The document discusses various aspects of kidney anatomy and physiology. It describes the structures and functions of the nephron, kidney vasculature, and how the kidney regulates fluid, electrolyte and acid-base balance. It also discusses factors that can influence renal function during anesthesia, such as choice of anesthetic, fluid management, ventilation settings and pre-existing kidney disease.

2.  Osmolality
 Acid –base & electrolyte balance
 Toxin removal
 Hormones (renin , prostaglandins , kinins)
 Vitamin D metabolism
 Erythropoietin

5.  Outer granular layer of the kidney that contains most of
the nephrons
 Highly vascular (85% -90% of RBF)
 Contains bowmans capsule and convoluted tubules

6.  Less vascular
 contains renal pyramids, renal papillae, renal calyces
(minor/major),renal pelvis
 part of nephron, not located in the cortex
 Site for salt, water and urea absorption

7.  Functional unit of kidney
 1 million functional unit in each kidney

8. Renal corpuscle Renal tubule
glomerulus Proximal convoluted tubules
Glomerular capsule Loop of henle
Distal convoluted tubule
Collecting duct
Juxtaglomerular apparatus

9. Cortical nephron juxtamedullary nephron
Short loop of henle Long loop of henle
Occupy renal cortex Deep into the renal medulla
Do not contain vasa recta Long loop of henle are accompanied
by the vasa recta
85% of nephrons are cortical nephrons Responsible for corticopapillary
osmotic gradient
15%of nephrons are juxta medullary
nephrons

11.  Glomerulus surrounded by a glomerular capsule
 Present with in the renal cortex

12.  Endothelial cells in glomeruli
 Epithelial cells of bowman's capsule
 Mesangial cells

13.  Ultrafiltration of blood
Filtation membrane therefore prevent the passage of :
 Blood cells
 Large proteins
 Most negatively charged molecule more than 8nm

14.  The PCT is responsible for the majority of the
reabsorption.
 Reabsorption : Na+ ,Cl-, water ,bicarbonate , glucose ,
protein ,amino acids , k+ , Mg2+ , Ca2+ , phosphate , uric
acid , urea
 Secretion: Organic anions and cations

15.  There are 3 sections to the loop of Henle:
 1. Thin descending limb
 2. Thin ascending limb
 3. Thick ascending limb
 Reabsortion : Na+, Cl+, water , k+ , Ca2+ ,Mg2+
,establishes concentration gradient within medulla

16.  countercurrent multiplier (the loop of Henle)
 countercurrent exchange (the vasa recta)

18.  Highly vascular
 20%to 25% of Cardiac output

20. Afferent Arteriole
 Transport arterial blood to glomerulus for filtration
 High –pressure capillary bed
Efferent Arteriole
 the blood that is not filtered begins its passage to the
venous system
 It offers resistance to blood flow

21.  transport reabsorbed materials from the PCT and DCT
into kidney veins
 Low –pressure bed formed by efferent vessel
Vasa recta :
 Hairpin loops
 Dip down among the loop of henle.

22.  Vasoconstriction of renal arterioles, which leads to a
decrease in RBF, is produced by activation of the
sympathetic nervous system and angiotensin II.
 At low concentrations, angiotensin II preferentially
constricts efferent arterioles, thereby “protecting”
(increasing) the GFR.

23.  20% of cardiac output goes to kidney
 Clearance: volume of blood that is completely cleared of
a substance per unit of time
 RPF most commonly measured by PAH clearance

24. • Kidney can maintain a nearly constant GFR despite
fluctuations in in systemic arterial BP
 Autoregulated between MAP of 50 and 150 mmhg
Mechanism :
a)Myogenic mechanism
b) Tubuloglomerular feedback
 RBF= RPF/(1- Hematocrit)

25.  Severity of renal impairment
 Cause of renal impairment
 Progression of renal disease

27. Urine output :
 simple method to evaluation of intaoperative
&postoperative renal function
 Oliguria – urine flow less then 0.5ml/kg/h
 It correlates with AKI .
 And fluid administration .

