The kidneys are a pair of highly vascular organs located in the lower back that filter waste from the blood and regulate fluid balance. They each contain around 1-1.5 million nephrons, the functional units of the kidney. The kidneys receive a high blood flow and precisely regulate glomerular filtration rate, reabsorption, and secretion to produce urine with the proper electrolyte and water content. Various tests can evaluate renal function by measuring glomerular filtration rate, tubular handling, or the levels of substances such as creatinine, urea, and electrolytes. Acute kidney injury is characterized by a sudden deterioration of renal function over hours to days that impairs waste excretion and fluid/electro

1. Dr. Ibrahim Elkathiri
11/April/2023

2. Introduction
 The kidneys are a pair of highly vascular organs located in the retroperitoneal space
against the posterior abdominal wall between the transverse process of T12-L3 vertebrae.
 They are approx. 12cm long & 150 gram each. The right kidney is lower than the left
kidney due to the position of liver.

3. Blood supply
 The renal arteries arise from the lateral aspect of the abdominal aorta
at L2 vertebral level & enters the kidney through the renal hilum.

4. Nephron
 Length of each nephron is 45-65nm
 Each adult kidney contains around 1-1.5 million nephrons

6. Juxtaglomerular apparatus
 Macula densa – specialised cells in the wall of the
tubule that are capable of sensing and responding to
the composition of tubular fluid.
 Afferent arteriole granular cells – specialised cells
in the wall of afferent arterioles that secrete renin.

8. RENAL BLOOD FLOW
 The kidneys receive a total blood flow of 20-25% of the
cardiac output.
 The blood flow is not evenly distributed throughout the
kidney and is not related to the level of metabolic activity.
 The cortex receives 80% of blood flow, which is the least
metabolically active, while only 10-15% goes to the more
metabolically active medulla.
 Cortex blood flow – 500ml/min/100g
 Outer medulla blood flow – 100ml/min/100g
 Inner medulla blood flow – 20ml/min/100g

9. Mechanisms of Urine Formation

10.  The glomerulus essentially acts as a filter, producing an ultrafiltrate of
the plasma from the glomerular capillaries that enters the Bowman’s
space.
 Structure of the filter:

11.  The degree to which solutes are filtered is dependent on two
physical properties:
 Molecular weight
 • Less than 7000 Daltons – molecules will be freely filtered
 • Greater than 70 000 Daltons – molecules are essentially not
filtered at all
 • In between 7000 and 70 000 Daltons - the percentage of a
molecule that is filtered decreases with increasing weight
 • Electrical charge
 • For any given molecular weight between 7000 and 70 000
Daltons a lower percentage of negatively charged molecules will
be filtered
 • This is due to the basement membrane having a negative
charge and therefore repelling negatively charged molecules

12. Glomerular Filtration
 Volume of fluid filtered from the glomerular
capillaries into bowman’s capsule per unit time.
Governed by (and directly proportional to)
 • Total surface area available for filtration
 • Filtration membrane permeability
 • NFP
Normal values 120 +/- 25 ml/min (male)
95 +/- 20 ml/min (female)
Calculated using inulin or creatinine clearence
 filtration fraction GFR/RPF = 20%

13. REGULATION OF GLOMERULAR
BLOOD FLOW
 GFR is regulated using three mechanisms
 1. Renal Autoregulation
 2. Neural regulation
 3. Hormonal regulation

14. Renal Autoregulation
 Goal: maintain constant filtration under variations in
arterial pressure
• Maintains a nearly constant GFR when MAP is in the
range of 80–180 mm Hg
• Two types of renal autoregulation
• Myogenic mechanism
• Tubuloglomerular feedback mechanism,
which senses changes in the juxtaglomerular apparatus.

