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Renal Physiology and Pathophysiology

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Cook County Urology

on 19 February 2015

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Transcript of Renal Physiology and Pathophysiology

Increased thirst, water intake
Basic renal anatomy


Renal Hemodynamics


Control of vascular tone


Tubular function


Diuretic Effects


Handling of Water


Electrolyte disorders



Acid-Base disorders


Renal Tubular Acidosis

Renal [Patho]Physiology
Renal blood flow
= blood to kidneys (1200ml/min)

Renal plasma flow
= plasma delivered to kidneys (600ml/min)

Glomerular filtration rate
= plasma filtered per min (100-125ml/min)

Filtration fraction
= 20% of RPF is filtered.

80% unfiltered plasma > efferent arteriole > peritubular capillary circulation (counter-current multiplying system)

Essential for concentration of urine
GFR reflects renal function
balance of hydrostatic, oncotic pressures
hydrostatic controlled by pre/post glomerular arteriolar tone
(hormonal control)
GFR approximated by creatinine clearance (filtered, not resorbed, slightly secreted)
Convenient tool to approximate renal function:
endogenous
Vascular tone is net result of vasoconstrictive and vasodilatory forces
Vasoconstrictors:
Endothelin (most potent)
Angiotensin II
Vasopressin
Norepinephrine
Atrial natriuretic peptide (counter-intuitive)
Vasodilators:
Prostaglandins
Acetylcholine
Nitric oxide (potent)
Carbon monoxide (potent)
Renin-Angiotensin-Aldosterone
"low Na/GFR? Secrete renin"
Maintain water, acid, electrolyte balance
Solutes actively reabsorbed
Water passively reabsorbed
Thiazides
HCTZ, Chlorthalidone

Inhibit Na, Cl reabsorption in DCT

Reduce GFR, RBF, diluting capacity of nephron

Reduce urinary Ca
Loop Diuretics
Furosemide, Ethacrinic Acid, Bumetanide

Inhibit N/K/Cl cotransporter thick ascending limb

Increased diuresis, excretion Na, K, Cl, Ca, Mg

Diminishes medullary solute concentration, impairs urinary concentrating and diluting capacity.
Response to water loss...
Increased plasma osmolality, decreased circulating volume (arterial)
Increased ADH, decreased water excretion
Disorders of Water/Sodium
Primary Goals...
Maintain BP
Excrete wastes
Mechanisms...
Thirst
ADH
RAS
Urine Osmolality
Plasma Osmolality
Na+
K+
Ca++
Hyponatremia
Nausea, malaise, headache
lethargy, obtundation, disorientation
stupor, seizures, coma
Hypernatremia

Lethargy, weakness, irritability
twitching, seizures, coma
Hypokalemia
Weakness, ileus, cramps, parathesias
ST segment depression, U-waves
Flattened T-waves
Hyperkalemia
Weakness, paralysis, conduction abnormality
peaked T-waves, wide QRS, arrhythmias
Hypocalcemia
tetany, neuromuscular irritability
fatigue, anxiety, depression
papilledema, seizures
Hypercalcemia
Fatigue, weakness, abd pain
constipation, depression
renal tubular dysfunction,
nephrolithiasis
(<120mEq/L)
Urine sodium concentration
used to distinguish between
volume depletion
vs
euvolemic hyponatremia
low [U]
>30mmol/L
Beware rapid correction!!!
Central Pontine myelinosis
Primary defect is impaired
water intake
Primary defect is renal
water handling
Can correct rapidly in acute setting
Must correct slowly in chronic setting:
(1-2mmol/L/hr until symptoms resolve)
then normalize over next 24-48hrs
Mostly Intracellular

Driven by insulin, bicarbonate
beta-agonists

Results from increased loss (GI, Urine)
or intracellular shifts (alkylosis)
Iatrogenic Causes Common...
diuretics, laxatives, amphotericin,
theophylline, postobstructive diuresis
Reflects decreased renal excretion
or shift out of cells (acidosis)
Most common causes:
Renal failure, K+sparing diuretics
ACE inhibitors, beta-blockers,
chronic acidosis (RTA type 4),
hyperaldosteronism
Management:
Calcium gluconate (reduce risk of V-fib)
Sodium bicarbonate (lasts 30 min)
Glucose + Insulin (temporary intracellular shift)
Sodium polystyrene sulfonate
(exchanges Na+ for K+; binds K+ in gut)
Vitamin-D and PTH
Vitamin-D increases intestinal absorption of calcium, phosphorus, and renal
absorption of calcium.

PTH increases bone resorption, renal reabsorption of calcium and excretion of phosphorus, and stimulates calcitriol production.
Majority of filtered Ca++ is passively
reabsorbed in the
proximal convoluted
tubule
and
thick ascending limb
of the
loop of Henle.
Normal arterial pH 7.37-7.43

Maintained by lungs, kidneys
Check arterial pH
pH < 7.4
acidosis
pH > 7.4
alkalosis
pCO2 > 40mmHg
Respiratory acidosis
Hypoventilation
pCO2 <40mmHg
Metabolic Acidosis
with compensation
Check anion gap
= (Na+) - ((Cl-) + (HCO3-))
High anion gap:
ketoacidosis (diabetes)
lactic acidosis
renal failure
intoxication
Normal (8-12 mEq/L)
GI alkali loss
Renal tubular acidosis
interstitial renal disease
ureterosigmoidostomy
ureteroileal conduit
acetazolamide therapy
ammonium chloride injestion
pCO2 <40mmHg
Respiratory alkalosis
Hyperventilation
pCO2 >40mmHg
Metabolic acidosis
with compensation
Vomiting
Diuretic use
antacid use
hyperaldosteronism
Family of metabolic acidosis syndromes
resulting from defects in tubular H+ secretion
and urinary acidification
RTA Type 1
Most common

distal nephron affected

calcium phosphate stones
(high U pH, Ca++, Low citrate)

diagnosed by urine pH >5.5

Treat: oral alkalinization and citrate
RTA Type 2
Failed bicarbonate reabsorption
in
proximal tubule

Children

Normal citrate, no stones

Growth retardation

Treat: NaHCO3
RTA Type 4
Impaired cation exchange in
distal tubule
with reduced secretion of H+ and K+

Hyperkalemia

Treatment aimed to reduce potassium
Variables:
bowel segment
length used
time of exposure
solute concentration
renal function
urine pH
Stomach
Hypochloremic, hypokalemic, metabolic alkalosis

Worse if co-morbid renal insufficiency

Treat: with PPI, acidification with dilute hydrochloric acid
Jejunum
Hyponatremic
, hypochloremic, hyperkalemic metabolic acidosis

Treat: NaCl replacement and thiazide diuretics
Ileum and Colon Diversions
Hyper
chloremic metabolic acidosis

Treat: Sodium bicarbonate and/or nicotinic acid (chloride transport inhibitor)

Note: Urea and creatinine are reabsorbed by ileum and colon (serum concentration less accurate measure of renal function after diversion)

May produce osteoporosis/malacia with less calcium reabsorption, impaired Vit-D metabolism, and chonric acidosis

May have diminished Vit-B12, bile acid absorption (ileum primary absorption site)

If more than 100cm of ileum resected, can have fat solube vitamin malabsorption (DEAK)
Effects of diversion
Principle cell sodium channel up-regulation.
K+ Sparing
-
Na
Na
Na
Na
Na
Low Na
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