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126 Cards in this Set

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Summary of Kidney Functions
Excretion of metabolic waste products: urea, creatinine, bilirubin, hydrogen
Excretion of foreign chemicals: drugs, toxins, pesticides, food additives
Secretion, metabolism, and excretion of hormones
renal erythropoetic factor
1,25 dihydroxycholecalciferol (Vitamin D)
Renin
Regulation of acid-base balance
Gluconeogenesis: glucose synthesis from amino acids
Control of arterial pressure
Regulation of water & electrolyte excretion
Main job of kidney is to excrete urea which is the by product of protein metabolism

2nd job is to maintain acid base balance,

then water/salt balance
Capsule has reticular tissue-no stretch-maintains________ hydrostatic pressure
high
functional unit of the kidney
Nephron:
tissue at Bottom of henle is ?
squamous
Prox has _________, none on distal
villi (BRUSH border)
Juice goes out through ______ into bowmans’ capsule
Renin adjusted by ?
podocytes

juxta-aparatuys
Incr symp activity will _______ GFR
drop
GFR is
how much juice gets pushed through the podocytes per minute
regulation of GFR

sympathetic nerves

afferent arteriole?
GFR?
baroreceptors/higher brain centers

constricts
decresases
regulation of GFR

low BP

afferent arteriole?
GFR?
dilates
no change
regulation of GFR

increased BP

afferent arteriole?
GFR?
constricts
no change
Proximal convoluted tubular cells –
can actively transport molecules from filtrate back into blood. By reabsorption
protien
not filtered
sam % in renal artery
zero clearnace
insulin
filtered, not reabsorbed or secreted
less % than in renal artery
clearance = to GFR
urea
filtered partially reabsorbed
less % than in renal artery
clearance less than GFR
glucose
filtered completely reabsorbed
% = renal artery
zero clearance
PAH
filtered and secreted
% less than RA, (appraches zero)
clearance graeter than GFR (up to total plasma flow rate)
K
filtered, reabsorbed and secreted
variable % in renal vein
variable clearance
Excretion of Metabolic Waste Products
Urea (from protein metabolism)
Uric acid (from nucleic acid metabolism)
Creatinine (from muscle metabolism)
Bilirubin (from hemoglobin metabolism)
Excretion of Chemicals
Pesticides
Food additives
Toxins
Drugs
Secretion, Metabolism,
and Excretion of Hormones

Hormones produced in the kidney
Renal erythropoetic factor
1,25 dihydroxycholecalciferol (Vitamin D)
Renin
Secretion, Metabolism,
and Excretion of

Hormones metabolized and excreted by the kidney
Most peptide hormones (e.g., insulin, angiotensin II, a zillion of ‘em.)
Counter current multiplier
Pumping out of NaCl out of the ascending limb makes the interstitium more conc.

Vasa recta pick up salt

Salt is actively pumped out
Urea keeps the filtrate concentrated in the distal tubule
Water is pulled back into the filtrate because of high concentrations of urea
proximal tubule-active transport?

passive?
na

Cl- ,water,urea
descending loop of henle
active transport?

passive?
none

maybe na, water, no urea
Thin segment of ascending limb

active transport?

passive?
no active

nacl, no water, urea
Thick segment of ascending limb

active transport?

passive?
na

cl-, no water, no urea
distal tubule

active transport?

passive?
na

cl-, no water (exc ept the lat part of tubule), no urea
collectin duct (dep[ends on adh_)
active transport?

