Renal - Embryo, Anatomy, and Physiology

usmlevan's version from 2015-04-13 06:30


Question Answer
PronephrosWeek 4 then degenerates
MesonephrosFns as interim kidney for 1st trimester
later contributes to male genital system
MetanephrosPermanent - first appears in 5th week gestation
Nephrogenesis continues through 32-36 weeks gestation
Ureteric budderived from caudal end of mesonephros
gives rise to ureter, pelvises, calyces, collecting ducts (collectin sys)
fully canalized by 10th week
Metanephric mesenchymeureteric bud interacts with this tissue; interaction induces differentiation and formation of glomerulus through to distal convoluted tubule
Ureteropelvic junctionlast to canalize
Most common site of obstruction (hydronephrosis) in the fetus
Potter's syndromeOligohydramnios → compression of fetus → limb deformities, facial deformities (low-set ears, retrognathia), and pulmonary hypoplasia (cause of death), clubbed feet (Talipes equinovarus)
Causes of Potter's syndromeARPKD, posterior urethral valves, bilateral renal agenesis
Renal disease associated with Turner syndromeHorseshoe kidney
Kidney gets snagged by inferior mesenteric artery as it's ascending, function: normal
Multicystic dysplastic kidneyBad interaction between ureteric bud and metanephric mesenchyme → non-fn'l kidney of cysts and connective tissue
Unilateral (most common) - asymptomatic with compensatory hypertrophy of contralateral kidney
Dx'd prenatally via ultrasound
Ureters courseunder uterine artery and under ductus deferens (retroperitoneal)
"water passes under the bridge"
What % of our body weight is water?60%
What % of our total body water is in the ICF?66%
What % of our total body water is in the ECF?33%
What is the % composition of the ECF?25% plasma volume
75% interstitial volume
Inulin measures...Extracellular volume
Plasma volume measured by.... Radiolabled albumin
Renal clearance formulaCx = UxV/Px
C=clearance of X (mL/min)
U=urine clearance of X
P=plasma concentration of X
V=urine flow rate
The relationship between Cx and GFRCCx < GFR: net tubular reabsorption of X
CCx > GFR: net tubular secretion of X.
CCx = GFR: no net secretion or reabsorption eg Inulin
Equations for GFR =Uinulin X V/Pinulin = Cinulin = Kf[(PGC - PBS) - (πGC - πBS)]
πBS normally equals 0
How well does creatinine clearance approximate GFRvery well, but Creatinine clearance slightly overestimates GFR due to moderate, constant secretion of Creatinine by renal tubules
ERPF (effective renal plasma flow) can be estimated byusing PAH clearance = (UPAH)(V/PPAH)
RBF =RPF/(1 - Hct)
ERPF underestimates true RPF by~10% (perfuses renal capsule)
Filtration fraction =GFR/RPF
Filtered load =GFR x [plasma]x: rate at which a substance is filtered into Bowman's space
Effects of NSAIDs on filtrationInhibits prostaglandins which normally dilate afferent arterioles → ↑ RPF, → GFR so the FF remains constant
ACE inhibitors affect flitration byInhibiting Angiotensin II which normally constricts the efferent arteriole → ↓ RPF, ↑ GFR so the FF increases
Excretion rate =UxxV
Reabsorption = filtered - excreted
Secretion =excreted - filtered
Glucose is normally reabsorbed where?Proximal tubule by Na/glucose cotransporter
Threshold of glucosuriais ~200 mg/dL
at 375 mg/dL all transporters are fully saturated. (Tm)
Glucosuria and aminoaciduria is normal during pregnancy

Nephron physiology

Question Answer
Early proximal tubule functionReabsorbs all of the glucose, amino acids, and most of the HCO3-, Na (65-80%), Cl, PO4, K and water.
Also generates and secretes ammonia which acts as a buffer for secreted H+
PTH's effect on proximal tubuleinhibits Na/phosphate cotransport → phosphate excretion
AT II's effect on proximal tubule↑ stimulates Na/H exchange → ↑ Na, H20, and Bicarb reabsorption (permitting contraction alkalosis)
Function of thin descending looppassively reabsorbs water making urine more concentrated (hypertonic)
Purpose of think ascending loopMakes urine less concentrated n ISF more conc as it ascends: Impermeable to H2O
actively reabsorbs Na, K, and Cl
Indirectly induces the paracellular reabsorption of Mg and Ca via the backleak of K+
Purpose of distal convoluted tubuleMakes urine hypotonic (dilutes urine), Impermeable to H2O
Actively absorbs Na (5-10%) and Cl.
PTH's effect on distal convoluted tubule↑ Ca/Na exchange → Ca reabsorption
Purpose of collecting tubulesreabsorbs Na (3-5%) and secretes K and H
Aldosterone's effect on collecting tubulesmiceralcorticoid receptor → insertion of Na channel on luminal side
ADH's effect on collecting tubulesV2 receptor → insertion of aquaporin H20 channels on luminal side

