Lyrics · 完整歌詞
The kidneys generate approximately 180 litres of glomerular filtrate each day,
with filtration governed by opposing hydrostatic and oncotic pressures.
Net filtration pressure equals capillary hydrostatic pressure minus Bowman's capsule pressure minus plasma oncotic
pressure,
a margin of only about 10 mmHg.
When a ureteric stone obstructs flow,
pelvic pressure is transmitted back to Bowman's capsule
and filtration falls at once,
a direct consequence of pressure rather than a reflex.
Afferent dilatation or efferent constriction raises capillary pressure and filtration,
whereas a rise in plasma protein lowers it.
Ultrafiltration belongs to the glomerulus alone; the tubule reabsorbs and secretes.
The proximal tubule reclaims glucose, amino acids,
bicarbonate and most filtered sodium and water.
Glucose enters through apical SGLT2 and leaves through basolateral GLUT2,
and nowhere else along the nephron.
The basolateral sodium-potassium pump supplies the gradient for every secondary active transporter.
The thick ascending limb carries NKCC2, the furosemide target,
and dilutes urine because it is impermeable to water.
The distal tubule carries NCC, the thiazide target,
while collecting duct principal cells carry ENaC under aldosterone
and aquaporin-2 under antidiuretic hormone.
The kidneys generate approximately 180 litres of glomerular filtrate each day,
with filtration governed by opposing hydrostatic and oncotic pressures.
Concentration depends on a hypertonic medulla built by sodium chloride transport in the thick
ascending limb
and urea recycling in the inner medullary collecting duct.
A prolonged low-protein diet therefore lowers hepatic urea,
weakens the medullary gradient and reduces concentrating ability.
Antidiuretic hormone acts on V2 receptors,
raising cyclic AMP and protein kinase A,
which move aquaporin-2 vesicles onto the apical membrane.
Water then follows the gradient passively,
whereas aquaporin-1 sits permanently in the proximal tubule and descending limb.
In chronic kidney disease the endocrine role fails first.
As filtration falls, phosphate is retained; hyperphosphataemia, not hypophosphataemia, is the rule.
Renal 1-alpha-hydroxylase declines, calcitriol falls and gut calcium absorption drops,
while phosphate binds calcium and lowers it further.
High phosphate, low calcium,
low calcitriol and an early rise in FGF-23 together drive secondary hyperparathyroidism.
Sustained parathyroid hormone excess accelerates bone resorption and produces osteitis fibrosa cystica,
with lytic brown tumours and subperiosteal resorption.
Oversuppression produces adynamic bone instead,
so KDIGO 2017 keeps parathyroid hormone between two
and nine times the assay's upper limit in dialysis patients.
Phosphate is lowered towards the normal range, calcium-based binders are restricted,
and calcimimetics, calcitriol or vitamin D analogues restrain the glands.
When severe hyperparathyroidism resists medical therapy, parathyroidectomy follows,
with vigilance for hungry bone syndrome.
Hypospadias repair preserves the urethral plate and foreskin and corrects chordee,
with at least six months between staged operations.
In a duplex kidney the Weigert-Meyer rule places the upper-pole ureter inferomedially,
prone to ureterocele, and the lower-pole ureter superolaterally, prone to reflux.
Storage is sympathetic,
through beta-3 receptors that relax the detrusor
and alpha-1 receptors that close the bladder neck.
Voiding is parasympathetic through M3 receptors,
which drive contraction although M2 receptors are more numerous.
In a child with a neurogenic bladder,
storage pressure of 40 cmH2O or more injures the upper tract.
Catheterisation and antimuscarinics therefore aim for low pressure,
large capacity and complete emptying.
The kidneys generate approximately 180 litres of glomerular filtrate each day,
with filtration governed by opposing hydrostatic and oncotic pressures.