3. Anatomical Position
The kidneys lie retroperitoneally (behind the peritoneum) in the abdomen, either side of the
vertebral column.
They typically extend from T12 to L3, although the right kidney is often situated slightly lower due
to the presence of the liver.
Each kidney is approximately three vertebrae in length.
The adrenal glands sit immediately superior to the kidneys within a separate envelope of the renal
fascia
4. Kidney Structure
The kidneys are encased in complex layers of fascia and fat. They are arranged as follows (deep to
superficial):
•Renal capsule – tough fibrous capsule.
•Perirenal fat – collection of extraperitoneal fat.
•Renal fascia (also known as Gerota’s fascia or perirenal fascia) – encloses the kidneys and the
suprarenal glands.
•Pararenal fat – mainly located on the posterolateral aspect of the kidney.
5. The renal parenchyma can be divided into two main areas – the outer cortex and
inner medulla.
The cortex extends into the medulla, dividing it into triangular shapes – these are
known as renal pyramids.
The apex of a renal pyramid is called a renal papilla. Each renal papilla is
associated with a structure known as the minor calyx, which collects urine from
the pyramids.
Several minor calices merge to form a major calyx. Urine passes through the
major calices into the renal pelvis, a flattened and funnel-shaped structure.
From the renal pelvis, urine drains into the ureter, which transports it to the bladder
for storage.
The medial margin of each kidney is marked by a deep fissure, known as the renal
hilum. This acts as a gateway to the kidney – normally the renal vessels and
ureter enter/exit the kidney via this structure.
6. Arterial Supply
The kidneys are supplied with blood via the renal
arteries, which arise directly from the abdominal
aorta, immediately distal to the origin of
the superior mesenteric artery.
Due to the anatomical position of the abdominal
aorta (slightly to the left of the midline), the right
renal artery is longer, and crosses the vena cava
posteriorly.
The renal artery enters the kidney via the renal
hilum. At the hilum level, the renal artery forms
an anterior and a posterior division, which carry
75% and 25% of the blood supply to the kidney,
respectively. Five segmental arteries originate
from these two divisions.
7. The segmental branches of the renal undergo further divisions to supply the renal parenchyma:
•Each segmental artery divides to form interlobar arteries. They are situated either side every renal pyramid.
•These interlobar arteries undergo further division to form the arcuate arteries.
•At 90 degrees to the arcuate arteries, the interlobular arteries arise.
•The interlobular arteries pass through the cortex, dividing one last time to form afferent arterioles.
•The afferent arterioles form a capillary network, the glomerulus, where filtration takes place. The capillaries come
together to form the efferent arterioles.
8. GUYTON AND HALL TEXTBOOK OF MEDICAL PHYSIOLOGY, 12TH ED., PAGE 305 8
FUNCTIONAL ANATOMY
OF NEPHRON
• Each kidney in the human contains
about 800,000 to 1,000,000 nephrons,
each capable of forming urine.
• After age 40, the number of functioning
nephrons usually decreases about 10
percent every 10 years.
• This loss is not life threatening because
adaptive changes in the remaining
nephrons allow them to excrete the
proper amounts of water, electrolytes,
and waste.
9. GUYTON AND HALL TEXTBOOK OF MEDICAL PHYSIOLOGY, 12TH ED., PAGE 306 9
NEPHRON
• Functional difference between 2
types of Nephrons is
Juxtamedullary Nephron is
involved in Concentration of
urine.
12. GUYTON AND HALL TEXTBOOK OF MEDICAL PHYSIOLOGY, 12TH ED., PAGE 310
12
FORMATION OF URINE
Urinary excretion rate =
Filtration rate -
Reabsorption rate +
Secretion rate
• A large amount of fluid
that is virtually free of
protein is filtered from
the glomerular
capillaries into
Bowman’s capsule.
• Concentration in the
glomerular filtrate in
Bowman’s capsule is
almost the same as in
the plasma.
13. GUYTON AND HALL TEXTBOOK OF MEDICAL PHYSIOLOGY, 12TH ED., PAGE 312 13
RATE
• Glomerular filtration rate (GFR) is defined as the
total quantity of filtrate formed in all the
nephrons of both the kidneys in the given unit of
time.
• Normal GFR is 125 mL/minute or about 180
L/day.
• Filtration fraction = GFR/Renal plasma flow.
