Anatomy and Physiology of the kidney Flashcards
Blood flow of the kidney
Artery goes into the kidney -> afferent arteriole goes into the Nephrone - renal corpuscle (Browman’s corpuscle + Glomerus) -> efferent arteriole -> down to the vasa recta (straight arteriole + straight venules) into the juxtamedullary nephron (MEDULLA)-> from venules of the vasa recta the blood leaves the kidney through the vein
Urine flow
Glomerus -> the filtrate is collected in the Browman’s capsule -> goes through the proximal convoluted tube -> descending loop of Henle (going down into the Medulla)-> thin and then thick ascending loop of Henle (up towards the cortex) -> goes through the distal convoluted tube -> urine goes into the collecting duct -> Ureter
Anatomy of the Renal Corpuscle
Renal Corpuscle
Podocytes on the capillary provide a barrier for molecules that should not leave the blood
Bowman’s capsule: collects the filtrate
Fenestra: little gaps on the capillary
basement membrane in between
Slit pores and foot processes in front of the urinary space
What is the predominant barrier molecules have to cross in order to get filtered in the kidney?
Basement membrane
Which molecules are likely to get filtered?
small hydrophilic molecules
Which molecules are not likely to get filtered?
large hydrophobic molecules
-drugs bound to albumin
-cells
-proteins
What is the Glomerular Filtration Rate (GFR)
The rate at which glomerular filtrate is formed (blood is filtered)
What determines the filtration rate (GFR)?
depends on
-the pressure in the glomerulus
-the blood flow to the glomerulus
Forces in the glomerulus
Glomerular blood pressure P(GC) 60mmHg - relatively high for a capillary BP
Fluid pressure in the Bowman’s space P(BS) - 15mmHg -> AGAINST
Osmotic force due to protein in plasma in the glomerular capillary O(GC) - 29 mmHG -> AGAINST
Net pressure: 60 - 15 - 29 = 16 mmHg towards the Bowman’s space
How does GFR change with change in glomerulus capillary (afferent, efferent)
-vasoconstriction of afferent capillary -> less blood flow -> decrease in GFR
-vasoconstriction of efferent capillary -> increase of pressure -> increase in GFR
What determines Renal clearance?
Filtration
Reabsorption
Secretion
Renal clearance equation
C = UV / P
Clearance (ml/min or ml/24h)
U: Urine concentration (mg/ml)
V: Urine volume (ml/min)
P: plasma concentration (mg/ml)
Which molecule is used to approximate GFR?
The clearance of creatinine
-> So it must be filtered and excreted but not secreted and not reabsorbed to be used for renal function calculations
-> In reality some are secreted in the proximal tubule
Which molecule is used to approximate renal plasma flow?
The clearance of PAH
we want to measure the plasma that is in the kidney and doesn’t leave the kidney
-> It is filtered and completely secreted, but NOT excreted, NOT reabsorbed
What is the difference between primary active transport and secondary active transport?
Primary active transport: uses ATP to go against the gradient
Secondary active transport: often uses Na+ to go against the gradient (low Na+ on the other side)
f.e. Glucose transport needs symport with Na+ to go against the gradient
Where does most of Reabsorption occur?
Proximal convoluted tube
How does Glucose behave in the kidney with an increase in concentration?
-Filtration goes up - NO SATURATION
-Reabsorption goes - SATURATION bc the transporters (Na-Glucose-Cotransporter) are limited
-Excretion goes up - NO SATURATION -> Glycosuria (sign of diabetes)
At which concentration does the Na-Glucose transporter start to get saturated?
200 mg/dl
200 mg/ 100ml
Reabsorption of Na at the ascending limb
Which limp is permeable to H2O and Na+?
Descending limb: impermeable to Na+ and permeable to water
Ascending limb: permeable to Na+ due to NKCC transporter, impermeable to H2O due to tight junctions
Consequences of blocking the NKCC transporter at the ascending limb
Na+ and K+ stays in the tubule -> water follows -> Excretion in the urine
Hypokalemia -> Patients using loop diuretics may have to supplement POTASSIUM
Reabsorption of Na at the collecting duct
Na+ Reabsorption is regulated based on the body’s needs
-regulated with Aldosterone (gets into the cell and activates a transcription factor for the Na-K pump)
-Aldosterone upregulates the Na-K pump at the basolateral membrane -> more Na+ gets reabsorbed in the interstitial fluid
more K+ goes into the duct cells -> diffusion into the tubule (urine)
How does Spirolactone affect Na and K?
Na+ stays in the tubule (urine), Na and water reabsorption decreased -> DIURETIC
K+ stays in the interstitial fluid (cells) -> K-sparing drug
How is ADH release stimulated?
Renin -> Angiotensin II
Where and how does Vasopressin (ADH) work?
in the distal convoluted + cortical and medullary collecting duct
-Vasopressin binds to Vasopressin receptors on the basolateral membrane of the collecting tube (or distal tube) -> activated adenylate cyclase -> conversion of ATP to cAMP -> more Aquaporins on the luminal membrane of the collecting tube -> water crosses from the tubular lumen (urine) into the cell -> crosses the cell into the interstitial fluid
-> Concentrated Urine
What are the two roles of Vasopressin (or ADH)
-VASOPRESSIN: Binding on V1 receptors on smooth muscle cells: Vasoconstriction of smooth muscle cells (GI, respiratory, renal, eye, genital)
-ADH: Binding V2 receptors of the distal tubules: causing reabsorption of H2O via an increase in Aquaporins
Where is Vasopressein produced?
-posterior pituitary gland (also oxytocin)
-it is a peptide
-administered IV, IM
-short half-life (15 min)
What are the advantages of Desmopressin?
-a synthetic form of Vasopressin (short long-life)
-longer half-life
-more antidiuretic action (4000x) than vasoconstrictor -> more potent as antidiuretic
-administered IV, SC, intranasally, orally
Vasopressin in Diabetes insipidus
-Treatment of pituitary (central cranial) diabetes -> insufficient ADH production from the pituitary gland
-Supplement ADH
-> Vasopressin (caution with patients cardiac conditions bc of vasoconstriction action) -> Desmopressin is the better option in those patients
-adverse effects: headache, nausea, abdominal cramps
-overdose: seizures, hyponatremia (ADH works too well -> the reabsorbed water is diluting the Na in the blood)
What are the two forms of Diabetes insipidus
-Renal: enough ADH but it is not working on the kidney
-Pituitary: the pituitary is not secreting enough ADH