passive?
slight na

no salt, water (adh) or slight with no ADH, urea
ADH secretion and action

increased osmolality (dehydration)
osm rec's in hypothalamus
increased ADH
decreased urine volume
increased water retention
decreased blood osmolality
ADH secretion and action

decreased osmolality
osm rec's in hypothalamus
decreased ADH
water loss (increased urine volume)
increased blood osm
ADH secretion and action

increased blood volume
stretch receptors in left atrium
decreased ADH
increased urine volume
decreased blood volume
ADH secretion and action

decreased blood volume
stretch receptors in left atrium
increased ADH
decreased urine vol
increased blood volume
adh from?
poterior pituitary
Secretion is
the active transport of molecules from the peritubular cap.s into the filtrate
Inulin –
a polysaccharide produced by onions, artichokes and garlic – is not reabsorbed or secreted. It’s a good indicator of renal clearance and GFR
PAH = para-aminohippuric acid
PAH is both filtered and secreted
It is a good measure of renal blood flow
Excretion = Filtration –
Reabsorption + Secretion
Filtration: somewhat variable, not selective (except for proteins), averages 20% of renal plasma flow

Reabsorption: highly variable and selective, most electrolytes (e.g. Na+, K+, Cl-) and nutritional substances (e.g. glucose) are almost completely reabsorbed; most waste products (e.g. urea) poorly reabsorbed

Secretion: variable; important for rapidly excreting some waste products (e.g. H+), foreign substances (including drugs), and toxins
The reabsorption of Na+ and the secretion of K+ and H+ in the distal tubule. High H+ conc in the blood can lower secretion of K+ (K+ will be lost in the urine)
You lose K if you are acidotic
when a substance is secreted by the nephron, it's renal plasma clearance is ________ than the GFR
greater
Glomerular Filtration
GFR = 125 ml/min = 180 liters/day
Plasma volume is filtered 60 times per day
Glomerular filtrate composition is about the same as plasma, except for large proteins
Filtration fraction (GFR/Renal Plasma Flow) = 0.2 (i.e., 20% of plasma is filtered)
Glomerular Capillary Membrane Filtration Barrier
Endothelium (fenestrated, 160-180 A pores)
Basement Membrane (70-80 A pores), negative charged proteoglycans, restriction site for proteins
Epithelial Cells (podocytes, 80-80 A pores) restriction site for proteins
Glomerular Capillary Filtration
Normally not highly variable
Disease that can reduce Kf (filtration constant) and GFR
chronic hypertension
obesity / diabetes mellitus
glomerulonephritis

Atg/antibodies can get lodges in the glomerulus….like lupus, arthritic conditions
The Ability of a Solute to Penetrate the
Glomerular Membrane Depends on:
Molecular size ( small molecules > filterability)
Ionic charge (cations > filterability)
Bowman’s Capsule Hydrostatic Pressure (PB)
Normally changes as a function of GFR, not a physiological regulator of GFR
Tubular Obstruction
kidney stones
tubular necrosis
Urinary tract obstruction
Prostate hypertrophy/cancer
Glomerular Hydrostatic Pressure (PG)
Is the determinant of GFR most subject to
physiological control?

Factors that influence PG:
arterial pressure (effect is buffered by autoregulation)
afferent arteriolar resistance
efferent arteriolar resistance
Regulation of Arterial Pressure
Endocrine Organ
renin-angiotensin system
prostaglandins
kallikrein-kinin system

Control of Extracellular Fluid Volume
regulation of renin and aldosterone secretion

decreased blood volume
increased renin
increased AT-2
increased aldosterone

low blood volume stimulates renal baroreceptorsa, granular cells release renin
regulation of renin and aldosterone secretion

increased blood volume
decreased renin
decreased AT-2
decreased aldosterone

increased blood volume inhibits baroreceptors.
increased NA in distule tubule acts via
macula densa to inhibit renin release
regulation of renin and aldosterone secretion

increased K+
no effect on renin
no effect on AT-2
increased aldosterone

direct stimulation of adrenal cortex
Regulation of Arterial Pressure
Endocrine Organ
renin-angiotensin system
prostaglandins
kallikrein-kinin system