15. Myogenic Mechanism
BP : constriction of afferent arterioles
• Helps maintain normal GFR
• Protects glomeruli from damaging high BP
BP : dilation of afferent arterioles
• Helps maintain normal GFR

16. Tubuloglomerular Feedback Mechanism
 Flow-dependent mechanism directed by the Macula densa cells.

17. Neural regulation of GFR
 Kidneys are supplied by sympathetic ANS fibres that cause
vasoconstriction of afferent arterioles.
 • At rest, sympathetic activity is minimal renal blood
vessels are maximally dilated renal autoregulation
predominates.
 • With moderate sympathetic stimulation, both afferent
& efferent arterioles constrict equally blood flow
decreases decreases GFR slightly.
 • With extreme sympathetic stimulation ( exercise or
hemorrhage), vasoconstriction of afferent arterioles
reduces blood flow reduces GFR lowers urine output &
permits blood flow to other tissues.

18. Hormonal regulation of GFR
 • Renin-Angiotensin Mechanism
 • Renal prostaglandins
 • Atrial natriuretic peptide (ANP)
 • Nitric oxide
 • Endothelin

19. Renin-Angiotensin Mechanism

20.  Renal prostaglandins:
 When renal blood flow is compromised.
 Afferent arteriole vasodilatation & maintain
glomerular blood flow and GFR.
 Atrial natriuretic peptide:
 ANP is released in response to increased atrial stretch
 cause vasodilatation of the afferent arterioles
 increase GFR.

21. Tubular reabsorption & Secretion

22. The Proximal Tubule
 • Of the Ultrafiltrate formed in Bowman’s capsule 65–75%
is normally reabsorbed in the proximal tubules.
 • The first part of the proximal tubule reabsorbs about
100% of the filtered glucose, lactate, and amino acids.
 • The major function of the proximal tubule is Na+
reabsorption. Sodium is actively transported out of
proximal tubular cells at their capillary side by Na-K-
ATPase.
 • H+ are extruded into the tubule in exchange for
bicarbonate by a sodium-H+ antiporter system.

23. THICK ASCENDING LOOP OF HENLE
• It reabsorbs about 20% of the filtered sodium, chloride,
potassium, and bicarbonate.
• In thick ascending loop, sodium is actively reabsorbed, but water
remains.
• In this so-called diluting segment of the kidney, tubular fluid
osmolality decreases to less than 150 mOsm/kg.
• An important symporter protein system couples the reabsorption
of sodium, chloride, and potassium across the apical membrane.
• Blockade of this system is the major site of action of loop
diuretics.

24. DISTAL TUBULE AND COLLECTING
DUCT
• The proximal segment of the distal tubule is structurally and
functionally similar to the thick ascending limb.
• Sodium reabsorption is mediated by an apical cell membrane
NaCl symporter system, which is the site of action of thiazide
diuretics.
The last part of the distal tubule is composed of two types of cells.
• Principal cells reabsorb sodium , water and secrete potassium
via the Na-K-ATPase pump
• Intercalated cells secrete H+ and reabsorb bicarbonate

25. Urine Concentration And Dilution
Importance:
 When there is excess water: osmolarity is reduced,
the kidney can excrete urine with an osmolarity as low
as 50 mOsm/liter.
 Conversely, when there is deficiency of water and
extracellular fluid osmolarity is high, the kidney can
excrete urine with a concentration of about 1200 to
1400 mOsm/liter.

28. Renal function test

29. Why test renal function?
 To assess the functional capacity of kidney.
 Severity and progression of the impairment.
 Monitor the safe and effective use of drugs which are
excreted in the urine.
 Monitor response to treatment.
 Early detection of possible renal impairment.

