Renal General Principles Flashcards
Ureter location relative to uterine artery and ductus deferns
Water under the bridge…ureters pass UNDER the uterine artery and UNDER the ductus deferens
Human % body water
60%
ECF vs ICF volume distribution
2/3rds ICF, 1/3rd ECF
ECF volume distribution
1/4th plasma, 3/4ths interstitial
Normal serum osmolality
290 mOsm
Composition of the glomerular filtration barrier
Fenestrated capillary endothelium, Fused basement membrane with heparan sulfate, epitherlial layer consisting of podocyte foot process
Charge of the glomerular podocytes
Negative due to heparan sulfate
Glomerular capillary type
Fenestrated (size barrier)
Clearance formula of X (Cx)
Cx = Ux*V/Px (Ux = urine osm, Px = plasm osm, V = urine flow rate)
Cx < GFR means?
Net reabsorption
Cx > GFR means?
Net secretion
Cx = GFR
Filterable, no reabsorption or secretion.
GFR calculation
Use x=inulin Cx=Ux*V/Px…inulin is not secreted or reabsorbed
Normal GFR value
100 mL/min
Effective renal plasma flow (ERPF) formula
Use x=PAH Cx=Ux*V/Px…PAH is filtered AND secreted meaning it can tell us the amount of flow throughout the tubule
Renal blood flow (RBF) formula
RBF = RPF/(1-hematocrit) ERPF unerestimates RPF by ~10%.
Filtration fraction formula
FF = GFR/RPF *RENAL PLASMA FLOW, not renal blood flow
Normal filtration fraction value
FF = 20%
Filtered load formula
Filtered load = GFR * plasma concentration
Best substance to estimate GFR? Best substance to estimate RPF?
GFR = creatinine or inulin; RBF = PAH
Effect on NSAIDs on afferent arteriole
Prevent prostaglandins from dilating thus distrubting filtration fraction and GFR regulation.
Does angiotensin II preferentially constrict the afferent or efferent arteriole?
Efferent; increses GFR and decreases RPF thus increases FF.
Excretion rate formula
Excretion rate = V * Ux
Effect of afferent arteriole constriction on RPF, GFR, and FF
Decrease RPF, GFR, no change of FF
Effect of efferent arteriole constriction on RPF, GFR, and FF
Decrease RPF, increase GFR, increase FF
Effect of increased plasma protein concentration on RPF, GFR, and FF
No change on RPF, decrease GFR and decrease FF
Effect of decreased plasma protein concentration on RPF, GFR, and FF
No change on RPF, increase GFR and increase FF
Effect of ureter constricction on RPF, GFR, and FF
No change on RPF, decrease GFR and decrease FF.
Glucose clearance by kidney…how much is normally excreted/secreted?
Glucose is completely reabsorbed by the proximal tubule…at glucose levels of 160 mg/dL (threshold)…we start to get glucosuria
What happens at the thin descending loop?
Passive reabsorption of water…makes urine hypertonic
What happens at the thick ascending loop?
Active reabsorb Na, K, and Cl- (triple cotransport)…Mg2+ and Ca2+ is also reabsorbed
What happens at early distal convuluted tubule?
Active reabsorb Na, Cl-…makles urine more hypotnic
What happens at the collecting tubules?
Reabsorb Na in exchange for K and H+; ADH causes retention of H2O
Where does isotonic absorption occur in the nephron
PCT
Early proximal tubule…what occurs here in terms of reabsorption/secretion?
Reabsorbs: All Glucose, All Amino acids, Most bicarb., Na, Cl, Phosphate, and water ….generates and secretes ammonia and H+
Effect of PTH and AT-II on the PCT
PTH inhibits sodium/phosphate cotransport, increasing phosphate exretion. AT-II stimulates sodium/hydrogen exchanger, increasing sodium/water reabsorption (contraction alkalosis).
% Na absorbed at the PCT, DCT, TAL, CT
PCT = 65-80%, DCT = 5-10%, TAL = 10-20%, CT = 3-5%
Where are amino acids reabsorbed in the nephron
PCT
Where is glucose reabsorbed in the neprhon
PCT via SGLT
Is water or salt permeable in the thin vs thick loop of henle
Thin: water permeable, salt impermeable. Thick: water impermeable, salt permeable.
Effect of PTH on the DCT
Increases calcium reabsorption via calcium/sodium exchanger.
Function of intercalated vs principal cell
Intercalated cell secretes H+ via an ATPase; principal cell secretes potassium.
