine ratio; CKD, chronic kidney disease. and respiratory symptoms.
a
Relative to young adult level. Mild dehydration may be treated with oral rehydration. If the
b
Including nephrotic syndrome (ACR usually >220 mg/mmol).
enteral route is unavailable or the level of dehydration is more
Table 2
profound intravenous fluid will be required. The nature of fluid

ANAESTHESIA AND INTENSIVE CARE MEDICINE 16:6 263 Ó 2015 Published by Elsevier Ltd.
 NEPHROLOGY
replacement will to some degree be guided by the ion de-
rangements that will usually accompany dehydration (particu-
larly sodium) though, as a rule, potassium-containing fluids are
best avoided in anuric patients. Administration of sodium chlo-
ride may result in hyperchloraemic acidosis, which can worsen
hyperkalaemia. Metabolic acidosis can reduce cardiac contrac-
tility, cardiac output and decrease renal blood flow. Hyper-
chloraemia itself can decrease renal blood flow and GFR.
Intravenous fluid therapy should be administered with caution as
overload may precipitate pulmonary oedema which may be more
challenging to treat in this population.
Diuretic therapy can be appropriate to treat fluid overload in
patients with remaining renal function. High-dose loop diuretics
such as furosemide 250e500 mg, given as an infusion, are often
required to produce a diuresis is in renal failure. In patients with
pulmonary oedema or with oliguric/anuric renal failure haemo-
dialysis or haemofiltration will provide more rapid and predict-
able correction of fluid balance.
Sodium
Sodium levels in renal failure will usually be related to fluid
shifts. Maximum sodium excretion is a function of GFR. Patients
with renal dysfunction are at risk of both hypo- and
hypernatraemia.
Increased loss of free water or reduced water intake will result
in hypernatraemia (sodium >145 mmol/litre). Reduced water
intake due to inability to drink (nausea and vomiting) or
inability to respond to thirst (excessive water restriction, intu-
bated patients, and those with reduced conscious level) will
result in water depletion. Conditions such as diarrhoea and
vomiting or increased sweat loss will be associated with a degree
of sodium loss but if free water loss is greater hypernatraemia
will result. Patients with certain kidney disorders such as cystic
kidney disease are at risk of acquired nephrogenic DI. This re-
sults in the production of dilute urine and hypernatraemia.
Administration of sodium bicarbonate or increased oral intake of
sodium chloride may result in sodium overload.
Initial management of hypernatraemia associated with dehy-
dration should be aimed at restoring normovolaemia. Once vol-
ume status has been restored water deficit can be corrected with
5% dextrose. It is important to remember that many drugs,
including antibiotics and soluble or effervescent medications,
may contain a large amount of sodium.
Patients usually present with hypervolaemic hyponatraemia.
Hyponatraemia (sodium <135 mmol/litre) results from dispro-
portionate sodium and water loss or excessive free water. The
kidney is required to reabsorb 99% of the filtered sodium. In
some patients with renal dysfunction and normal or high urine
output loss of reabsorbtive power will result in hyponatraemia
with or without hypovolaemia. Other causes of increased sodium
loss such as diarrhoea and vomiting, diuretic use, and Addison’s
syndrome are often associated with hypovolaemia. When pa-
tients are anuric fluid intake should be restricted to insensible
loss. If intake is increased water overload with dilutional hypo-
natraemia can develop. Dilution may also occur with osmotic
diuretic administration in anuric patients. Water overload may
also occur as a result of water retention due to raised aldosterone
levels (such as in CHF) or SIADH. Loop diuretics can be used to
treat these patients (furosemide 1 mg/kg).
ANAESTHESIA AND INTENSIVE CARE MEDICINE 16:6
If the patient is hypovolaemic administration of 0.9% saline is
appropriate to treat mild hyponatraemia. Some authors recom-
mend hypertonic saline (3%) for severe symptomatic hypona-
traemia (Naþ <125 mmol/litre with seizures or coma). However
rapid correction of chronic hyponatraemia is associated with a
risk of central pontine myelinolysis. Patients with hypokalaemia,
malnutrition, cirrhosis, burns, alcoholism and young menstruant
females are at higher risk of brain damage. Correction should be
limited to 1e2 mmol/litre/hour in serious cases and no more
than 10 mmol/litre in a 24-hour period. After sodium concen-
tration has reached 125 mmol/litre treatment should be by water
restriction. Brain swelling disappears at a sodium level of
130 mE/litre so correction to normal levels is not required.5 In
intensive care hypovolaemic hypotonic hyponatraemia is most
commonly treated with haemodialysis or haemofiltration.