Control of Extracellular Fluid Volume
regulation of renin and aldosterone secretion

decreased blood volume
increased renin
increased AT-2
increased aldosterone

low blood volume stimulates renal baroreceptorsa, granular cells release renin
regulation of renin and aldosterone secretion

increased blood volume
decreased renin
decreased AT-2
decreased aldosterone

increased blood volume inhibits baroreceptors.
increased NA in distule tubule acts via
macula densa to inhibit renin release
regulation of renin and aldosterone secretion

increased K+
no effect on renin
no effect on AT-2
increased aldosterone

direct stimulation of adrenal cortex
Diuretics
Work on different parts of the nephron to promote the excretion of water.
Electrolytes can leave with the water – that may be bad.
Other Factors That Influence GFR
Prostaglandins: increase GFR; non-steroidal
anti-inflammatory agents can decrease GFR,
especially in volume depleted states
Fever, pyrogens: increase GFR
Glucorticoids: increase GFR
Aging: decreases GFR ~10%/decade after 40 yrs
Dietary protein: high protein increases GFR
low protein decreases GFR
Hyperglycemia: increases GFR (diabetes mellitus)
loop diretics
inhibit na transport
thick segments of scending limbs
thiazides
inhibit na transport
last part of ascending limb and first part of distal
carbonic anhtdrase inhi8bitors

acetazolamide
inhibit reabsorption of bicarb
prox tubule
osmotic diretics
reduces osmotic reabsorption of water by reducing gradient
last part of distal tubule and cortical collecting duct
K-sparing

spironolactone
inhibits na reabsorbtion and K secretion

last part of distal tubule and cortical collecting duct
Functions of Renal Blood Flow
To deliver enough plasma to kidneys for
glomerular filtration

To deliver nutrients to kidney so that the
renal cells can perform their functions (only about 20% of renal blood flow needed for this function)
Regulation of Erythrocyte Production
by kidneys

increased o2 delivery to bean increases EPO which increased RBC production in marrow
Regulation of Vitamin D Activity
by kidney

Kidney produces active form of vitamin D
(1,25 dihydroxy vitamin D3 )

Vitamin D3 is important in calcium and
phosphate metabolism
Regulation of Acid-Base Balance – along with lungs
Excrete acids (kidneys are the only means
of excreting non-volatile acids)

Regulate body fluid buffers
( e.g. Bicarbonate)

Acidification of the urine
Glucose Synthesis
Gluconeogenesis: kidneys synthesize glucose
from precursors (e.g., amino acids) during prolonged fasting
Clinical Significance of Proteinuria
Early detection of renal disease in at-risk patients
hypertension: hypertensive renal disease
diabetes: diabetic nephropathy
pregnancy: gestational proteinuric hypertension (pre-eclampsia)
annual “check-up”: renal disease can be silent
Assessment and monitoring of known renal disease
“Is the dipstick OK?”: dipstick protein tests are not very sensitive and not accurate: “trace” results can be normal & positives must be confirmed by quantitative laboratory test.
Microalbuminuria
Definition: urine excretion of > 25-30 but < 150mg albumin per day