• The fraction of the renal plasma flow that is
filtered (the filtration fraction) averages about 0.2.
• This means that about 20 percent of the plasma
flowing through the kidney is filtered through the
glomerular capillaries.
14. GUYTON AND HALL TEXTBOOK OF MEDICAL PHYSIOLOGY, 12TH ED., PAGE 316 & 318 14
RATE
15. STOELTING'S PHARMACOLOGY & PHYSIOLOGY IN ANESTHETIC PRACTICE, 5TH ED., PAGE 420 15
FORMATION OF URINE
• Tubular secretion accounts for significant amounts of potassium ions,
hydrogen ions, and a few other substances that appear in the urine.
• Tubular reabsorption is highly selective. Some substances, such as
glucose and amino acids, are almost completely reabsorbed from the
tubules, so the urinary excretion rate is essentially zero.
• sodium, chloride, and bicarbonate, are also highly reabsorbed, but their
rates of reabsorption and urinary excretion are variable, depending on
the needs of the body.
• Waste products, such as urea and creatinine, conversely, are poorly
reabsorbed from the tubules and excreted in relatively large amounts
16. STOELTING'S PHARMACOLOGY & PHYSIOLOGY IN ANESTHETIC PRACTICE, 5TH ED., PAGE 422 16
FLOW
• Kidneys receive 20% to 25% of the cardiac output.
• Renal blood flow is approximately 400 mL/100 g/minute,
compared with 70 mL/ 100 g/minute for the heart and liver.
• The ability to autoregulate keeps renal blood flow relatively
constant across a range of systemic mean arterial pressures.
• Approximately 90% of the renal blood flow is distributed to
the renal cortex, with less than 10% of renal blood flow going
to the medulla.
• The generous delivery of blood to the cortex supports flow-
dependent functions such as glomerular filtration and tubular
reabsorption processes of the cortex.
• Low blood flow in the medulla maintains a high interstitial
fluid osmolarity, which in turn permits concentration of the
urine.
• Low blood flow also makes the medulla more susceptible to
17. STOELTING'S PHARMACOLOGY & PHYSIOLOGY IN ANESTHETIC PRACTICE, 5TH ED., PAGE 423 17
AUTOREGULATION
The Myogenic Mechanism of the
Renal Blood Flow Autoregulation
• Whenever the blood flow to kidneys
increases, it stretches the elastic wall of
the afferent arteriole.
• Stretching of the vessel wall increases
the flow of calcium ions from
extracellular fluid into the cells.
• The influx of calcium ions leads to the
contraction of smooth muscles in
afferent arteriole, which causes
constriction of afferent arteriole.
• So, the blood flow is decreased.
18. Stoelting's Pharmacology & Physiology in Anesthetic Practice, 5th Ed., Page 423
18
AUTOREGULATION
Tubuloglomerular Feedback
• The juxtaglomerular
apparatus is where the
distal renal tubule passes
between the afferent and
efferent arterioles
• In response to decreased
renal blood flow,
juxtaglomerular cells
release renin into the
circulation. Renin converts
angiotensinogen to
angiotensin I, which is then
converted to angiotensin II.
• Effects of angiotensin II
include thirst,
vasoconstriction, and salt
and water reabsorption by
the kidneys to maintain
circulating volume and
19. PRIMARY ROLES OF KIDNEYS
Blood & ECF volume
maintenance
Blood volume is maintained over a narrow
range despite large daily variations in fluid
and solute intake or loss.
Regulation of Osmolality
Kidney helps to maintain Plasma osmolality
by maintaining the concentration of ions in
the body.
Plasma Concentrations
of Ions & Urea
Kidney controls the concertation of Sodium,
Potassium, Urea, Calcium, Magnesium and
also Hydrogen ion, thus maintaining acid
base balance.
STOELTING'S PHARMACOLOGY & PHYSIOLOGY IN ANESTHETIC PRACTICE, 5TH ED., PAGE 423
19
20. BLOOD AND EXTRACELLULAR FLUID
VOLUME
Hypovolemia: Patients with hypovolemia, for example, from haemorrhage,
gastrointestinal loss, or preoperative fasting, are commonly encountered in the
perioperative period. This activates the renin-angiotensin-aldosterone
response, and releases AVP.