Potassium
Plasma potassium usually remains normal until onset of Stage 5
CKD. This is usually because of increased excretion per func-
tioning nephron and increased excretion in stools.
Acidosis in renal failure will result in potassium shift out of
the cells (in acute acidosis K will rise by w0.5 mmol per drop in
pH of 0.1). For this reason ventilated patients should not be
allowed to develop respiratory acidosis if hyperkalaemic. While
chronic hyperkalaemia is better tolerated than acute hyper-
kalaemia, potassium levels greater than 6.5 mmol/litre may be
associated with serious complications such as hypotension,
weakness, and ventricular dysrhythmias. Potassium levels
greater than 6.5 mmol/litre or hyperkalaemia associated with
ECG changes (P wave flattening, tenting of T waves, and QRS
widening) should be treated as a matter of urgency.
Treatment of hyperkalaemia is aimed firstly at reducing
plasma potassium levels by increasing intracellular movement of
potassium and secondly be increasing potassium excretion.
Calcium is required to protect the myocardium, this may be given
as either calcium chloride (5 ml 10% over 5 minutes) or gluco-
nate (10 ml 10% over 5 minutes).
Increased intracellular shift:
 insulin and dextrose (50 ml 50% dextrose with 10 iU
Actrapid over 20 minutes)
 correct acidosis with sodium bicarbonate (50 ml 8.4% over
1 hour via central access in emergencies or 500 ml 1.26%
over 6 hours)
 salbutamol nebulizers (5 mg).
Increased excretion:
 furosemide if some urine output
 calcium Resonium oral 15 g four times daily, or rectally if
oral is not tolerated (binds K)
 haemodialysis or haemofiltration.
Less commonly hypokalaemia (K <3.5) may develop. This is
frequently related to treatments such as diuretics. In patients
with renal tubular acidosis potassium is lost in exchange for
hydrogen ions. Treatment with K supplementation should be
performed cautiously in patients with serious renal dysfunction
as life-threatening hyperkalaemia may develop.
Magnesium
Magnesium is actively excreted by the kidney and renal
dysfunction will lead to raised magnesium levels (indeed
264 Ó 2015 Published by Elsevier Ltd.
 NEPHROLOGY
magnesium levels often follow potassium levels). Symptoms and
signs tend to develop at levels greater than 2 mmol/litre. Early
features will be nausea and flushing. As levels increase muscle
weakness and hypotension may develop. Magnesium levels
above 8 mmol/litre may be associated with respiratory weak-
ness, AV block, and cardiac arrest.
The treatment of clinically significant hypermagnesaemia is
calcium administration. This may be given as calcium chloride or
calcium gluconate. Other treatments are aimed at either pro-
moting intracellular shift (insulin and dextrose) or excretion
(fluid loading, diuretics and haemodialysis).
Treatment of renal dysfunction with diuretics or increased
loss from other sources may rarely reduce magnesium levels.
Calcium and phosphate
Plasma calcium levels are frequently reduced in renal failure.
Reduced production of active vitamin D (calcitriol) will result in
reduced absorption of calcium from the gut. Phosphate is actively
excreted from the kidney and will accumulate in end stage renal
disease. Phosphate will bind calcium and is then deposited in
tissues. Presentation is frequently with signs of increased nerve
and muscle excitability such as paraesthesia and carpo-pedal
spasm. More serious problems such as cardiac dysrhythmias
and laryngospasm may develop.
Treatment of clinically significant hypocalcaemia is intrave-
nous calcium (chloride or gluconate). Longer term measures
include oral calcitriol and oral calcium carbonate to bind phos-
phate and increase calcium intake. Haemodialysis and haemo-
filtration will help reduce phosphate levels.