Causes: early diabetes, hypertension, glomerular hyperfiltration

Prognostic Value: diabetic patients with
microalbuminuria are 10-20 fold more
likely to develop persistent proteinuria
Three renal processes
Glomerular filtration
Tubular resorption
Tubular secretion
Glomerular filtration
Glomerular membrane is more than 100X more permeable than capillaries elsewhere.
Hydrostaic pressure is the main filtration pressure
The most prominent factor in changing GFR is hydrostatic pressure.
Kidneys receive 20% - 25% of C.O.
Prox Conv Tube and descending Henle’s
65% of filtrate is reabsorbed through PCT walls back into body. Molecules and water.
Filtrate remains isosmotic- tube is permeable to water
Reabsorption occurs constantly, regardless of hydration level.
20% more is reabsorbed constantly, by the descending Henle loop
PCT and descending Henle’s unaffected by hormones – ADH and aldosterone
6% of total body energy is given over to reabsorption
The remaining 15% of the filtrate (which would amount to 27 L/day) has to be further reduced in ascending Henle’s, DCT, and collecting ducts to maintain body fluid
A person with normal hydration produces 1.5L/day of urine.
99.2% of the ultrafiltrate is reabsorbed
Tubular reabsorption
Tubular reabsorption involves trans-epithelial transport
Active transport moves Na+ across the membrane
Aldosterone promotes Na+ reabsorption (in the DCT and early collecting duct)
Atrial natriuretic peptide inhibits Na+ absorption
Glucose and A.A.s are reabsorbed by secondary active transport, linked to Na+
With the exception of Na+, all actively transported molecules have a transport maximum
Active pumping of Na+ is responsible for the passive movement of Cl-, water, and urea
In general waste products are not reabsorbed
Reabsorption
Na+ is actively pumped through prox conv tubular cells back into the body (cap.s). This is Primary active transport
Glucose and amino acids move through the nephron cell walls in a co-transport mechanism (using a protein carrier molecule). This is secondary active transport. Virtually all the glucose and A.A. molecules presented to the membrane are reabsorbed.
Tubular walls are permeable to water
Desc. Henle’s is very perm to water. Urea diffusion helps make medulla salty. Urea is trapped in the asc. DCT. End of DCT is also imperm to urea and it becomes more conc.
Urea becomes more conc. In DCT & collecting duct, because water is being reabsorbed under the influence of vasopressin.
When vasopressin is secreted in the presence of water deficit, urea recycling concentrates in urine
Urea Recirculation
Urea is passively reabsorbed in proximal tubule.
In the presence of ADH, water is reabsorbed in distal and collecting tubules, concentrating
urea in these parts of the nephron.
The inner medullary collecting tubule is highly
permeable to urea, which diffuses into the
medullary interstitium.
ADH increases urea permeability of medullary
collecting tubule.
Cellular Ultrastructure and Transport Characteristics of Thin Loop of Henle
very permeable
to H2O and doesn’t pump Na
Cellular Ultrastructure and Transport Characteristics of Thick Loop of Henle
not permeable to
to H2O, pumps Na out of filtrate into tissue. H+ secreted into filtrate
Henle
The descending limb is impermeable to salt diffusion
Water is drawn out and the filtrate concentrates
Ascending limb pumps salt out
The increased hypertonicity of the medulla is the main driving effect to pull water out of the nearby collecting ducts.
Cellular Ultrastructure and Transport Characteristics of Early Distal Tubules and Collecting Tubules
not permeable
to H2O
not very
Permeable to
urea
Cellular Ultrastructure and Transport Characteristics of Late Distal Tubules and Collecting Tubules
permeablility
to H2O
depends on ADH
not very
Permeable to
urea
Tubular Secretion
First step is simple diffusion from peritubular
capillaries to interstitial fluid
Enter into tubular cell can be active or passive
Exit from tubular cell to lumen can be active or
passive
Examples: potassium, hydrogen, organic acids,
organic bases, NH3
The most important tubular secretion processes are those for
K+ and H+ (and some organic ions)
Early Distal Tubule
Functionally similar to thick ascending loop
Not permeable to water (called diluting segment)
Active reabsorption of Na+, Cl-, K+, Mg++
Contains macula densa
The Vasa Recta Preserve Hyperosmolarity of Renal Medulla
The vasa recta
serve as
countercurrent
exchangers

Vasa recta blood
flow is low
(only 1-2 % of
total renal
blood flow)
Factors That Contribute to Buildup of Solute in Renal Medulla - Countercurrent Multiplier
Active transport of Na+, Cl-, K+ and other ions from thick
ascending loop of Henle into medullary interstitium
Active transport of ions from medullary collecting ducts
into interstitium
Passive diffusion of urea from medullary collecting ducts
into interstitium
Diffusion of only small amounts of water into medullary
interstitium

