PCT

if bound to albumin: secretion not filtration

S1: Na and HCO3- reabsorption
S2: organic anion and cation secretion
S3: pars recta
Na-K ATPase: found everywhere except descending limb, no Na reabsorption
occurs
HCO3-: most important solute that promote passive transport, present in highest
concentration, accompanies Na at the first half
Cl-: accompanies NA in the second half
determinant of PCT Na and water reabsorption: Na-K ATPase, Na-H exchanger
anions such as formate maintain the continued reabsorption of Cl-
aquaporin-1: PCT water channels
reabsorption of Na and HCO3-: driving force for passive reabsorption of water by
osmosis, transtubular osmotic gradient
Na reabsorbed down its electrochemical gradient
kidneys major sites of catabolism of plasma proteins including polypeptide
hormones
renal disease: increase hormone levels since it is not degraded
urea: lipid soluble, passive diffusion
urea recycling: at straight PT and Henles loop
urea reabsorption: increase osmolarity in the medullary interstitium, also caused by
Na
patients with protein and energy malnutrition no urea (end product of protein),
difficulty in concentrating their urine
patients with arrhythmia, coadministration of organic acids will increase plasma
conc of both drugs drug toxicity
glomerulotubular balance: tubular reabsorption directly related to GFR
tubuloglomerular feedback: autoregulation

hyperkalemia increase K, hyperpolarization of cardiac cells, arrhythmia

glomerular injury protein in urine
glucosuria urinary excretion of glucose, happens in diabetes mellitus
diabetic necropathy is the leading cause of end-stage kidney disease
osmotic diuresis increased urination
classic cystinuria diminished cysteine reabsorption and formation of cysteine
stones, loss of function of Na-independent transport of cysteine and dibasic aa
nephrotic syndrome albumin reabsorbed by low affinity, high capacity endocytic
process, when filtered in greater than normal amounts
prerenal azotemia rise in BUN due to rise in urea due to rise in Na and water
reabsorption
organic anions bile salts, hippurates, oxalate, prostaglandins, exogenous
substances (acetazolamide, chlorathiazide, salicylates)
organic caitons creatinine, epinephrine, histamine, serotonin, norepinephrine,
exogenous substances (atropine, cimetidine, morphine, procaine, quinine)
Bartter syndrome mutation in NKCC2, mutation in ROMK, loss of function of CLC-
NKB
hypomagnesemia low levels of Mg in blood
hypercalciuria high levels of Ca in urine
nephrocalcinosis high levels of Ca in kidneys
polyhydramnios xs accumulation of amniotic fluid
furosemide NKCC2
ouabain Na-K ATPase
acetazolamide carbonic anhydrase inhibitor, diuretic acting at PCT
cimetidine H2 receptor antagonist, treat gastric ulcers, competes for the secretory
pathway with procainamide, an antiarrhythmic drug
antenatal Barrters syndrome: severe systemic disorder, electrolyte wasting,
polyhydramnios, hypercalciuria, nephrocalcinosis
classic Barterrs syndrome: polyuria, impaired urinary concentrating ability

Loop of Henle
collecting tubule not water-permeable unless there is ADH
most potent diuretic are the ones acting on NKCC2 on TAL
NKCC2 sensitive to furosemide, used to inhibit transepithelial Cl transport by TAL
Maxi K: Ca activated
90% of K transported is recycled through ROMK and Maxi-K
K recycling creates lumen + potential
half of Na, Ca, Mg reabsorption is through paracellular pathway
transport stoichiometry of NKCC2: additional Na transported through paracellular
pathway
claudin: cation selectivity of TAL tight junction, mutation will lead to
hypomagnesemia, hypercaliuria, nephrocalcinosis
thiazide NCC, used to treat HP, edema, nephrolithiasis
amiloride EnaC
Gitelman syndrome loss of function of NCC, low to normal BP, elevated renin,
hypokalemia, metabolic alkalosis, hypocalciuria, hypomagnesemia
Barrter syndrome loss of function of CLC-NKB and Barttin
ClC-Kb channel mutation mixed Barter/Gitelman phenotype, severe neonatal salt
wasting disorder, sensorineural deafness