Initially, the GFR and filtered load of sodium decrease. Sodium reabsorption in
the proximal tubule is increased from about 66% to 80%. Sodium delivery to the
thick ascending loop of Henle, distal tubule, and collecting duct is decreased,
but aldosterone promotes reabsorption of sodium at these sites.
Under the influence of AVP, water is also avidly reabsorbed in the collecting
duct so that the urine becomes highly concentrated (osmolality 600 mOsm/kg)
but with virtually no sodium (10 mEq/L).
MILLER'S ANAESTHESIA, 9TH ED., PAGE 458
20
21. BLOOD AND EXTRACELLULAR FLUID
VOLUME
Hypervolemia: Expansion of the extracellular volume by hypervolemia is
countered by an increase in the GFR and filtered sodium load due to a
combination of reflex decreases in sympathetic and angiotensin II activity
and the release of ANP.
Together with the increase in peritubular capillary hydrostatic
pressure, these responses cause sodium reabsorption in the proximal
tubule to decrease from 67% to 50%.
The decline in plasma aldosterone decreases sodium absorption from
the Distal Convoluted tubule.
The presence of ANP and absence of AVP impairs water absorption at
the collecting duct so that a dilute urine (osmolality 300 mOsm/ kg)
with abundant sodium (80 mEq/L) is produced.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 458
21
22. REGULATION OF OSMOLALITY
Plasma osmolality is closely regulated between 275
and 300 mOsm/L.
Acute alterations in osmolality, either hypoosmolality
or hyperosmolality, can result in serious neurologic
symptoms and death as the result of water movement
in the brain.
Normal patients can dilute and concentrate urine
within the range of 40 to 1400 mOsm/L.
Maintenance of plasma osmolality is linked to the
regulation of sodium concentration and water balance
by the tubular system and the collecting ducts in
concert with the vasa recta blood supply of the
tubules through differences in tubular permeability to
water and the control of sodium transport.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 456 22
23. ROLE OF UREA IN REGULATING
OSMOLALITY
A healthy person excretes 20% to 50% of the filtered load of
urea.
The concentration of urea entering the tubular system is
related to the prerenal plasma concentration and the GFR.
Urea contributes 40% to 50% of the osmolality of the
medullary interstitium.
The PCT are freely permeable whereas the loop of Henle,
distal tubules, and the collecting ducts have little permeability
to urea.
As water absorption increases with AVP action, the
concentration of urea in the tubules progressively increases.
With this high concentration, urea diffuses into the interstitial
fluid facilitated by specific urea transporters that are activated
by AVP in the CD.
As the concentration of urea increases in the medullary
interstitium, it diffuses through the thin limb of the loop of
Henle and transits through the ascending system again before
it is excreted. This recirculation enhances the increased
osmotic pressure in the medulla.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 458 23
24. PLASMA CONCENTRATION OF IONS
AND UREA
Urea: Urea is the most abundant metabolic waste product. Without adequate
clearance of urea, excessive accumulation in body fluids prevents normal
function of multiple systems.
Urea elimination depends on the plasma concentration of urea (blood urea
nitrogen or BUN) and the GFR.
Approximately 50% of the urea that is filtered into the renal tubules is
eliminated in the urine; the remainder is reabsorbed.
When the GFR is low, tubular filtrate flow is relatively slow, thus increasing the
proportion of urea that is reabsorbed. This effectively increases the BUN by
decreasing urinary elimination of urea.
Conversely, when GFR increases, less urea is reabsorbed in the tubules,
increasing its elimination in the urine, and BUN decreases.
STOELTING'S PHARMACOLOGY & PHYSIOLOGY IN ANESTHETIC PRACTICE, 5TH ED., PAGE 426
24
25. Regulation of Sodium Concentration: The kidneys control the concentration of
sodium through the process of reabsorption.
Two-thirds of the sodium in glomerular filtrate is reabsorbed in the proximal renal
tubule, and less than 10% of sodium is expected to reach the distal renal tubule.
In case of Hypotension RAAS is activated and nearly all the filtered Sodium is
reabsorbed.
Typically, only 1% of the filtered sodium is excreted in the urine.
STOELTING'S PHARMACOLOGY & PHYSIOLOGY IN ANESTHETIC PRACTICE, 5TH ED., PAGE 425 25
26. Regulation of Potassium Concentration:
Potassium, after being filtered in the glomerulus, is then
reabsorbed by the proximal tubule and loop of Henle.