Hydrogen and bicarbonate
Acidebase homeostasis is maintained by the renal excretion of
hydrogen ions and the production and reabsorption of bicar-
bonate. With a normal diet a 70-kg man will produce 50e80
mmol of hydrogen ions per day. To maintain the normal pH
of 7.4 hydrogen ion concentration must be kept at about
40 nmol/litre and the kidney must actively excrete the majority
of this hydrogen load. Patients with renal dysfunction will
develop acidosis due to hydrogen retention and reduced bicar-
bonate production. In some patients there may also be excessive
bicarbonate loss from the kidney (renal tubular acidosis). Pre-
operative assessment of plasma bicarbonate level can be helpful.
Acidosis may be managed with bicarbonate administration
(dose in mmol ¼ (desired bicarbonate e serum bicarbabonate)
 weight  0.5), but will also be corrected by haemodialysis or
haemofiltration.
Perioperative fluid therapy in patients with kidney disease
There are three distinct groups to consider when considering
preoperative preparation and fluid therapy for patients with renal
disease: patients with renal dysfunction whose kidneys are still
functioning, patients with dialysis-dependent end stage renal
failure and patients with a transplanted kidney. Electrolytes
should be checked on the morning of surgery e fasting may
provoke a hyperkalaemic state and checking too soon after dial-
ysis may give a false hypokalaemic picture. Oxygen delivery in
patients with CKD may be compromised by factors like chromic
anaemia, heart failure, endothelial dysfunction, poor microvas-
cular circulation and coagulopathy due to platelet dysfunction.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 16:6
Recent evidence indicates liberal fluid therapy might cause
and aggravate AKI in critically ill patients.9,5 Targeted fluid re-
striction does not seem to have the same effect. In general, daily
requirements ¼ losses þ approximately 500 ml (for insensible
losses). In anuric patients without extra losses this may mean
that they only require 500 ml daily. Fluid overload occurs
because of increased capillary permeability and reduced sodium
excretion in acutely ill patients even before AKI actually sets in.
Fluid overload can lead to intra-abdominal hypertension and
abdominal compartment syndrome which in turn increases renal
venous pressure and decreases renal blood flow. As the kidney is
an encapsulated organ, renal interstitial oedema itself could lead
to decreased renal blood flow.
Both hypervolaemia and hypovolaemia are avoided by goal-
directed fluid therapy using cardiac output monitoring. Oeso-
phageal Doppler monitoring and transoesophageal echocardiog-
raphy are commonly used to measure intravascular volume and
blood flow. Chronically uraemic patients seem to adapt well
to anaemia and no studies have shown an improved outcome
with liberal preoperative blood transfusions. However recent
evidence shows the more blood transfusions a patient receives
before transplantation, the greater the chances of a functioning
transplant.5
In 2013 the use of intravenous fluids containing hydroxyethyl
starches (HES) was suspended by the Medicines and Healthcare
products Regulatory Agency (MHRA). This was due to a number
of studies in critically ill patients that suggested an increased risk
of kidney injury requiring RRT in patients receiving intravenous
fluids containing high-molecular-weight starches. Mechanisms of
renal injury with use of colloids are incompletely understood
but may be due to direct molecular effects and effects of high
oncotic pressures. The Saline versus Albumin Fluid Evaluation
(SAFE) study did not show any difference in renal effect between
the study fluids. Albumin and gelatins are used as colloids if
needed.
The hyperchloraemic acidosis caused by large volumes of
0.9% saline has been discussed above. Potassium-containing
balanced crystalloids do not cause hyperkalaemia At present
buffered crystalloid solutions such as compound sodium lactate
seem to be the best fluid to use in critically ill patients to avoid
renal injury.
A suggested alternative crystalloid is a K-free bicarbonate
buffered dialysis solution such as Hemosol. A
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 NEPHROLOGY
6 Eilers H, Liu K, Grauber A, et al. Chronic kidney disease: implications
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ANAESTHESIA AND INTENSIVE CARE MEDICINE 16:6
FURTHER READING
British Consensus Guidelines on Intravenous Fluid Therapy for Adult
Surgical Patients GIFTASUP Guidelines. http://www.bapen.org.uk/pdfs/
bapen_pubs/giftasup.pdf (accessed 10 January 2015).
Chronic kidney disease: early identification and management of chronic
kidney disease in adults in primary and secondary care. NICE guide-
lines [CG182] Published date: July 2014.
Ronco C, Bellomo R, Kellum J. Critical care nephrology. 2nd edn. Saunders
Elsevier, 2009.
266 Ó 2015 Published by Elsevier Ltd.