Urea is one of the players that keeps the counter current mech running
Net Effects of Countercurrent Multiplier
1. More solute than water is added to the renal medulla
(i.e., solutes are “trapped” in the renal medulla).
2. Fluid in the ascending loop is diluted.
3. Most of the water reabsorption occurs in the cortex
(i.e., in the proximal tubule and in the distal
convoluted tubule) rather than in the medulla.
4. Horizontal gradient of solute concentration established
by the active pumping of NaCl is “multiplied” by countercurrent flow of fluid.
Summary of Water Reabsorption and Osmolarity in Different Parts of the Tubule
Proximal Tubule: 65 % reabsorption, isosmotic
Desc. loop: 15 % reabsorption, osmolarity increases
Asc. loop: 0 % reabsorption, osmolarity decreases
Early distal: 0 % reabsorption, osmolarity decreases
Late distal and coll. tubules: ADH dependent
water reabsorption and tubular osmolarity
Some substances have a maximum rate of tubular transport
due to saturation of carriers, limited ATP, etc.
Transport Maximum: Once the transport maximum is
reached for all nephrons, further increases in tubular
load are not reabsorbed and are excreted.

Threshold is the tubular load at which transport maximum is
exceeded in some nephrons. This is not exactly the same
as the transport maximum of the whole kidney because
some nephrons have lower transport max’s than others.

Examples: glucose, amino acids, phosphate, sulfate
The figure below shows the concentrations of inulin at
different points along the tubule, expressed as the tubular
fluid/plasma (TF/Pinulin) concentration of inulin. If inulin is
not reabsorbed by the tubule, what is the percentage of the
filtered water that has been reabsorbed up to that point.
remains at each point? What percentage of the filtered water
has been reabsorbed up to that point?
Inulin is not reabsorbed and not secreted
Know how to calculate GFR
Clearance is a general concept that describes the
rate at which substances are removed (cleared)
from the plasma.
Renal clearance of a substance is the volume of
plasma completely cleared of a substance
per min by the kidneys.
How fast can these cells pump molecules out?
Carrier mediated transport (like Glu and A.A.s) has a maximum – when all the carriers are full. Transport Max for Glu is 375mg/min.
Fasting blood Glu = about 100mg/dl or 1mg/ml.
GFR = about 125 ml/ min.
Glu is filtered about 125 mg/min.
Carriers are saturated at 375 mg/min
Glucose – for example – arrears in the urine when more Glu passes through the tubule than the cells can pump.
Glu begins to appear in the urine when plasma conc.s are 180-200ml/dl. (some nephrons have a lower threshold than others.)
Calculate the GFR from the following data:
Pinulin = 1.0 mg / 100ml
Uinulin = 125 mg/100 ml
Urine flow rate = 1.0 ml/min
gfr=C.inulin=Uinulin x V divided by Pinulin

gfr=125x1.0 divided by 1.0

gfr =125ml/min
A uninephrectomized patient with uncontrolled diabetes has a
GFR of 90 ml/min, a plasma glucose of 200 mg/dl (2mg/ml), and a transport max (Tm) shown in the figure. What is the glucose excretion for this patient?
30 mg/min
T max
Glucose 320 mg/min
Urates 15 mg/min
Plasma proteins 30 mg/min
Vit. C 1.77 mg/min
Hgb 1 mg/min
Clearances of Different Substances
Substance Clearance (ml/min
inulin 125
PAH 600
glucose 0
sodium 0.9
urea 70

