Renal Flashcards
pronephros develops by
Week 4, then degenerates
Mesonephros
interim kidney during 1st trimester, later contributes to male genital system
metanephros
permanent kidney
When does metanephros appear? contiues through
5th week of gestation. Nephrogenesis continues through 32-36 weeks.
When is ureteric bud fully canalized by?
10th week
What is ureteric bud derived from?
caudal end of mesonephric duct
What does ureteric bud give rise to?
ureter + pelvises + calyces + collecting ducts
what does metanephric mesenchyme give rise to?
Glomerulus through to DCT.
what are congenital malformations of kidney often due to?
aberrant interaction between ureteric bud and metanephric mesenchyme.
causes of Potter disease
ARPKD + obstructive uropathy (posterior urethral valves) + bilateral renal agenesis + chronic placental insufficiency
Potter sequence presentation
POTTER (pulmonary hypoplasia, Oligohydramnios (trigger), Twisted face, Twisted Skin, Extremity defects, Renal failure (in utero.
horseshoe kidney assocations
1) hydronephrosis (ureteropelvic junction obstruction.
2) renal stones
3) infection
4) chromosomal aneuploidy syndromes (13,18,21)
5) renal cancer (rarely)
Diagnosis of unilateral renal agenesis
US
cause of unilateral renal agenesis
Ureteric bud fails to develop and induce differentiation of metanephric mesenchyme.
kidney consisting of cysts and connective tissue
multicystic dysplastic kidney
cause of multicystic dysplastic kidney
ureteric bud fails to induce differentiation of metanephric mesenchyme
Causes of duplex collecting system
1) 2 ureteric buds reaching and interacting with metanephric blastema
2) bifurcation of ureteric bud before it enters the metanephric blastema, creating a Y-shpaed bifid ureter.
Why do duplex collecting systems create problems?
1) vesicoureteral reflux
2) ureteral obstruction
3) increased risk for UTIs
what usually happens with congenital solitary functioning kidney?
1) majority asymptomatic
2) compensatory hypertrophy of kidney
3) anomalies in contralateral kidney common though.
which kidney is usually taken during donor transplantation?
left (longer renal vein)
Renal blood flow
renal artery –> segmental artery –> interlobar artery –> arcuate artery –> interlobular artery –> afferent arteriole –> glomerulus –> efferent arteriole –> vasa recta/peritubular capillaries –> venous outflow
angiotensin II affects
1) Potent vasoconstrictor with preferential affects on the efferent arteriole, thus increasing FF to preserve GFR in low vlume states.
2) increases NE release by renal sympathetic nerves, thus stimulating aldosterone release
3) secondary effect is to increase HCO3- reabsorption (permitting contraction alkalosis)
4) Affects baroreceptor function; limits reflex bradycardia.
5) stimulates hypothalamus –> thirst
6) Acts at AT II receptor on vascular smooth muscle –> vasoconstriction –> increased BP.
8) stimulates ADH release from anterior pituitary.
9) increases PCT Na/H activity –> Na, HCO3, H2O reabsorption (can permit contraction alkalosis).
macula densa location
Lines the wall of the cortical thick ascending limb, at the transition to the DCT.
function of macula densa
when GFR drops, NaCl presentation to the macula is reduced , macula densa signals to juxtaglomerular cells in the afferent arteriole, causing them to release renin and activate the RAAS. Thus causing efferent arteriole vasoconstriction and increased GFR.
common complication of gynecologic procedures (ligation of uterine or ovarian vessels)
Damage to ureter, leaking to ureteral obstruction or leak.
relation of ureter to vas
Ureter passes UNDER vas deferens
percent of total body weight of total body water, ICF, ECF
60-40-20. 60% of your body water is total body water, of which 40% is ICF and 20% is ECF.
How is plasma volume measured?
Radiolabeling albumin.
How is ECF volume measured?
Inulin or mannitol
osmolality
285-295 mOsm/kg H2O
How to calculate HCT
roughly 3 x [Hb] in g/dL
RBC volume
2.8 L
ECF breakdown
interstitial fluid comprises 75% of ECF, Plasma comprises 25% of ECF
what component of the glomerular filtration barrier is lost in nephrotic syndrome?