30. When should we assess renal
function?
 Older age
 Family history of Chronic Kidney disease (CKD)
 Diabetes Mellitus (DM)
 Hypertension (HTN)
 Autoimmune disease
 Systemic infections
 Urinary tract infections (UTI)
 Nephrolithiasis
 Obstruction to the lower urinary tract
 Drug toxicity

31. Biochemical Tests of Renal
Function
 Measurement of GFR
 Clearance tests
 Plasma creatinine
 Urea, uric acid and β2-microglobulin
 Renal tubular function tests
 Osmolality measurements
 proteinuria
 Glycosuria
 Urinalysis
 Appearance
 Specific gravity
 pH
 Glucose
 Protein
 Urinary sediments

32. Glomerular Filtration Rate
 GFR = rate (mL/min) at which substances in plasma
are filtered through the glomerulus.
 Best indicator of overall kidney function
 In the normal adult, this rate is about 120 ml/min;
about 180 litres/Day

33. Measurement of GFR
 Clearance tests
 Plasma creatinine
 Urea, uric acid and β2-microglobulin

34. Clearance
 Clearance is defined as the volume of plasma cleared
of a substance per unit time.
 C = (U x V)/P
▫ C = clearance
▫ U = urinary concentration
▫ V = volume of urine produced/min
▫ P = plasma concentration

35. Markers of GFR
 • Ideal characteristics:
 Freely filtered at the glomerulus
 No tubular secretion or reabsorption
 No tubular metabolism
 Types of markers:
• Exogenous –Inulin, 124I-iothalamate, 48Cr-EDTA
• Endogenous -- Creatinine.

36. Inulin clearance
 The Volume of blood from which inulin is cleared or
completely removed in one min is known as the inulin
clearance and is equal to the GFR.
Male-110 to 140 mL/ min/1.73m2
Female- 95 to 125 mL/min/1.73m2
 Limitations
 ▫ Expensive, hard to obtain.
 ▫ Difficult to assay & invasive.

37. Creatinine
 1-2% of muscle creatine spontaneously converts to
creatinine daily and released into body fluids at a constant
rate.
 Since Creatinine is released into body fluids at a constant
rate and its plasma levels is maintained within narrow
limits Creatinine clearance may be measured as an
indicator of GFR.
 Endogenous creatinine produced is proportional to muscle
Mass the production varies with age and sex.

38. Creatinine Clearanace
 Creatinine clearance in adults is normally about of 120
ml/min.
 Advantages
 ▫ Endogenous
 ▫ Produced at a constant rate per day
 ▫ Routinely measured
 ▫ Freely filtered at glomerulus
 Disadvantages
 ▫ 10% is secreted by renal tubules

40. Creatinine Clearance
 Plasma creatinine derived from muscle mass
which is related age, weight, sex.
MODIFICATION OF DIET IN RENAL DISEASE
 eGFR(ml/min) = 175 x sr. creat(-1.154) x age(-0.203)
For females, the derived eGFR is multiplied by 0.742

41. The Schwartz equation (less then 18 years old)
eGFR(ml/min/1.73m2)= length in cm x K
sr. creatinine(mg/dl)
K= 0.33 for premature infants
K= 0.45 for term infants to 1year
K= 0.55 for 1 year to 13 years
K= 0.70 in adolescent males ( females- 0.55)

42. Blood urea nitrogen
 • Blood urea nitrogen is directly related to protein catabolism and
inversely related to glomerular filtration.
 The reference interval is 8-20 mg/dl.
 Plasma concentrations also tend to be slightly higher in males than
females.
 Measurement of plasma creatinine provides a more accurate
assessment than urea because there are many factors that affect urea
level.
 Non renal factors can affect the BUN level:
 Mild dehydration
 high protein diet
 increased protein catabolism, muscle wasting as in starvation
 GIT haemorrhage
 Rhabdomyolysis

43. Clinical Significance
 Condition associated with elevated levels of BUN are
referred to as azotemia.
 Causes of BUN elevations:
 Prerenal: renal hypoperfusion
 Renal: acute tubular necrosis, glomerulonephritis
 Postrenal: obstruction of urinary flow.