Clearance of inulin (Cin) = GFR
Clearance creatinine (Ccreat) ~ 140 (used to estimate GFR)
Clearance of PAH (Cpah) ~ effective renal plasma flow
Clearance Technique
Renal clearance of a substance is the volume of
plasma completely cleared of a substance per min.
Sodium Chloride and Potassium Transport in Thick Ascending Loop of Henle
In the thick segment, Na+ and K+ together with 2 Cl- enter the tubular cells. Na+ is then pumped out into the interstitial space (and Cl- follows passively). The K+ can diffuse back into the filtrate. Loop diuretics block Na+ from entering the cells in the first place
Regulation of Tubular Reabsorption
Glomerulotubular Balance
Peritubular Physical Forces
Hormones
- aldosterone
- angiotensin II
- antidiuretic hormone (ADH)
- natriuretic hormones (ANF)
- parathyroid hormone
Sympathetic Nervous System
Arterial Pressure (pressure natriuresis)
Osmotic factors
Aldosterone Actions on Late Distal, Cortical and Medullary Collecting Tubules
Increases Na+ reabsorption
Increases K+ secretion
Increases H+ secretion
Abnormal Aldosterone Production
Excess aldosterone - Conn’s syndrome
Na+ retention, hypokalemia, alkalosis,
hypertension

Aldosterone deficiency - Addison’s disease
Na+ wasting, hyperkalemia, hypotension
Control of Aldosterone Secretion
Factors that increase aldosterone secretion
Angiotensin II
Increased K+
adrenocorticotrophic hormone (ACTH)
(permissive role )

Factors that decrease aldosterone secretion
Atrial natriuretic factor (ANF)
Increased Na+ concentration (osmolality)
Angiotensin II Increases Na+ and Water Reabsorption
Stimulates aldosterone
Directly increases Na+ reabsorption
(proximal, loop, distal, collecting tubules)
Constricts efferent arterioles
- decreases peritubular capillary
hydrostatic pressure
increases filtration fraction, which increases
peritubular colloid osmotic pressure)
Angiotensin II Blockade Decreases Na+ Reabsorption and Blood Pressure
ACE inhibitors (captopril, benazipril, ramipril)
Ang II antagonists (losartan, candesartin, irbesartan)

decrease aldosterone
directly inhibit Na+ reabsorption
decrease efferent arteriolar resistance

leads to Natriuresis and Diuresis + Blood Pressure
Antidiuretic Hormone (ADH)
Secreted by posterior pituitary

Increases H2O permeability and reabsorption in
distal and collecting tubules
Allows differential control of H2O and solute
excretion
Important controller of extracellular fluid osmolarity
Stimuli for ADH Secretion
Increased osmolarity
Increased osmolarity
Decreased blood pressure (arterial baroreceptors)
Other stimuli :
- input from cerebral cortex (e.g. fear)
- angiotensin II ?
- nausea
- nicotine
- morphine
Factors that Decrease ADH Secretion
Decreased osmolarity
Increased blood volume (cardiopulmonary reflexes)
Increased blood pressure (arterial baroreceptors)
Other factors:
- alcohol
- clonidine (α-2 adrenergic agonist)
- haloperidol (antipsychotic, tics,Tourette’s)
- caffeine
Stimuli for Thirst
Increased osmolarity
Decreased blood volume
(cardiopulmonary reflexes)
Decreased blood pressure
(arterial baroreceptors)
Increased angiotensin II
Other stimuli:
- dryness of mouth
Factors that Decrease Thirst
Decreased osmolarity
Increased blood volume
(cardiopulmonary reflexes)
Increased blood pressure
(arterial baroreceptors)
Decreased angiotensin II
Other stimuli:
-Gastric distention
Abnormalities of ADH
Inappropriate ADH syndrome (excess ADH)
- decreased plasma osmolarity, hyponatremia