Charge barrier
Composition of glomerular filtration barrier
1) fenestrated capillary endothelium (size barrier)
2) Fused BM w/ heparan sulfate (negative charge and size barrier)
3) epithelial layer consisting of podocyte foot processes (negative charge barrier)
Renal clearance equation
Cx = Ux V/Px (FA 556)
clearance and GFR relationship
Cx net reabsorption
Cx>GFR –> net secretion
Cx = GFR –> no net secretion or reabsorption
How to calculate GFR
1) Clearance of inulin. (given by above equation)
2) creatinine clearance
Normal GFR
100 mL/min
Describe creatinine clearance as a measure of GFR
Approximate. Slightly overestimates GFR because creatinine is moderately secreted by renal tubules.
How to estimate effective renal plasma flow (eRPF)? why?
PAH clearance. This is because between filtration and secretion there is nearly 100% excretion of all PAH that enters the kidney. It rises rapidly and is not reabsorbed anywhere.
eRPF as an estimate of RPF
It UNDERestimates true renal plasma flow slightly.
Normal FF
20%
How to calculate filtered load (mg/min)
GFR (mL/min) x plasma concentration (mg/mL)
How do prostaglandins affect FF?
No effect on FF because they increase both RPF and GFR
angiotensin II affect on FF
Increase FF because they decrease RPF and increase GFR by constricting efferent arteriole.
Effect of ureter constriction on GFR and FF
Decrease GFR + FF (backup causes increased hydrostatic pressure)
Effect of dehydration on GFR, RPF, and FF
Decrease GFR and decrease RPF BUT increase FF (RPF decreased to a greater degree than GFR).
Filtered load equation
Filtered load = GFR x Px
Excretion rate equation
V x Ux
Reabsorption/secretion
just difference between filtered and excreted
FEna
Na+ excreted/Na+ filtered
Glucose clearance
at a normal plasma level, glucose is completely reabsorbed in PCT by Na+/glucose ACTIVE cotransport.
When does glucosuria begin?
around 200 mg/dL
when do glucose glucose transporters become fully saturatd (Tm)?
375 mg/min
Why are glucosuria and aminoaciduria common in pregnancy?
pregnancy decreases ability of PCT to reabsorb glucose and amino acids.
What is “splay”?
Region of substance clearance between threshold and Tm. Basically, individual nephrons vary in absorptive capacity, so beyond the threshold there are still some nephrons capable of reabsorption.
PCT functions
1) reabsorbs all glucose and amino acids and most HCO3-, Na+, Cl-, PO4, K+, H2O, uric acid
2) generates and secretes NH3, which acts as a buffer for secreted H+ (which is secreted when Na+ is absorbed)
PTH action in the proximal tubule
Inhibits Na+/PO4 cotransport, cauisng phosphate excretion.
Fraction of Na+ reabsorbed in the proximal tubule
65-80%
Function of thin descending loop of henle
passive reabsorption of H2O via medullary hypertonicity (impermeable to Na). Thus, this is a concentrating segment.
Fraction of Na reabsorbed in the thick ascending limb
10-20%
Ca2+ and Mg2+ transport
Paracellular absorption in thick ascending limb through positive lumen potential generated by K+ backleak.
Thick ascending limb and affect on tonicity
Impermeable to H2O. Makes urine less concentrated as it ascends.
Early DCT affect on tonicity
Reabsorbs Na, Cl- thus diluting urine.
PTH action in the early DCT
Increases Ca/Na exchange leading to Ca reabsorption.
Fraction of Na absorbed in the DCT
5-10%
triamterene
K+-sparing diuretic
collecting tubule function
Reabsorbs Na+ in exchange for secreting K+ and H+ (regulated by aldosterone).
Sodium absorption in the collecting tubule
3-5%
Fanconi syndrome defect
Generalized reabsorptive defect in PCT. Associated with increased excretion of nearly all amino acids, glucose, HCO3-, and PO4.
Causes of fanconi syndrome
Wilson disease, tyrosinemia, glycogen storage disease, cystinosis, ischemia, MM, nephrotoxins/drugs (ifosfamide, cisplatin, tenofovir, expired tetracyclines), lead poisoning.
Which is more severe, gitelman’s or bartter’s syndrome?
Barter’s
differentiating barter’s from gitelman’s in metabolic profile
gitelman’s causes hypocalciuria, Bartter’s causes hypercalciuria
Example of a gain of function mutation
Liddle syndrome
Syndrome of apparent mineralocorticoid excess
1) pathophys
2) presentation
3) treatment
hereditary deficiency of 11beta-hydroxysteroid dehydrogenase, which normally converts cortisol into cortisone in mineralocorticoid receptor-containing cells before cortisol can act on the mineralocorticoid receptors. /excess cortisol in these cells from enzyme deficiency leads to increased mineralocorticoid receptor activity. /presentation = hypertension + hypokalemia + metabolic alkalosis. /low serum aldosterone. /can acquire disorder from glycyrrhetic acid (present in licorice), which blocks activity of 11beta-hydroxystroid dehydrogenase. /treatment = corticosteroids (exogenous corticosteroids decrease endogenous cortisol production, leading to decreased mineralocorticoid receptor activation).