28.  Transient oliguria is almost invetable
 Due to : hypotension ( hypovolemia or surgical stress)
 Anuria suggests post renal obstruction

29.  Best measure of renal function
 Calculated from timed urine volume +urinary and
plasma creatine concentration
 Or from direct measurement of the clearance of either
endogenous or exogenous substance

30.  GFR: 125Ml /min -140 ml /min
 Decreases 1% per year after age of 20
 Clinical manifestation of urenia appear when GFR falls
below 15ml/min/1.73m3

31.  Factors governing filtration rate at capillary beds
1. Total surface area available for filtration
2. Filtration membrane permeability
3. Net filtration pressure
 Ratio GFR to RPF called filtration fraction (FF);
normally 20%

32.  The driving force for glomerular filtration is the net
ultrafiltration pressure across the glomerular
capillaries.
 GFR can be expressed by the Starling equation:
 GFR=Kf [(PGC −PBS )−(πGC −πBS )]
 Kf is the filtration coefficient

34.  Creatinine is endogenous marker of renal filtration
 results from the metabolism of creatine in the liver
 It is freely filtered and not reabsorbed
 Most reliable measure of GFR

35.  0.6 to 1.0 mg /dl in women
 0.8 to 1.3 mg/dl in male
 Varies with muscle mass, rate of catabolism
 Protein intake and physical activity
 low GFR overestimate renal function as little creatinine
is secreted

36.  Urea is formed in liver by deamination of amino acids
and conversion to ammonia by arginine cycle
 Not an indicator of GFR
 Rapidly reabsorbed by the tubules

37.  Absorption of blood from G.I tract ,steroids and sepsis
BUN
 Malnutrition or liver disease BUN
 Ratio of BUN to serum creatinine ratio
10 and 15 to 1
 useful in diagnosis of renal failure from prerenal causes
vs acute tubular necrosis

38.  It is assessed by measuring the urine concentrating
ability
 Protein urea reflect renal tubular damage

39.  Urinary specific gravity is an index of renal tubular
function
 Specific gravity higher than 1.018 suggests that the
ability of renal tubules to concentrate is adeqate

40.  Transient proteinuria is associated with fever ,CHF
seizure activity ,pancreatitis and exercise
 Microalbuminuria is the earliest sign of diabetic
nephropathy
 Severe proteinuria may result in hypoalbuminemia
 Associated in plasma oncotic pressure and in
unbound drug concentration

41.  Measure of the % of filtered sodium that is excreted in
the urine

42.  Useful in differentiating pre-renal and renal cause of
azotemia
 FeNa higher than 2% suggestive of acute tubular
necrosis
 FeNa of less then 1% suggestive of prerenal azotemia

43.  Urinalysis :
a. Gross appearance
b. Microscopic
 Serum and urine electrolytes
 Dipsticks
 Imaging studies
a. CT scan
b. MRI

44.  Markers for GFR :
a. Cystatin C
b. Beta -2 microglobulin
 Biomarkers for tubular function:
a. Albumin
b. Transferrin
c. Lambda and kappa light chain
d. Immunoglobulin C

45.  Biomarkers reflecting tubular cell response to
stress :
a. Neutrophil gelatinase associated lipocalin
b. Urinary interleukin 18
c. Kidney injury molecule1

46.  Decrease GFR and intraoperative urine flow due to
decreased cardiac output and arterial blood pressure .
 Renal injury occurs unless there is preexisting renal
disease , nephrotoxic drug ,hypovolemia or
combination.

47.  Volatile anesthetics induce mild to moderate reduction
in RBF and GFR mainly due myocardial depression and
vasodilatory effects
 Can be attenuated by prior intravenous hydration

48.  Decrease in GFR by decreasing renal perfusion
pressure either by decreasing systemic vascular
resistance (isoflurane or sevoflurane) or cardiac output
(halothane).
 This decrease in GFR is exacerbated by hypovolemia
and the release of catecholamines and antidiuretic
hormone as a response to painful stimulation during
surgery.