Potassium is either reabsorbed or secreted in the distal tubule
and collecting duct, depending on the level of aldosterone.
An increase in aldosterone increases potassium ion secretion into
the renal tubules and consequently increases urinary potassium.
When aldosterone activity is blocked by certain diuretics, plasma
potassium concentration depends more on dietary intake of
potassium, making hypokalemia or hyperkalemia.
In the presence of alkalosis (e.g., vomiting and loss of gastric
acid), potassium is excreted in the urine in order to maintain
acid–base balance.
Metabolic acidosis will lead to the secretion of hydrogen ions and
retention of potassium, and plasma potassium concentration will
increase.
STOELTING'S PHARMACOLOGY & PHYSIOLOGY IN ANESTHETIC PRACTICE, 5TH ED., PAGE 425 26
27. ACID BASE BALANCE
The kidneys control acid-base balance by excreting either acidic or basic urine.
Excreting acidic urine (H+) reduces the amount of acid in extracellular fluid,
whereas excreting basic urine (HCO3-) removes base from the extracellular
fluid.
Kidney tries to conserve the primary buffer system of the extracellular fluid i.e.,
HCO3-
The kidneys regulate extracellular fluid H+ & HCO3- concentration through
three fundamental mechanisms:
(1) secretion of H+
(2) reabsorption of filtered HCO3 −
(3) production of new HCO3 −
GUYTON AND HALL TEXTBOOK OF MEDICAL PHYSIOLOGY, 12TH ED., PAGE 386 27
28. The kidneys secrete excess hydrogen ions by
exchanging a hydrogen ion for a sodium ion,
thus acidifying the urine.
In the presence of hypovolemia, bicarbonate
reabsorption by the kidneys will lead to
acidification of the urine and a metabolic
alkalosis.
GUYTON AND HALL TEXTBOOK OF MEDICAL PHYSIOLOGY, 12TH ED., PAGE 386 28
29. ACID BASE BALANCE IN LATE
DISTAL AND COLLECTING TUBULES.
The tubular epithelium secretes H+ by
primary active transport.
H+ is transported directly by a specific
protein, a hydrogen-transporting ATPase.
The main difference is that H+ moves across
the luminal membrane by an active H+ pump
instead of by counter-transport, as occurs in
the early parts of the nephron.
GUYTON AND HALL TEXTBOOK OF MEDICAL PHYSIOLOGY, 12TH ED., PAGE 386 29
30. ASSESSMENT OF RENAL FUNCTION
Thorough history and physical
examination important.
Though accurate clinical
assessment of kidney function is
difficult & relies heavily on
laboratory tests.
Incidentally patients may exhibit
evidence of renal dysfunction.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1932
30
31. GLOMERULAR
FILTRATION RATE
•Blood Urea Nitrogen (10- 20 mg/dL)
•Serum Creatinine (0.6- 1.3 mg/dL)
•Creatinine Clearance (>90 mL/min)
•Urinary Albumin Creatinine Ratio (<30 mg/g)
RENAL TUBULAR
FUNCTION
•Urine Specific Gravity (1.003- 1.030)
•Urine Osmolality (40- 1400 mOsm/L)
•Urine Sodium Excretion (<40 mEq/L)
•Glucosuria
K SEMBULINGAM - ESSENTIALS OF MEDICAL PHYSIOLOGY, 6TH ED., PAGE 334
31
Factors influencing RFT
1. Hydration status
2. Variable Protein Intake
3. GI Bleeding
4. Catabolism
5. Advance Age
6. Skeletal Muscle mass
7. Timing of Sample Collection
32. GLOMERULAR FUNCTION RATE
GFR best measure of glomerular function. Normal GFR ~ 125 mL/min.
However, manifestations of reduced GFR are not seen until the GFR has
decreased to 50% of normal.
When GFR decreases to 30% of normal, a stage of moderate renal insufficiency
ensues.
This stage is characterized by profound clinical manifestations of uremia and
biochemical abnormalities, such as acidemia; volume overload; and neurologic,
cardiac, and respiratory manifestations.
When the GFR is 5% to 10% of normal, it is called end-stage renal disease
(ESRD), and continued survival without renal replacement therapy becomes
impossible.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1933 32
33. SERUM CREATININE & CREATININE
CLEARANCE
Creatinine in serum results from turnover of muscle tissue and
depends on daily dietary intake of protein.