Components of the juxtaglomerular apparatus + function
Mesangial cells + JG cells + macula densa (NaCL sensor, part of DCT). Function is maintain GFR via RAAS.
JG cells + function
Modified smooth muscle cells of afferent arteriole. Secrete renin in response to decreased renal blood pressure and increased sympathetic tone (B1)
ANP, BNP effects
1) check on RAAS.
2) relaxes vascular smooth muscle via cGMP –> increased GFR + decreased renin
3) dilates afferent ateriole; constricts efferent
4) promotes natriuresis.
What activates RAAS?
1) Decreased BP
2) decreased Na+ delivery (macula densa cells)
3) increased sympathetic tone (B1-receptors)
angiotensin 1 –> angiotensin II
occurs in lungs
Aldosterone affects
Increases Na channel and 1) Na/K pump insertion in principal cells; enhances K+ and H+ excretion by way of principal cell K+ channels and alpha-intercalated cell H+ ATPases. Thus, creates favorable Na+ gradient for Na+ and H2O reabsorption.
2) summary –> Na reabsorption, K+ and H+ secretion.
active form of vitamin D
calcitriol, 1,25-(OH)2 vitamin D3
PTH action in vitamin D pathway
inhibits 1alpha-hydroxylase
calciferol
refers to either D2 or D3
Dopamine kidney actions
Secreted by PCT cells, promotes natriuresis. At low doses, dilates interlobular arteries, afferent arterioles, efferent arterioles –> increased RBF, little or no change in GFR. At higher doses, acts as vasoconstrictor.
PTH triggers
1) decreased plasma Ca
2) increased phosphate
3) decreased plasma 1,25-OH)2D3
PTH effects
1) increased Ca reabsorption (DCT)
2) decreased phosphate reabsorption (PCT)
3) increased vitamin D production
4) increased Ca and phosphate absorption from gut via vitamin D
Causes of hyperkalemia (things that shift K+ out of cells)
DOLABS. Digitalis, hyperOsmolarity, Lysis of cells, Acidosis, B-blocker, high blood Sugar
Causes of hypokalemia
Hypo-osmolarity, alkalosis, beta agonists, insulin
Presentation of hyponatremia
nausea + malaise + stupor + coma + seizures
hypernatremia presentation
irritability + stupor + coma
hypokalemia on ECG
U waves + flattened T waves
hyperkalemia on ECG
wide QRS and peaked T waves
caveat about hypercalcemia
not necessarily calciuria
hyperkalemia pnemonic
stones (renal), bones (pain), groans (abdominal pain), thrones (increased urinary frequency), psychiatric overtones (anxiety, altered mental status).
hypomagnesemia presentation
presentation = tetany + torsades de pointes + hypokalemia.
hypermagnesemia presentation
decreased DTRs + lethargy + bradycardia + hypotension + cardiac arrest + hypocalcemia
hypophosphatemia presentation
bone loss + osteomalacia (adults) + rickets (children).
hyperphosphatemia presentation
renal stones + metastatic calcifications + hypocalcemia
bicarb and PCO2 levels in metabolic alkalosis
increased PCO2 + increased HCO3
Using winters formula + what results mean
1) Use winters to predict respiratory compensation for a simple metabolic acidosis.
2) if measured PCO2>predicted PCO2, a concomitant respiratory acidosis is occurring
3) If measured PCO2 is leass than predicted PCO2, concomitant respiratory alkalosis is occurring.
Causes of normal anion gap
HARDASS: Hyperalimentation, Addison disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion
PCO2 cutoff for determining respiratory acidosis
44 mm Hg
HCO3- cutoff for determining metabolic acidosis
less than 20
PCO2 cutoff for determining respiratory alkalosis
less than 36
HCO3- cutoff for determining metabolic alkalosis
greater than 28
common causes of metabolic alkalosis
1) loop diuretics
2) vomiting
3) antacid use
4) hyperaldosteronism
hyperchloremic vs. hypochloremic metabolic acidosis
hyperchloremic = normal anion gap
hypochloremic - anion gap
Renal tubular acidosis (RTA)
disorder of renal tubules that leads to normal anion gap metabolic acidosis
Distal renal tubular acidosis (type 1)
Urine pH > 5.5. Defect in ability of alpha intercalated cells to secrete H+ –> no new HCO3- is generated, leading to metabolic acidosis. Associated with hypokalemia + increased risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover).