49. 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

51.  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

52.  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

53.  Hypertension
 Diabetes Mellitus
 Glomerulonephritis
 SLE
 HIV
 Sickle Cell Disease

54.  Metabolic acidosis
 Altered haemostasis
a. platelet dysfunction
b. prothrombotic tendency and reduced fibrinolysis
 Autonomic neuropathy
 delayed gastric emptying
 parasympathetic dysfunction

55.  Uremia
 Hypertension
 Fluid and electrolytes abnormalities
a. volume overload
b. hyperkalaemia
c. Hypocalcaemia
d. Hyponatraemia
 Hypoalbuminaemia
 Increased Cardiovascular mortality
 Increased risk for infections
 Bone disease

56.  The symptomatic and supportive treatment of
hypotension and hypovolemia.
 Diuretics for volume overload
 Correction electrolyte derangements (hyperkalemia,
acidosis, etc)
 Treatment of sepsis
 Removal of nephrotoxic agents

57.  These patients should be optimized using a
multidisciplinary approach as CKD affects all organ
systems.
 CKD is strongly associated with an accelerated form of
ischaemic heart disease and as such, all patients
should have a baseline ECG.

58.  Vascular access should be chosen carefully; current
and potential fistula sites should be avoided.
 Patients with chronic renal failure should receive
dialysis treatment 12-24hrs before planned surgery to
optimize their electrolyte, metabolic and volume status.

59.  Opioid- based anesthetics are considerably more
effective than volatile anesthetics in suppressing the
release of catecholamine's, angiotensin ll, aldosterone
 ketamine RBF but urine flow rate
(sympathetic activation)
Preserve RBF during hemorrhagic hypovolemia .

60.  Degraded in basic carbon dioxide absorbents (Barium
Hydroxide and Soda lime) into a vinyl ether called
compound A.
 Compound A has been implicated to cause renal injury
through fluoride toxicity (animal studies).

61.  High intra-renal fluoride concentrations impair the
concentrating ability of the kidney and may theoretically
lead to non-oliguric renal failure.
 It is considered safe even in patients with renal
impairment as long as prolonged low-flow anesthesia is
avoided. (Minimum flow ≥ 2 L/min)

62.  Caused dose-dependent abnormalities post-surgery.
 It causes vasopressin-resistant polyuria, serum
hyperosmolality, hypernatremia, increased
concentrations of serum urea nitrogen and inorganic
fluoride, and decreased urinary potassium, sodium,
osmolality, and urea nitrogen concentrations.
 Therefore, clinically it is no longer used

67.  Positive-pressure ventilation used during general
anesthesia can decrease venous return, cardiac output,
renal blood flow, and GFR.
 Decreased cardiac output leads to release of
catecholamine's, ADH, rennin, and angiotensin II with
the activation of the sympathoadrenal system and
resultant decrease in renal blood flow.

68.  Spinal and epidural anaesthesia only slightly decrease
GFR and RBF in proportion to the decrease in mean
arterial pressure.
 The preexisting intravascular volume and the quantity
of intravenous fluids given strongly influence the renal
response to spinal and epidural anaesthesia.
 There is also decreased diuresis and a marked fall in
sodium excretion.
 These trends are gradually reversed during recovery.

69.  Inhalational anaesthetics generally reduce GFR and
urine output, mainly by extra-renal effects that are
attenuated by pre- operative hydration.
 Opioids, barbiturates and benzodiazepines also reduce
GFR and urine output.

70.  The effects of regional anesthesia seem to be less than
those of general anesthesia and are related to changes
in systemic hemodynamic.
 Mechanical ventilation decreases urine volume and
sodium excretion to an extent that depends on the
increase in intrathoracic pressure.

71.  Miller anesthesia
 Stoelting’s anesthesia & co-exiting Diesease
 Pharmacology and physiology for anesthesia