44. Uric acid
 Renal handling of uric acid is complex and involves four
sequential steps:
 Glomerular filtration of virtually all the uric acid in capillary
plasma entering the glomerulus.
 Reabsorption of about 98 to 100% of filtered uric acid in PCT.
 Subsequent secretion of uric acid into the lumen of the distal
portion of the proximal tubule.
 Further reabsorption in the distal tubule.
 Hyperuricemia is defined by serum or plasma uric acid
concentrations higher than 7.0 mg/dl (0.42mmol/L) in men or
greater than 6.0 mg/dl (0.36mmol/L) in women.

45. Plasma β2-microglobulin
It is present on the surface of most cells & in low
concentrations in the plasma.
It is completely filtered by the glomeruli and is
reabsorbed and catabolized by proximal tubular
cells.
Being unaffected by diet or muscle mass, the
plasma concentration of β2-microglobulin is a good
index of GFR in normal people.
It is increased in certain malignancies and
inflammatory diseases.

46. Diuretics
Mannitol: 0.25 to 1 g/kg
 Most commonly used osmotic diuretic. There is no
evidence to suggest that mannitol provides renal
protection or lessens the severity of AKI. A rapid
intracellular to extracellular shift of water can
precipitate pulmonary edema in patients with limited
cardiac reserve. If fluid and electrolytes are not
replaced after diuresis, mannitol administration can
result in hypovolemia, hypokalemia, and hyper-
natremia.

47. Loop diuretics:
 Inhibit sodium and chloride reabsorption in thick
ascending limb. Commonly used in hypervolemic
states of sodium overload (e.g., heart failure, cirrhosis)
and hypertension. There is no evidence that loop
diuretics provide renal protection or lessen the severity
of AKI.

48. Thiazide diuretics:
 Act at the distal tubule, inhibiting sodium
reabsorption. Synergistic when used with a loop
diuretic. Indications include hypertension, edematous
disorders, hypercalciuria, and nephrogenic diabetes
insipidus.

49. Potassium-sparing diuretics:
 Overall weak diuretic agents. Typically used only to
counteract more potent diuretics and their potassium-
wasting effect.

50. Carbonic anhydrase inhibitors:
 Interfere with sodium reabsorption and hydrogen
secretion in proximal tubules. Used for correction of
metabolic alkalosis and alkalization of urine.
 acetazolamide, 250 to 500 mg

52. RENAL IMPAIRMENT- ACUTE KIDNEY INJURY
◾ Acute renal failure is characterized by the sudden and often reversible
deterioration of renal functions over a period of hours to few days or
weeks, resulting in failure of the kidneys to excrete nitrogenous waste
products and to maintain fluid, electrolytes and acid-base homeostasis.
◾ KDIGO defines AKI as any of the following:
◾ Increase in serum creatinine by 0.3mg/dL or more within 48 hours or
◾ Increase in serum creatinine to 1.5 times baseline or more within the last 7 days
or
◾ Urine output less than 0.5 mL/kg/h for 6 hours

53. ◾ It can be categories as:
◾ Pre-Renal ARI (~55%)- Diseases that cause renal hypoperfusion, resulting in ↓
function without frank parenchymal damage,
◾ Renal or Intrinsic ARI (~40%)- Diseases that directly involve the renal parenchyma,
◾ Post-Renal ARI (~5%)- Diseases associated with urinary tract obstruction.

54. ACUTE KIDNEY INJURY

55.  Patients with AKI can be oliguric or non-oliguric on the basis of their
urine production. (Oliguria <400ml/day, Non-oliguria >400ml/day)
◾ AKI can also be categorised into varying stages:
◾ RIFLE
◾ AKIN
 The prognosis of patients with AKI is related to the cause, the
presence or absence of pre-existing renal disease as well as the
duration of renal dysfunction prior to therapeutic intervention. The
condition was thought to be completely reversible, however some
patients may progress to chronic renal failure.