Causes of distal renal tubular acidosis (type 1)
Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract.
Proximal renal tubular acidosis (type 2)
Urine pH increased excretion of HCO3- in urine and subsequent metabolic acidosis. Urine is acidified by alpha-intercalated cells in collecting tubule. Associated with hypokalemia + increased risk for hypophosphatemic rickets.
Causes of proximal renal tubular acidosis (type 2)
Fanconi syndrome + carbonic anhydrase inhibitors
Hyperkalemic renal tubular acidosis (type 4)
Urine pH HYPERkalemia –> decreased NH3 synthesis in PCT –> decreased NH4+ excretion.
causes of hyperkalemic renal tubular acidosis (type 4)
decreased aldosterone production + aldosterone resistance (K+ sparing diuretics, nephropathy due to obstruction, TMP/SMX).
RBC casts found in
glomerulonephritis + malignant HTN
WBC casts found in
tubulointerstitial inflammation + acute pyelo + transplant rejection
Fatty casts (“oval fat bodies) found in
nephrotic syndrome. associated with “Maltese cross” sign.
waxy casts found in
ESRD/chronic renal failure
hyaline casts indicate…
nonspecific, can be normal, often seen in concentrated urine samples
focal vs. diffuse glomerulonephritis
diffuse involves >50% of glomeruli, focal less than
“proliferative” means…
hypercellular glomeruli
cause of nephritic syndrome
Inflammatory process. GBM disruption
general characteristics of nephritic syndrome
HTN (due to salt retention) + increased BUN and creatinine + oliguria + hematuria + RBC casts + azotemia + proteinuria (mild)
cause of nephrotic syndrome
Podocyte disruption –> charge barrier impaired.
general characteristics of nephrotic syndrome
massive proteinuria + hypoalbuminemia + hyperlipidemia + edema.
Nephritic-nephrotic syndrome
Severe nephritic syndrome can lead to profound GBM damage that damages the glomerular filtration charge barrier leading to nephrotic range proteinuria + concomitant features of nephrotic syndrome. Can occur with any nephritic syndrome.
nephritic-nephrotic syndrome most commonly seen with..
1) Diffuse proliferative glomerulonephritis.
2) Membranoproliferative glomerulonephritis.
massive proteinuria defined as
greater than 3.5 g/day
other impt features of nephrotic syndrome
hypercoagulable state (due to AT III loss in urine) + immunocompromised state (due to loss of immunoglobulins in urine and soft tissue compromise by edema).
What happens to GFR in diabetic glomerulonephropathy?
Increased due to glycosylation of efferent arterioles.
most common kidney stone presentation
calcium oxalate stone in patient w/ hypercalciuria and normocalcemia.
renal stone breakdown
80% calcium, 15% struvite, 5% uric acid
where would uric acid stones form?
DTC and collecting tubule (precipitate in decreased pH)
Other causes of hydronephrosis
retroperitoneal fibrosis + vesicoureteral reflux.
Renal cell carcinoma route of metastasise
invades renal vein then IVC and spreads hematogenously.
renal cell carcinoma treatment
Resection if localized. Immunotherapy (eg, aldesleukin) or targeted therapy for advanced/metastatic disease. Resistant to chemo and radiation.
usual presentation for RCC
metastatic neoplasm. “silent cancer”
renal oncytoma – presentation, etc.
codebook
Wilms tumor management
MOPP –> Mechlorethamine, Oncovin/vincristine, Procarbazine, Prednisone
WAGR complex
WAGR syndrome: Wilms tumor, Aniridia (absence of iris), Genitourinary malformations, mental Retardation/intellectual disability (WT1 deletion).
Denys-Drash syndrome
(codebook)
transitional cell carcinoma carcinogens
Phenacetin, Smoking, Aniline dyes, cyclophosphamide
nitrites indicate
gram negative organisms (especially e coli)
sterile pyuria indicates
urethritis by gonorrhoea or chlamydia
negative urine cultures with UTI presentation indicates
urethritis by gonorrhoea or chlamydia
other impt findings in pyelonephritis
tubulorrhexis (necrosis of epithelial lining) + microabscesses
CT finding in pyelo
striated parenchymal enhancement
chronic pyelo findings + xanthogranulomatous pyelo
codebook
ATN pathophys in intrinsic renal failure
Patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule, leading to decreased GFR.
