MindMap Gallery Renal Physiology
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Renal Physiology
This is a mind map talking about renal physiology.
Edited at 2020-09-27 12:31:12
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Renal Physiology
Nephron: Renal Corpuscle (Glomerulus) + Renal tubule
Cortical nephrons: cannot concentrate urine as much, don't go deep into medulla
Jextamedullay nephrons: make concentrated urine-go deep into medulla
Nephron structure
Glomerulus cell
1) Endothelial cells(1)-leakiest in the body located on top of a basement membrane
2) Mesangial cells (5a): may play a role in changing size of surface area of glomerus capillaries
3) Podocytes (3b): locate outside the basement membrane, these are arranged alongside each other, leaving filtration 'slits' between them. This allows small solutes to pass through but prevents albumin & larger proteins from exiting the blood stream
Bowman's space
This area is where all blood once passed through glomerular capillary membrane passes into. This space then drains into the proximal convoluted tubule
Arterioles: come off the renal arteries
Afferent arteriole conducts blood into the glomerulus
Efferent arteriole conducts the unwanted blood away from the glomerulus back to the circulation
Tubules
Loop of Henle
Sets up a counter-current mechanism that concentrated the urine
Ureters
Passes down to the bladder
Specialised Cells: Cells of the Juxtaglomeular apparatus
1) Juxtaglomerular (JG)/Granular cells (6)
Located in the wall of the afferent arteriole
They secrete renin in response to a) increased sympathetic (beta-1) stimulation & b) renal hypoperfusion caused by hypotension or volume retention c) stimulation by the macula densa cells
Macula Densa Cells (7)
Located in the distal convoluted tubule close to the glomerulus
Sense changes in NaCl concentration as a result of more reabsorption following a slower GFR as a result of decrease in BP. Respond in 2 ways
1) Decrease resistance to flow in the afferent arteriole thereby increasing hydrostatic pressure & increasing GFR
2) Stimulates release of Renin by JG cells via prostaglandins
Extraglomerular mesangial cells (5b)
Role is poorly understood but is believed to help with the renin-angiotensin-aldosterone system
Other Specialised cells outside the nephron (includes below):
Zona Glomerulosa Cells of the adrenal glands
Produce Aldosterone in response to 2 stimuli which increases ACTH & thus Aldosterone secretion:
1) Increased ANG2
2) Increased [K+]
Results in 1) Upregulation & activation of basolateral Na+/K+ pumps in the distal tubule & collecting duct. 2) Stimulating NaCl/H20 reabsorption in GIT, salivary & sweat glands 3)May stimulate Vasopressin/ADH release from posterior pituitary 4) Increases renal efferent tubule resistance, increasing hydrostatic pressure & thus GFR
Osmoreceptors in the Hypothalamus
If osmolarity becomes higher than normal, cells will shrink in the hypothalamus, which stimulutes thirst centres and the production of ADH
ADH has several effects:
1) Acts on V2 receptors, increasing water reabsorption in kidney through direct insertion of aquaporins in the collecting tubule
2) Acts on V2 receptors in arterial smooth muscle, resulting in vasoconstriction & increased BP
Other Effects of ANG 2 besides increase in Aldosterone
Atrial Natriuretic Peptide (ANP)
Secreted in the atria, it inhibits Na+/H20 reabsorption by decreasing secretion of Renin & Aldosterone. Also acts by vasodilating the afferent arteriole & increasing GFR & decreasing reabsorption of Na+. Overall effect is Total Blood Volume is reduced.
Disease
ACUTE RENAL FAILURE: Abrupt decline in GFR & accumulation of nitrogenous waste (creatinine + urea). COMPLICATIONS: Fluid overloas, pulmonary oedema, heart failure, hyperkalaemia.
Pre-Renal: SHOCK, Hypovolaemia, Renal artery stenosis.
Test: bland urinary sedement (little protein/cells, high serum urea compared to creatinine.
Intra-renal:
Tubulo-interstitial: 1) Acute tubular necrosis (usually resolves), from unresolved pre-renal problem 2) Interstitial nephritis: DRUGS like penicillins, aspirin, NSAIDS (Analgesic nephropathy).
Glomerular (presence of haemeturia, lipiduria & proteinuria): glomerularnephritis is usual cause & is divided into types:
1) Nephritic Syndrome: inflammatory condition associated with low urine volume & haematuria
2) Nephrotic Syndrome: associated with high proteinuria & caused from diseases such as Diabetes, Hep B, HIV, Obesity. Also associated with hyperlipidemia & oedema.
Vascular: Hypertension, Polyarteritis
Post-renal: Bladder outflow obstruction, neurogenic bladder, urethral stricture, ureteric obstruction (stone), carcinoma
Test: Hydronephrosis on abdominal U.S
CHRONIC RENAL FAILURE: Stage 1: GFR>90 Stage 4: GFR=15-29 Stage 5: GFR=<15% End Stage: GFR=<10% GFR
Causes: Diabetic Nephropathy (most common), Glomerulonephritis (unresolved acute form), Vascular dx, Obstructive uropathy
Consequences: CVS (WORSE): Hypertension goes with CFR, accelerated atherosclerosis, cardiac failure. Proteinurea is a VERY STRONG RISK FACTOR for CVS Death GIT (anorexia, nausea, vom), Resp (Acidosis, pulmonary oedema), Neuro (confusion, coma, peripheral), Derma (Pruritis, leukonichia), Musculo (muscle wasting, renal bone dx (hypocalcaemia)
DRUGS
No. 1: ACE INHIBITORS to disrupt renin-angiotensin system. ACts as an antihypertensive, anti A.M.I
Biochemical tests of renal function
Urinanalysis: for glucose, creatinine, drugs,
GFR Measurement: via creatinine, as they are freely filtered & not absorbed. Can compare blood creatinine vs urine creatinine. If ratio is high then decreased GFR & renal function. Good for comparing before & after of one patient, but not good for between pt's.