57. RENAL IMPAIRMENT- CHRONIC RENAL
FAILURE
◾Chronic Kidney Disease (CKD) refers to an
irreversible and progressive deterioration in
renal function which develops over months to
years.
◾It causes a multi-systemic dysfunction which can
be caused by the primary disease process, effects
of uremia or both.

58. STAGES OF CKD
◾Stage 1: Kidney damage with normal or ↑GFR
(≥90 ml/min)
◾Stage 2: Kidney damage with mild ↓GFR (60–89
ml/min)
◾Stage 3; Moderate ↓GFR (30–59 ml/min)
◾Stage 4: Severe ↓GFR (15–29 ml/min)
◾Stage 5: Kidney failure with GFR<15 or need to
dialysis

60. Aetiology of CKD
◾ Hypertension (
35%)
◾ Diabetes Mellitus
(15%)
◾ Glomerulonephri
tis (6%)
◾ SLE (6%)
◾ HIV (5%)
◾ Sickle Cell
Disease (4%)
◾ Others

61. SOME FEATURES OF CHRONIC KIDNEY DISEASE
◾ Metabolic acidosis
◾ Altered haemostasis
◾ - platelet dysfunction
◾ - prothrombotic tendency and
reduced fibrinolysis
◾ Autonomic neuropathy
◾ - delayed gastric emptying
◾ - parasympathetic dysfunction
◾ Uremia
◾ Hypertension
◾ Fluid and electrolytes
abnormalities
◾ volume overload
◾ hyperkalaemia – exacerbated
by acidaemia
◾ Hypocalcemia
◾ Hyperphosphatemia
◾ Hyponatraemia
◾ Hypoalbuminaemia
◾ Increased Cardiovascular
mortality
◾ Increased risk for infections
◾ Bone disease

62. Preoperative assessment of the patient
with kidney disease

63. History
 Cause, nature and course of the disease process should
be ascertained
 Does this patient present with AKI, CKD or Acute on
chronic kidney failure?
 Cause of AKI should be sought:
 prolonged hypotension?
 sepsis/ rhabdomyolysis/nephrotoxic drugs
 What is the patient’s fluid balance over the preceding
days?
 h/o Diabetes Mellitus and Hypertension?

64.  In patients with known CKD, assess the stage of the disease.
 If this is stage 5, does the patient receive RRT?
 What modality of RRT?
 When was RRT last provided, and when is the next due?
 What is the patient’s ‘DRY WEIGHT’?
 What is the urine output per day?
 Clinical indications for urgent RRT
 Acidosis
 Electrolyte abnormalities
 Intoxication
 Oedema/fluid overload
 Uremic consequenses

65. Symptoms
 Infections- fever, chest symptoms, dysuria
 Obstruction- difficulties in voiding or incontinence
 Fluid overload- orthopnea, PND
 Palpitations
 Uremic and/or anaemic- lethargy, malaise, reduced
appetite

66. Clinical examination
 volume status- hypovolaemia/ fluid overload
 CVS- HR, BP, pericardial rub (uraemia) or abnormal
HS(gallop rhythm in heart failure)
 RS- Crepitations, tachypnoea
 Neurological- signs of uremia, peripheral neuropathy
 Hyperpigmentations & rashes- in CKD (vasculitis,
lupus)
 Assessment of potential sites for IV access

67. Investigations & Diagnostic Tools
 CBC – Anemia, leucocytosis, thrombocytopenia
 S. urea(15-45 mg/dl)
 S.Creatinine (0.6-1.3 mg/dl)
 Creatinine clearence (110-150 ml/min)
 Serum Electrolytes- Hyperkalemia
 Urinalysis
 CXR
 ECG & ECHO
 ABG- Metabolic acidosis, hypoxemia

68. Pre Anaesthetic Optimisation
 Symptomatic and supportive treatment- hypotension,
hypovolemia, low cardiac output state- BP correction
 Treat underlying cause
 Correct fluids
 Electrolytes and acid-base derangements
 Dialysis