Consequences of renal failure
MADHUNGER: Metabolic Acidosis, Dyslipidemia (especially triglycerides), Hyperkalemia, Uremia, Na+/H2O retention (HF, pulmonary edema, HTN), Growth retardation and developmental delay, Epo failure (anemia), Renal osteodystrophy
urea vs ammonia vs protein
Excess nitrogen in the form of ammonia (NH3) is generated from the catabolism of amino acids, and is feed into the urea cycle to produce urea, which is then excreted by the kidney.
Uremia + presentation
Clinical syndrome marked by increased BUN. nausea and anorexia + pericarditis + asterixis + encephalopathy + platelet dysfunction.
Prerenal Lab Values:
1) Urine osmolality (mOsm/kg)
2) Urine Na+ (mEq/L)
3) FENa
4) Sserum BUN/Cr
1) >500
2) less than 20
3) less than 1%
4) greater than 20
Intrinsic renal Lab Values:
1) Urine osmolality (mOsm/kg)
2) Urine Na+ (mEq/L)
3) FENa
4) Sserum BUN/Cr
1) less than 350
2) greater than 40
3) greater than 2%
4) less than 15
Postrenal Lab Values:
1) Urine osmolality (mOsm/kg)
2) Urine Na+ (mEq/L)
3) FENa
4) Sserum BUN/Cr
1) less than 350
2) greater than 40
3) >1% (mild), >2% (severe)
4) varies
3 stages of ATN, and associated risks
- Inciting event.
- Maintenance phase–oliguric; lasts 1-3 weeks; risk of hyperkalemia, metabolic acidosis, uremia.
- Recovery phase–polyuric; BUN and creatinine fall; risk of hypokalemia.
Causes of ATN
1) Ischemic–secondary to decreased renal blood flow (eg, hypotension, shock, sepsis, hemorrhage, HF). Results in death of tubular cells that may slough into tubular lumen.
2) Nephrotoxic–secondary to injury resulting from toxic substances (eg., aminoglycosides, radiocontrast agents, lead cisplatin), crush injury (myoglobinuria), hemoglobinuria. PCT is particularly susceptible to injury.
papillary necrosis associations
sickle cell disease or trait + acute pyelonephritis + NSAIDs + diabetes mellitus
ADPKD treatment
ACE inhibitors or ARBs
Medullary cystic disease
Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine. Medullary cysts usually not visualized; shrunken kidneys on ultrasound. Poor prognosis.
ARPKD
cystic dilation of collecting ducts. Often presents in infancy. associated with congenital hepatic fibrosis. Significant oliguric renal failure can lead to Potter sequence.
sequela of ARPKD
Systemic HTN + progressive renal insufficiency + portal hypertension from congenital hepatic fibrosis.
Simple cysts
Filled with ultrafiltrate (anechoic (black) on US). Very common and account for majority of all renal masses. Found incidentally and typically asymptomatic.
Complex cysts
Septated, enhanced, or have solid components on imaging. Require follow-up or removal due to risk of RCC.
Mannitol MOA
Osmotic diuretic. Increases tubular fluid osmolarity, thereby increasing urine flow and decreasing.intracranial/intraocular pressure.
Mannitol clinical use
Drug overdose, elevated ICP/intraocular pressure.
Mannitol AE’s
pulmonary edema, dehydration, contraindicated in anuria, HF.
Acetazolamide mechanism
carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diureses and decreased total body HCO3- stores.
Acetazolamide clinical use
glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri
Acetazolamide AE’s
Proximal RTA, paresthesias, NH3 toxicity, sulfa allergy
Other mechanism point about loop diuretics
Stimulate PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs.
Loop diuretics adverse effects
ototoxicity, hypokalemia, dehydration, allergy (sulfa), metabolic alkalosis, interstitial nephritis, gout.
ethacrynic acid MOA
nonsulfonamide inhibitor of cotransport system of thick ascending limb of loop of henle.
ethacrynic acid AE’s
similar to furosemide, but more ototoxic.
metolazone
thiazide
Thiazide clinical uses
HTN, HF, idiopathic hypercalciuria, nephrogenic DI, osteoporosis
Thiazide AE’s
hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy
spironolactone and eplerenone MOA
competitive aldosterone receptor antagonists in cortical collecting tubule.
triamterene and amiloride MOA
Act at collecting tubule by blocking Na+ channels in the cortical collecting tubule.