Important ion channels and med effects on them

Question Answer
Where is the Na/H antiporter?Luminal side of proximal tubule
H is excreted (binds with HCO3- to recycle CO2), Na is reabsorbed
What acts on Na/H antiporter?Angiotensin II - stimulates reabsorption of Na (excretion of H)
Where do carbonic anhydrase inhibitors act?Lumen of proximal tubule to inhibit reabsorption of CO2 (actually inhibits breakup of H2CO3 into H20 and CO2)
Where is the Na, K, 2Cl symporter?Thick ascending loop
reabsorbs all three (Na/K/2Cl)
Where do loop diuretics act?Thick ascending loop
Blocks the reabsorption of Cl by blocking the Na/K/2Cl transporter
Where is the Na/Cl cotransporter?Distal convoluted tubule
Where do thiazide diuretics act?Distal convoluted tubule
Blocks Cl reabsorption by blocking the Na/Cl cotransporter
Where do amiloride and triamterene act?Collecting tubules
Block Na reabsorption
Where is the V2 receptor?Interstitium side of collecting tubule
Where does ADH act?Collecting tubule
inhibits aquaporins (water channels) placement on luminal side of CT via the V2 receptor

Renin-angiotensin-aldosterone system

Question Answer
AT II's effect on vascular smooth muscleVasoconstriction → ↑ BP
AT II's effect on FFconstricts efferent arteriole → ↑ FF (to preserve renal fn (GFR) in low volume states
AT II's effect on adrenal glandStimulates release of aldosterone → ↑ Na (principal cells)and H20 reabsorption and K (up regulates principal cells K channels)/H excretion(up regulates intercalated cell H+ ATPase)
AT II's effect on ADH↑ H20 channel insertion in principal cells → ↑ H20 reapsorption
AT II's effect on proximal tubule↑ Na, HCO3, and H20 reabsorption (can permit contraction alkalosis)
AT II's effect on hypothalamus↑ thirst
Atrial natriuretic peptideActs as a check on R-A-A system
↑ volume → ANP release from atria → elaxes smooth muscle via cGMP → ↑ GFR, ↓ renin
Renin's actionConverts angiotensinogen to angiotensin I
ACE's fnConverts angiotensin I to angiotensin II
Inhibits bradykinin
What promotes renin release?↓ BP (JG cells)
↓ Na delivery (MD cells)
↑ sympathetic tone (β1-receptors)
Juxtaglomerular apparatusModified smooth muscle of afferent arteriole (JG cells) and macula dense
secrete renin in response to ↓ renal blood pressure → ↓ NaCl delivery to distal tubule & ↑ sympathetic tone (β1)
Macula densaNaCl sensor
part of the distal convoluted tubule

Kidney and hormones

Question Answer
Erythropoietinhypoxia → release of EPO by interstitial cells in the peritubular capillary bed
1,25-(OH)2 vitamin DProximal tubule cells convert 25-vitD to 1,25-vitD via 1α-hydroxylase (which is activated by PTH)
Reninsecreted by JG cells in response to ↓ renal arterial pressure and ↑ renal sympathetic discharge (β1 effect)
ProstaglandinsVasodilates the afferent arterioles to ↑ GFR
ANP↑ GFR and ↑ Na filtration with no compensatory Na reabsorption in distal nephron
Angiotensin II↓ BP → efferent arteriole constriction → ↑ GFR and ↑ FF with compensatory Na reabsorption in proximal and distal nephron
Aldosterone↓ blood volume and ↑ plasma [K] → ↑ Na reabsorption, ↑ K secretion, ↑ H secretion