69. Monitoring
 All routine monitoring – ECG, NIBP, SpO₂, EtCO.
 Monitoring urinary output and intravascular volume
(desirable urinary output: 0.5 ml/kg/hr)
 Intra-arterial, central venous, pulmonary artery
monitoring are often indicated
 Intra-arterial blood pressure monitoring in poorly
controlled hypertensive patients

70. Pre-Medication
 Reduced doses of an opioid or BZD
 H2 blocker - Aspiration prophylaxis
 Metoclopramide -for accelerating gastric emptying,
prevent vomiting, ↓risk of aspiration
 Antihypertensive agents should be continued until the
time of surgery

71. Induction
drug Normal dosage Altered dosage
Thiopental 3-5 mg/kg 2-3 mg/kg
Propofol 1-2 mg/kg 1-2 mg/kg
Etomidate 0.2-0.4 mg/kg 0.2-0.4 mg/kg
Succinylcholine 1-2 mg/kg 0.5-1.5 mg/kg
Atracurium 0.6 mg/kg 0.6 mg/kg
Cisatracurium 0.15 mg/kg 0.15 mg/kg

72. Drug Metabolism/Excretion Efficacy
Succinylcholine Plasma cholinesterase Use cautiously in
hyperkalemia
Atracurium *Hoffman degradation safe
Cisatracurium Hoffman degradation safe
Vecuronium Renal elimination *active
metabolite
Prolonged duration of
action
Rocuronium Hepatic & renal clearance Prolonged duration of
action
Pancuronium Renal elimination Prolonged duration of
action

73. Drugs Drugs safe Drugs safe in
limited or
reduced
doses
Drugs that either
Contraindicated or
Unsafe
Premeditation Temazepam Diazepam Midazolam (unsafe)
Induction Propofol, Etomidate thiopentone
Maintenance Desoflurane,
Isoflurane, Halothane
Sevoflurane Enflurane,
Methoxyflurane
Muscle Relaxants Sch, Atracurium,
Cisatracurim
Vecuronium,
Rocuronium
Pancuronium
Opioids Remifentanil,
Fentanyl,
Alfentanil, Sufentanil
Morphine Pethidine
Local Anaesthetic Bupivacaine,
Lidocaine
Analgesic Paracetamol opioids NSAIDS

74. Reversal
 Neuro-muscular blockade is reversed with Neostigmine or
pyridostgmine in combination with anticholenergic.
 Neostigmine and pyridostgmine has 50% & 70% renal
elimination respectively.
 Glycopyrolate has 80% renal excretion so should be used
cautiously.
 Atropine undergoes 25% renal elimination and rest
undergoes hepatic metabolism to form metabolite
noratropine which has renal excretion.
 Extubation should be done after complete reversal of NM
blockage.

75. Post Operative
 Monitoring of fluid overload or hypovolemia-titrate
fluids
 Residual neuromuscular blockade
 Monitoring of urea and electrolytes
 ECG monitoring for detecting cardiac dysrhythmias
 Continue oxygen supplementation in post operative
period
 Analgesia
 Carefully titrated opioids, ↑CNS depression,
respiratory depression – naloxone.

76. SUMMARY
◾ Patients presenting for surgery with renal
insufficiency or failure present a significant challenge
for the anesthesiologist.
◾ The perioperative care of these patients should be
arranged and carried out by senior staff from surgery,
anaesthesia and renal medicine
◾ Failure to care for these patients well will impact their
perioperative morbidity and mortality.

77. OTHER CONCERNS

78. Thank you

79. REFERENCE
 Dr. Sathyaprabu
 Dr. ERROL WILLIAMSON
 Morgan & mikhail’s clinical anesthesiology 7th edition
 Stoelting’s pharmacology & physiology in anesthetic
practice
 Miller’s anaesthesia 8th edition