Normal values are 0.5 to 1.5 mg/100 mL.
Creatinine is freely filtered at the glomerulus; it is neither reabsorbed
nor secreted.
Serum creatinine measurements reflect glomerular function and
creatinine clearance is a specific measure of GFR.
Creatinine clearance can be calculated by the formula derived by
Cockcroft-Gault that accounts for age-related decreases in GFR, body
weight, and sex.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1933 33
34. SERUM CREATININE & CREATININE
CLEARANCE
Creatinine clearance (mL/min) = [(140− Age) ×
Lean body weight (kg)]/ [Plasma creatinine (mg/dL)
× 72
This value should be multiplied by 0.85 for women
because a lower fraction of body weight is
composed of muscle.
50% increase in serum creatinine concentration,
indicative of a 50% reduction in GFR, may go
undetected unless baseline values are known.
Excretion of drugs dependent on glomerular
filtration may be significantly decreased despite
what might seem to be only slightly elevated serum
creatinine values (1.5-2.5 mg/100 mL).
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1934 34
35. BLOOD UREA
NITROGEN
Not a reliable indicator of the GFR
unless protein catabolism is normal &
constant.
BUN is influenced by nonrenal
variables such as exercise, bleeding,
steroids, and massive tissue
breakdown.
BUN > 50 mg/dL : Associated with
impaired kidney function.
The more important factor is that BUN
is not elevated in kidney disease until
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1933
35
36. TUBULAR FUNCTION
Urine Concentrating Ability:
Urinary specific gravity : index of kidney’s concentrating ability, specifically renal tubular function.
Determination of urinary osmolality (i.e., measurement of the number of moles of solute [osmoles] per
kilogram of solvent) is a similar, more specific test.
Excretion of concentrated urine (specific gravity, 1.030; 1050 mOsm/kg) is indicative of excellent tubular
function, whereas a urinary osmolality fixed at that of plasma (specific gravity 1.010; 290 mOsm/kg)
indicates renal disease.
Protein:
Patients without renal disease can excrete 150 mg of protein per day.
Greater amounts may be present after strenuous exercise or after standing for several hours.
Massive proteinuria (i.e., >750 mg/day) is always abnormal and usually indicates severe glomerular
damage.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1934 36
37. TUBULAR FUNCTION & ADDITIONAL
DIAGNOSTIC TESTS
Glucose:
Glucose is freely filtered at the glomerulus and is subsequently reabsorbed in the proximal tubule.
Glycosuria signifies that the ability of the renal tubules to reabsorb glucose has been exceeded by an
abnormally heavy glucose load and is usually indicative of diabetes mellitus.
Glycosuria also may be present in hospitalized patients without diabetes who are receiving intravenous
glucose infusions.
Urinalysis and Appearance:
The gross appearance of urine may indicate the presence of bleeding or infection in the genitourinary tract.
Microscopic examination of urinary sediment may reveal casts, bacteria, and various cell forms, supplying
diagnostic information in patients with renal disease.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1934 37
38. ADDITIONAL DIAGNOSTIC TESTS
Urine and Serum Electrolytes With Blood Gases:
Sodium, potassium, chloride, and bicarbonate concentrations should be determined if impairment in renal
function is suspected.
However, the results of these tests usually remain normal until frank renal failure is present and
hyperkalemia does not occur until patients are uremic.
In significant renal disease patients develop metabolic acidosis.
Fractional Excretion of Sodium (FeNa)
FeNa : percentage of filtered sodium excreted in urine.
Useful in differentiating between prerenal & renal azotemia.
FeNa > 2% reflects tubular dysfunction.
FeNa < 1% : renal tubules are conserving sodium.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1934 38
FeNa = (uNa x sCr x 100) / (sNa x uCr)
1. uNa is Urine Sodium
2. sCr is Serum Creatinine
3. sNa is Serum Sodium
4. uCr is Urine Creatinine
39. NOVEL BIOMARKERS OF RENAL
FUNCTION
Although serum creatinine is most used as a marker of GFR and hence renal
function, it has some limitations in that it is influenced by nonrenal factors such
as age, gender, muscle mass and metabolism, diet, and hydration.
Furthermore, creatinine levels may take several hours or days to reach a steady
state to accurately reflect the GFR as indicator of renal function in acute kidney
injury (AKI).