Renal Plasma Flow: Use measurement of substance PAH as it is secreted by the tubules & only 20-30% filtered by glomerulus. 10% of plasma flow though goes to non-functioning parts of kidney.
Bicarbonate Handling
NET LOSS OF BICARBONATE IONS: When alkalosis occurs, for every 1H+ less in the body, 1 HCO3- is also lost as they are usually required as a pair. In effect this is like adding 1 H+ to the blood, so pH goes up.
PRODUCTION OF 'NEW' HCO3-: via ammonium (below) & phosphate. Everytime a H+ is excreted in this way, has the effect of adding 1 'new' HCO3- to the body. Also glutamine metabolism creates 2 new HCO3- molecules while also producing 2 NH4+ ions.
SECRETION OF H+: More H+ is secreted than HCO3- is absorbed
AMMONIUM SYNTHESIS: Ammonium can bind to Cl- & H+ & be secreted as a compound in the urine. Only a small amount can be excreted this way. When ammonia is formed from glutamate, 2 ammonium ions & 2 bicarbonate ions are formed which are reabsorbed. The collecting duct however secretes NH3 which can combine to H+ and form NH4+ which is then excreted due to impermeability to this ion. Systemic acidosis & hypokalaemia promotes this function.
PHOSPHATE BUFFER: H+ can bind to phosphate & be excreted in the urine. Only small amounts of phosphate in body though.
NET ACID EXCRETION = NH4+ EXCRETION + URINARY TITRATABLE ACID (PHOSPHATE) - HCO3- EXCRETION
Drugs: Diuretics
THIAZIDES
Hydrochlorothiazide acts on the Na+/Cl+ co-transporter in the late distal tubule
LOOP
Frusemide acts on the Na+/2Cl-/K+ co-transporter in the thick ascending limb
K+ SPARING
Spironolactone inhibits the Na+/K+/ATP pump in the late distal tubule that is usually up-regulated by Aldosterone. It is an aldosterone antagonist. Prevents hypokalemia in vulnerable pt's.
Reabsorption along different parts of the Nephron
PROXIMAL TUBULE
Solutes absorbed: water & Na+ (65%),90% HCO3- (90%), K+ (>90%)
Specialisations: Brush border filled with protein carrier molecules & Na+/K+/ATP pumps. Also a Na+/H+ pump in luminal membrane & a basolateral HCO3-/Na+ co-transporter for bicarbonate handling.
Bicarbonate reabsorption: H+ from Na+/H+ pump combines with HCO3- in lumen forming H2CO3. This then dissociates into CO2 + H20. These then diffuse into tubular cell. They thnen reform and H+ is pumped out while HCO3 is co-pumped with Na+ into capillary.
THIN DESCENDING LIMB
Solutes absorbed: only 10% water. A little urea & Na+ passive diffuses as well.
Specialisations: Part of the counter current mechanism in the vasa recta. H20 is drawn out via oncotic pressure differences and not via active transport
THICK ASCENDING LIMB
Solues absorbed: impermeable to H20. NaCl, K+, Ca2+, Mg2+, HCO3- (all 25%),
Specialisations: Na+/K+/ATPase pumps in basolateral membrane. A co-transporter that moves 1Na+, 2Cl-, 1K+ into tubular cell. This also drives Ca2+ & Mg2+ into cell. This section is also part of counter-current mechanism.
LATE DISTAL TUBULE
Solutes absorbed: NaCl (5%). Fine tuning System. Influenced by Aldosterone. Without =2%, with=5%
Specialisations: Na+/K+/ATPase pump in basolateral membrane that may be up-regulated by Aldosterone. Also a Na+/Cl+ co-transported using energy from other pump to drive.
COLLECTING TUBULE
Solutes absorbed: Na+ (5%), usually impermeable to H20, however, H20 (5% in water loading, >24% in dehydration). Influenced by ADH.
Na+/K+ antiporter in luminal membrane. ADH causes insertion of aquaporins, increasing H20 reabsorption.
Urine Formation
Composition: 95% water + urea Nitrogenous waste=uric acid +creatinine
Na+ Reabsorption
2 Steps:
1) PASSIVE carrier mediated facilitated diffusion (channel) into tubular cell
2) Na+/K+/ATPase pumps move Na+ into capillary & K+ into tubular cell then into lumen by diffusion
Glucose Reabsorption
2 Steps:
1) Co-symporter with Na+
2) Via Secondary Active Transport. Energy from Na+/K+/ATP pump facilitates glucose moving against its concentration gradient into capillary
Transport Maximum
Transport Maximum (Tm): when there is saturation of available carrier molecules for a particular solute.
Green graph shows normal glucose reabsorption. Orange graph shows Transport maximum being met, at which point, purple graph shows proportion of glucose that is then excreted into the urine. As amount of glucose entering kidneys increases, more & more is excreted until at the point of graph intersection, more glucose is being excreted than absorbed. This is the case in diabetic patients where high levels of blood glucose mean carrier molecules are quickly saturated.