Effect of ADH on the nephron
Increases water and urea reabsorption via luminal aquaporins at the medullary collecting tubule.
Where is urine most hypotonic assuming ADH is present?
Distal convoluted tubule
Tubular fluid to plasma concentration ratio TF/P >1
When solute is reabsorbed less quickly than water (urea, chloride), when solute is not absorbed at all (inulin, mannitol, creatinine) or there is a net secretion (PAH)
Tubular fluid to plasma concentration ratio TF/P <1
When solube is reabsorbed more quickly than water (glucose, amino acids, HCO3, phosphate).
Tubular fluid to plasma concentration ratio TF/P =1
When solute and water are reabsorbed at the same rate (potassium, sodium).
Three stimuli for renin secretion
Low blood pressure (JG cells at afferent arteriole), beta-1 adrenergic stimulation, low salt delivery to macula densa (DCT/TAL border).
Two functions of ACE
Degrades bradykinin, converts A-I to A-II.
Angiotensin II functions
Affects baroreceptor function; limits reflex bradycardia which would normally accompany its pressor effects. Stimulates thirst. Constricts efferent arteriole to increase GFR and FF (lowers RBF).* Increaes aldosterone and ADH release.* Contraction alkalosis via stimulating proximal tubule Na/H activity.
Atrial naturetic peptide
Stimulates cGMP vasodilation; increases sodium excretio. Decreases renin, increases GFR.
Is ADH release more dependent on volume loss or osmolality decrease?
More dependent on volume loss.
How can NSAIDS induce caute renal failure?
Prevent vasodilation of afferent arteriole, preventing GFR maintence.
What two mormones are produced in the kidney
EPO and 1,25-(OH)2 Vitamin D
1,25-(OH)2 vitamin D function
Increases intestinal absorption of calcium and phosphate.
What hormone stimulates 1,25-(OH)2 vitamin D synthesis
PTH.
Two effects of PTH on the nephron
Increases phosphate excretion (via PCT Na/PO4- cotransporter inhibition), and increases calcium reabsorption (via DCT calcium/sodium exchanger).
PGE2 effect on nephron
Dilates the afferent arteriole.
Aldosterone effects
Increases sodium reabsorption (principal cells), increases potassium secretion (principal cells), increases H+ secretion (intercalated cells); hypokalemic metabolic alkalosis.
Effect of A-II on the CNS.
Stimulates thirst via the hypothalamus
Six factors that shift potassium out of cells (causing hyperkalemia)
Beta antagonists (decrease Na/K-ATPase), cell lysis, digitalis (inhibits Na/K-ATPase), hyperosmolarity, acidosis/severe exercise (increases K/H+ exchanger), insulin (decrease Na/K-ATPase) deficiency.
Four factors that shift potassium into cells (causing hypokalemia)
Beta agonists / insulin (increase Na/K-ATPase), alkalosis (decreases H/K+ exchanger), hypoosmolarity. (INsulin shifts potassium IN).
Henderson-Hasselbach equation
pH = pKa + log [HCO3/(0.03*PCO2)]
Winter’s formula for respiratory compensationi reponse to metabolic acidosis
PCO2 = 1.5 * (HCO3) + 8 +/- 2
For every 0.7 mm Hg increase in PCO2, how much mEq/L HCO3 increases?
1
What is the juxtaglomerular apparatus?
Consists of JG cells and the macula densa (detects NaCl in the DCT…remember that this it next to the glom. App because it loops back up)…..JG cells secrete renin in response to lower renal blood pressure, decrease NaCl DCT, and increased sympathetic tone
What are four things that the kidney secretes?
Erythropoitetin (in response to hypoxia), 1.25 -(OH)2 vitamin D (proximal tubule cells convert and release this active form of vitamin D back into the blood), Renin, prostaglandins (used to increase GFR by dilating afferent arteriols)
Metabolic Acidosis…main disturbance? Compensatory response?
Decreased pH from Decreased HCO3-….Hyperventilation (decreases PCO2 which gets rid of “acid”)
Metabolic Alkylosis…main disturbance? Compensatory response?
Increased pH from increased HCO3-…Hypovent (increases PCO2 which keeps “Acid” in)
Respiratory Acidosis…main disturbance? Compensatory response?
Decreased pH from increased pCO2…Increase renal [HCO3] reabsorbtion
Respiratory Alkylosis…main disturbance? Compensatory response?
Increased pH from decreased pCO2…Decrease renal {HCO3] reabsorbtion