Serum cystatin C, a ubiquitous protein that is exclusively excreted by
glomerular filtration, is less influenced by variations in muscle mass and
nutrition than is creatinine.
It may better predict risk of death and ESRD across diverse populations.
Other novel biomarkers such as N-acetyl-β-d glucosaminidase, kidney injury
molecule-1, interleukin-18, uromodulin, and microRNA are also showing
promise at early detection of kidney injury.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1934 39
40. IMAGING STUDIES & ECG
Renal Ultrasound: It is the first-line examination in patients with renal
dysfunction for assessing kidney size and the presence or absence of
hydronephrosis and obstruction.
Computed Tomography Scan of Kidneys: A stone protocol computed
tomography (CT) scan of the kidneys, ureter, and bladder has become the study
of choice for the detection of kidney stones because of its ability to detect
stones of all kinds, including uric acid stones and non obstructing stones in the
ureter.
Computed Tomography Angiography: CT angiography is used for the evaluation
of renal artery stenosis.
Magnetic Resonance Imaging With Magnetic Resonance Angiography: . It is a
good alternative to contrast-enhanced CT, especially in patients who cannot
tolerate iodinated contrast material and in patients for whom reduction of
radiation exposure is desired, such as pregnant women and children.
Electrocardiogram: The electrocardiogram reflects the toxic effects of
potassium excess more closely than determination of the serum potassium
concentration.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1934 40
41. ANAESTHESIA
AND THE
KIDNEYS
STOELTING'S PHARMACOLOGY & PHYSIOLOGY IN ANESTHETIC PRACTICE, 5TH ED., PAGE 429 41
An understanding of kidney function is
important for the anesthesiologist, as
fundamental concepts of perioperative
management include the maintenance of normal
circulating volume, the regulation of electrolytes
and acid– base status, and the clearance of
metabolites and drugs. Perioperative AKI has an
estimated overall incidence of 1% and is
associated with an eightfold increase in risk of
mortality.
42. EFFECTS OF VARIOUS
ANESTHETICS ON RENAL
FUNCTION
GFR, Glomerular
filtration rate; PEEP,
positive end-expiratory
pressure; RBF, renal
blood flow; ↔, no
significant change; o,
significant data; ↓,
decrease.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1938 42
43. EFFECTS OF DRUGS IN PATIENTS
WITH REDUCED RENAL FUNCTION
Opioids
•Morphine, Meperedine should be avoided.
•Fentanyl congeners clinical pharmacology is not grossly altered
by renal failure.
Inhaled Anaesthetics
•Data suggests that renal blood flow is maintained with
Halothane, Isoflurane and Desflurane.
•But RBF is decreased in Sevoflurane.
Intravenous
Anaesthetics
•Thiopental dose to produce and maintain anesthesia should be
reduced.
•Prolonged infusion of Propofol produce green urine though it
doesn’t alter renal function.
MILLER'S ANAESTHESIA, 9TH ED., PAGE 1937 43
45. ANESTHESIA AND RENAL BLOOD
FLOW
Several perioperative factors affect renal blood flow either directly by
hemodynamic effects or indirectly through actions of the sympathetic
nervous system or AVP.
Regardless of the immediate cause, a fall in renal blood flow tends to
decrease the GFR by diminishing blood flow to the renal cortex.
Likewise, decreased renal blood flow puts the renal medulla at risk
for ischemia because the blood supply to this region is already low at
baseline.
The sum effect of these changes is conservation of sodium and water
and, consequently, a decrease in urine output.
STOELTING'S PHARMACOLOGY & PHYSIOLOGY IN ANESTHETIC PRACTICE, 5TH ED., PAGE 430 45
46. 46
Sympathetic stimulation leads to increased renal vascular resistance,
which has two significant effects
First, blood is shunted away from the kidneys to other organs, preserving
perfusion of critical organs such as the brain and heart.
Second, constriction of the afferent renal arterioles lowers glomerular
capillary pressure and decreases the GFR.
• Any factor that decreases the cardiac output will also lead to a release of AVP and an
increase in the activity of both the sympathetic nervous system and the renin-
angiotensin-aldosterone system.
• AVP and aldosterone tend to restore both normal circulating volume and normal renal
blood flow by retaining sodium and water.
• Hypovolemia from acute haemorrhage also increases sympathetic tone, again
reducing renal blood flow.