Electrolyte and Acid/Base physiology

Question Answer
What causes shifts of K out of the cell (hyperkalemia)Pts with hyperkalemia? DO Insulin LAβ work
Insulin deficiency
Lysis of cells
β-adrenergic antagonist
Effect of low serum [Na]Nausea and malaise, stupor, coma
Effect of low serum [K]U waves on ECG, flattened T waves, arrhythmias, muscle weakness
Effects of low serum [Ca]Tetany, seizures,QT prolongation
Effects of low serum [Mg]Tetany, arrhythmias (Torsades de pointes)
Effects of low serum [PO4]Bone loss, osteomalacia
Effects of high serum [Na]Irritability, stupor, coma
Effects of high serum [K]Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness
Effects of high serum [Ca]Stones, bones, groans, and psychiatric overtones
renal, bone pain, abdominal pain, anxiety, altered mental status
Effects of high serum [Mg]↓ DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
Effects of high serum [PO4]renal stones, metastatic calcifications, hypocalcemia
Metabolic acidoses causes what?immediate hyperventilation → ↓ Pco2
Metabolic alkalosis causes what?immediate hypoventilation → ↑ Pco2
Respiratory acidosis causes what?delayed ↑ renal HCO3 reabsorption
Respiratory alkalosis causes what?delayed ↓ renal HCO3 reabsorption
Henderson-Hasselbalch equationpH = 6.1 + log(HCO3/(0.03xPco2))
Predicted respiratory compensation for simple metabolic acidosisPco2 = 1.5(HCO3) + 8 +/minus 2
Causes of repiratory acidosisHypoventilation causes:
airway obstruction
acute/chronic lung disease
Opioids, sedatives
weakening of respiratory muscles
muscle relaxants
sleep apnea
restrictive lung disease
NM defects: MS, muscle dystrophy
Obesity hypoventilation syndrome
Causes of anion-gap metabolic acidosis with compensationMUDPILES:
Methanol (formic acid)
Diabetic ketoacidosis
Iron tablets or INH
Lactic acidosis
Ethylene glycol (oxalic acid)
Salicylates (late)
Causes of metabolic acidosis with compensation and normal anion gapHARD-ASS:
Addison's disease
Renal tubular acidosis
Saline infusion
Causes of respiratory alkalosisHyperventilation:
Hypoxemia (e.g high altitude)
Salicylates (early)
Pulmonary embolism
pneumothorax (cause atelecthasia --> shunt and remaining hyperventilation)
ventilation-perfusion inequality (due to hypoxemia)
Causes of metabolic alkalosis with compensationLoop diuretics
Antacid use
Type 1 renal tubular acidosisDistal
Defect in collecting tubule's (intercalated cells) ability to excrete H--> new HCO3- is not generated
Urine pH>5.5
Assoc w hypokalemia
↑ risk for calcium phosphate kidney stones ( increase urine pH, increase bone turnover)
Type 2 renal tubular acidosisProximal
Defect in proximal tubule HCO3 reabsorption--> ↑HCO3 excretion and metabolic acidosis
Urine pH < 5.5: acidified by alpha intercalated cells in collecting tubule
Assoc w hypokalemia
↑ risk of hypophosphatemic rickets
Type 4 RTAHypoaldosteronism or lack of CT response to aldosterone, K sparing diuretics → hyperkalemia → impairs ammoniagenesis in the PT → ↓ buffering capacity and ↓ urine pH

Rapid fire - Acid/Base

Question Answer
Hypoventilationrespiratory acidosis
Methanol (formic acid)↑ anion gap metabolic acidosis with compensation
Uremia↑ anion gap metabolic acidosis with compensation
Diabetic ketoacidosis↑ anion gap metabolic acidosis with compensation
Propylene glycol↑ anion gap metabolic acidosis with compensation
Iron tablets↑ anion gap metabolic acidosis with compensation
INH↑ anion gap metabolic acidosis with compensation
Lactic acidosis↑ anion gap metabolic acidosis with compensation
Ethylene glycol (oxalic acid)↑ anion gap metabolic acidosis with compensation
Salicylates (late)↑ anion gap metabolic acidosis with compensation
Hyperalimentationnormal anion gap metabolic acidosis with compensation
Addison's diseasenormal anion gap metabolic acidosis with compensation
Renal tubular acidosisnormal anion gap metabolic acidosis with compensation
Diarrheanormal anion gap metabolic acidosis with compensation
Acetazolamidenormal anion gap metabolic acidosis with compensation
Spironolactonenormal anion gap metabolic acidosis with compensation
Saline infusionnormal anion gap metabolic acidosis with compensation
Hyperventilationrespiratory alkalosis
early high-altitude exposurerespiratory alkalosis
salicylates (early)respiratory alkalosis
loop diureticsMetabolic alkalosis with compensation
vomitingMetabolic alkalosis with compensation
antacid useMetabolic alkalosis with compensation
hyperaldosteronismMetabolic alkalosis with compensation

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