K+ sparing diuretics use
hyperaldosteronism, K+ depletion, HF
hepatic ascites treatment
spironolactone
nephrogenic DI treatment
amiloride
K+ sparing diuretics AE’s
hyperkalemia (arrhythmias) + endocrine effects with spironolactone (gynecomastia, antiandrogen effects).
diuretics associated with alkalemia
loop diuretics + thiazides
alkalemia mechanism with diuretics
1) volume contraction –> increased AT II –> increased Na+/H+ exchange in PCT –> increased HCO3- reabsorption
2) K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells.
3) in low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule –> alkalosis and “paradoxical aciduria”
bradykinin actions
potent vasodilator
ACEI’s clinical use
HTN, HF (decreased mortality), proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a result of chronic HTN.
ACEI mechanism in diabetic nephropathy
decrease intraglomerular pressure, slowing GBM thickening.
ACEI’s AE’s
cough, angioedema, teratogen, increased creatinine, hyperkalemia, Hypotension
ACEI’s contraindicated in
bilateral renal artery stenosis (can further decrease GFR)
ARB clinical uses
HTN, HF, proteinuria, diabetic nephropathy with intolerance to ACE inhibitors
ARB AE’s
hyperkalemia + decreased GFR + hypotension + teratogen
Aliskiren MOA
direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I
Aliskiren AE’s
hyperkalemia, decreased GFR, hypotension. Relatively contraindicated in patients already taking ACEI’s or ARBs.
Inulin and mannitol
Used to help measure GFR (volume of fluid filtered from the renal glomerular capillaries into the Bowman’s capsule per unit time) because it is not secreted or absorbed. Thus, inulin clearance is constant. Very similar to creatinine. Concentration basically steadily rises, except for a slight dip in distal tubule.
Potassium regulation in the kidney
2 vacuums in proximal tubule + thick ascending limb sucking bananas from tubules/most K+ is resorbed in the proximal tubule + loop of Henle. /late distal and cortical collecting tubules are the primary sites for regulation of K+ concentration. Imagine faces of Principal ted from highschool puking bananas into the late DTC + collecting duct/principal cells in the late distal convoluted tubule + cortical collecting ducts secrete K under conditions of normal or increased K+ load.
Phosphorus regulation in the kidney
80-90% of filtered load of phosphate is reabsorbed. Phosphines stuck into proximal tubule with salt piled on top/most reabsorption occurs in the proximal tubule by secondary active transport mediated by Na+-phsophate cotransporters (NAPT). This is a transport maximum process. /primarily regulated by PTH, which reduces proximal tubule phosphate reabsorption. /calcitriol (1,25-OH2-vitamin D), increases phosphate reabsorption (by increasing NAPT). /Thus PTH inhibits renal phosphate reabsorption.
Tubular fluid osmolarity
Hambones frozen in ice lining proximal tubule/300 in the proximal tubule + *isotonic (both solutes and water reabsorbed). Lined with hooks/descending limb = 700 (variable tho). Lined with ivy/thin ascending limb = 800. Stuffed with hens/thick ascending limb = 200. Filled with hats/distal convoluted tubule = 100. Lined with bode miller hula-hooping/collecting duct (IN THE PRESENCE OF ADH) = 900. Dead bode covered in lice/in the absence of ADH, tubular fluid is most dilute in the collecting ducts. /most NaCl absorption occurs in the thick and thin ascending limbs, so fluid becomes hypotonic here. Thus, these are called the diluting segments of the kidney. Salt plug in the bottom of the loop of henle/in the absence of ADH, highest osmolarity occurs at the bottom of the loop of henle.
Permeabilities of segments:
- Descending limb is permeable to water, but not solutes - fluid becomes hypertonic. -Thick ascending limb is impermeable to water and electrolytes are resorbed fluid becomes hypotonic.
- DTC reabsorbs solutes + is impermeable to water tubular fluid becomes more hypotonic.
- Collecting ducts depends on ADH impermeable to water in its absence, thus becoming more hypotonic.
Effect of hematocrit on GFR
Increased hematocrit will decrease GFR because increased hematocrit means decreased plasma volume (plasma holds water and protein).
In the absence of ADH, where is fluid most diluted in the kidney?
Collecting duct