“Central” Diabetes insipidus (insufficient ADH)
- increased plasma osmolarity, hypernatremia,
excess thirst
Disorders of Urine Concentrating Ability
Failure to produce ADH: “Central” diabetes insipidus
Failure to respond to ADH: “nephrogenic” diabetes insipidus
- impaired loop NaCl reabs. (loop diuretics)
- drug induced renal damage: lithium, analgesics
- malnutrition (decreased urea concentration)- kidney disease: pyelonephritis, hydronephrosis,
chronic renal failure
Atrial Natriuretic Peptide Increases Na+ Excretion
Secreted by cardiac atria in response to stretch
(increased blood volume)
directly inhibits Na+ reabsorption
inhibits renin release and aldosterone formation
increases GFR
helps to minimize blood volume expansion
Parathyroid Hormone Increases Renal Ca++ Reabsorption
Released by parathyroids in response to
decreased extracellular Ca++
Increases Ca++ reabsorption by kidneys
Increases Ca++ reabsorption by gut
Decreases phosphate reabsorption Helps to increase extracellular Ca++
Sympathetic Nervous System Increases Na+ Reabsorption
Directly stimulates Na+ reabsorption

Stimulates renin release

Decreases GFR and renal blood flow
Increased Arterial Pressure Decreases Na+ Reabsorption (Pressure Natriuresis)
Increased peritubular capillary hydrostatic pressure
Decreased renin and aldosterone
Increased release of intrarenal natriuretic factors
- prostaglandins
- EDRF
Osmotic Effects on Reabsorption
Water is reabsorbed by osmosis
Decreasing the amount of solutes reabsorbed
in the tubules decreases water reabsorption
i.e. diabetes mellitus: unreabsorbed glucose in
tubules causes diuresis and water loss
i.e. osmotic diuretics (mannitol)
Abnormal Tubular Function: Increased Reabsorption
Conn’s Syndrome: primary aldosterone excess
Renin secreting tumor: excess Ang II formation
Inappropriate ADH syndrome: excess ADH
Abnormal Tubular Function: Decreased Reabsorption
Diabetes Insipidus: decreased water reabsorption,
hypernatremia, increased thirst
- nephrogenic
- lack of ADH
Addison’s disease: decreased Na+ reabsorption and
decreased K+ secretion; lack of aldosterone
Abnormal Tubular Function: Decreased Reabsorption
Fanconi syndrome: generalized decrease in reabsorption
often in proximal tubules;
causes: genetic, heavy metal damage,
drugs (tetracyclines), multiple myeloma,
tubular necrosis (ischemia)
Renal tubular acidosis: decreased H+ secretion, acidosis
causes: genetic, renal injury, etc
Assessing Kidney Function
Albumin excretion (microalbuminuria)
Plasma concentration of waste products
(e.g. BUN, creatinine)
Urine specific gravity, urine concentrating ability
Imaging methods (e.g. MRI, PET, arteriograms,
iv pyelography, ultrasound etc)
Isotope renal scans
Biopsy
Clearance methods (e.g. 24-hr creatinine clearance)
etc
Concentration and Dilution of the Urine
Primarily controlled by ADH
Maximal urine concentration
= 1200 - 1400 mOsm / L
(specific gravity ~ 1.030)
Minimal urine concentration
= 50 - 70 mOsm / L
(specific gravity ~ 1.003)
Water diuresis in a human after ingestion of 1 liter of water
Even though water excretion rates change, solute excretion rates remain fairly constant
Formation of a Dilute Urine
Continue electrolyte reabsorption
Decrease water reabsorption
Mechanism:
1. decreased ADH release
2. reduced water permeability in distal and collecting tubules
Formation of a Concentrated Urine
Continue electrolyte reabsorption
Increase water reabsorption
Mechanism:
Increased ADH release which increases water
permeability in distal and collecting tubules
High osmolarity of renal medulla
Countercurrent flow of tubular fluid
Formation of a Concentrated Urine when Antidiuretic Hormone (ADH) Levels are High
Cells of the DCT and collecting duct reabsorb water
Obligatory Urine Volume
The minimum urine volume in which the excreted
solute can be dissolved and excreted.

Example:
If the max. urine osmolarity is 1200 mOsm/L,
and 600 mOsm of solute must be excreted each
day to maintain electrolyte balance, and excrete
metabolic waste toxins,the
obligatory urine volume is:

600/1200=0.5liter per day