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Clinical Fluid Analysis in Renal Function

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4 views7 pages

Clinical Fluid Analysis in Renal Function

Uploaded by

Thomas
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
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MLSC 3054 Clinical Fluid Analysis

Charity Accurso, PhD


MLS Program
University of Cincinnati

 Kidneys
 Two areas
 Cortex
 Medulla
 Ureters
 Bladder
 Urethra
 Functional unit of the kidney
 → Nephron

 Glomerulus

 Proximal convoluted tubule


– PCT

 Loop of Henle – LoH

 Distal convoluted tubule –


DCT

 Collecting duct – CD

Charity Accurso, PhD, MT(ASCP) 1


MLSC 3054 Clinical Fluid Analysis

Afferent arteriole
Renal Nephron
artery capillaries

Glomerulus

Peritubular
Renal Efferent
capillaries and
vein arteriole
vasa recta

•Renal blood flow is ~1200 mL/min


•Total renal plasma flow 600-700 mL/min
•Based on average body size of 1.73 m2 of surface

 Vascular pole
 Secretory granules – renin
 Renin released
 Decreased blood pressure or blood volume
 Decreased sodium
 Increased potassium
 Vascular hemorrhage
 Causes angiotensin formation and aldosterone
secretion
 Outcomes in the kidney:
 Retention of sodium and water

 Main function urine formation


 Eliminate metabolic waste
 Maintain electrolyte and water balance
 Regulate acid/base balance

 180,000 mL of plasma filtered per day


 Final output: 600-1800 mL per day

 Three main processes


1. Glomerular filtration
2. Reabsorption of selective components
3. Secretion of selective components

Charity Accurso, PhD, MT(ASCP) 2


MLSC 3054 Clinical Fluid Analysis

Component Initial Ultrafiltrate, Final Urine, mmol % Reabsorption


mmol

Water 9,500,000.00 67,000.00 99.3%

Urea 910.00 400.00 44.0%

Chloride 37,000.00 185.00 99.5%

Sodium 32,500.00 130.00 99.6%

Potassium 986.00 70.00 92.9%

Glucose 900.00 0.72 100.0%

Albumin 0.02 0.001 95.0%

 Molecular size barrier


 67,000 Daltons

 Three structures
 Capillary endothelium – negatively charged surface that is
fenestrated with large pores – 50-100 nm in diameter
 Trilayer basement membrane
 Podocytes with filtration diaphragms in between
 End result
 Restriction of large proteins
 Passage of water and small molecules

Charity Accurso, PhD, MT(ASCP) 3


MLSC 3054 Clinical Fluid Analysis

 Active transport – must  Passive transport –


combine with a carrier movement across the
protein in membranes of membrane due to difference
renal tubular cells in concentration or electrical
 Electrochemical energy potential on opposite sides
created by interaction of membrane – gradients
transfers the substance  Water in PCT, DLOH, CT
across the cell membranes  Urea in PCT and ALOH
and back into bloodstream
 Sodium ALOH
 Glucose, amino acids, salts
from PCT
 Chloride in ALOH
 Sodium in DCT

Charity Accurso, PhD, MT(ASCP) 4


MLSC 3054 Clinical Fluid Analysis

[Link]

Reabsorption Secretion

 Selective  Eliminate metabolic wastes


 Reabsorbs what is needed for  Eliminate other substances
maintenance of homeostasis not normally present in
 Water plasma
 Salts  Adjust acid-base equilibrium
 Glucose
 Secreted items: hydrogen
 Amino acids
ions, ammonia, potassium,
 Proteins weak acids and bases

 Tubular secretion – helps regulate acid-base equilibrium


 Blood pH – 7.35-7.45
 Disease states: 7.00-7.80
 Endogenous acids
 Oxidative metabolism of foods
 Catabolism of dietary proteins and phospholipids
 Acid production from pathologic or physiologic conditions
 pH maintained
 Blood buffer system – hemoglobin, bicarbonate, inorganic
phosphate
 Pulmonary system
 Renal system

Charity Accurso, PhD, MT(ASCP) 5


MLSC 3054 Clinical Fluid Analysis

1. Recovery of bicarbonate 3. Formation of


 Secretion of H+ by PCT ammonium ions
 Combines with HCO3- to  Ammonia is secreted by
form carbonic acid the DCT
 Dissociation into CO2 and  Combines with excess
H2O eventually leads to a H+ to form NH4+
conversion back to HCO3-  Ammonium ion is
for reabsorption and H+ excreted
for secretion

 Disruption to any of theses


2. Formation of titratable acids processes can result in
 Secretion of excess H+ metabolic acidosis or renal
 Combines with filtered tubular acidosis
phosphate
 Formed acid is secreted

 Tm – maximal reabsorptive capacity

 When plasma conc of substance normally completely


reabsorbed reaches abnormal level
 Substance appears in urine
 Renal threshold
 Glucose 160-180 mg/dL
 Useful to distinguish excess solute filtration and renal
tubular damage
 Glucose in urine with normal blood levels – tubular
damage

 Distal convoluted tubule


 Active reabsorption of sodium
 Controlled by aldosterone
 Secretion of potassium
 Collecting duct
 Reabsorption of water controlled by vasopressin (ADH)
and osmotic gradient
 ADH renders walls of DCT and CD permeable or
impermeable to water

 ↑ ADH (↓ body hydration) = ↑ Permeability = ↑ Reabsorption


= Low-volume, conc urine
 ↓ ADH (↑ body hydration) = ↓ Permeability = ↓ Reabsorption
= High-vol, dilute conc

Charity Accurso, PhD, MT(ASCP) 6


MLSC 3054 Clinical Fluid Analysis

 AKA - vasopressin
 Controls water reabsorption in
collecting tubules
 ADH is produced in
hypothalamus but released into
blood from posterior pituitary
gland
 Causes a change in tubule
epithelium, and increased water
reabsorption occurs
 Release of ADH controlled by
negative feedback with arterial
blood pressure and positive
feedback with plasma osmolality

[Link]

Charity Accurso, PhD, MT(ASCP) 7

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