Kidney Flashcards
(33 cards)
Homeostatic functions of kidney
Excretion of metabolic waste products
Regulation of water & electrolyte balance
Regulation of body fluid osmolality and electrolyte conc
Regulation of arterial pressure
Regulation of acid-base balance
Regulation of electrolyte production
Secretion, metabolism and excretion of hormones
Gluconeogenesis
Urinary excretion rate =
Filtration rate - reabsorption rate + secretion rate
What % of cardiac output goes to kidney
25%
What % of renal plasma flow is GFR
~20% (125ml/min)
Layers of glomerular capillary membrane
Endothelium of capillary
Basement membrane
Layer of epithelial cells (podocytes)
Adaptions to glomerulus for filtration
Capillary endothelium: thousands of fenestrations. Endothelial Proteins have fixed negative charges that hinder passage of plasma proteins
Basement membrane: mesh work of collagen and proteoglycan fibrillae have spaces for water and small solutes. Proteoglycans have negative charges.
Epithelial (podocytes): foot processes of podocytes create gaps called ‘slit pores’ which filtrate moves. Epithelial cells also negatively charged.
Net filtration pressure =
Glomerular hydrostatic pressure (PG) - Bowman’s capsule pressure (PB) - glomerular oncotic pressure + osmotic pressure of Bowman’s Capsule (usually zero)
Variables for glomerular hydrostatic pressure
Arterial pressure
Afferent arteriolar resistance
Efferent arteriolar resistance
Increased afferent arteriolar resistance causes
Lower glomerular hydrostatic pressure and lower GFR
Increased efferent arteriolar resistance causes
Increased glomerular hydrostatic pressure
Biphasic effect on GFR. Increased if <2 x normal
(If it increased threefold GFR actually REDUCES)
What is the mechanism by which increased efferent arteriolar resistance decreases GFR
Increased resistance causes reduced renal blood flow and increased filtration fraction.
Greater filtration fraction leads to more filtration of water therefore greater colloid osmotic pressure (increase in conc of proteins).
Greater oncotic pressure decreases net filtration pressure (PG - PB - glomerular oncotic pressure).
Reduced net filtration pressure decreases GFR.
Factors that decrease GFR (and causes)
⬇️ Kf (surface area of glomerular capillaries) - Renal disease/DM/hypertension
⬆️ PB - urinary track obstruction
⬆️ glomerular oncotic pressure - reduced renal blood flow/ increased plasma proteins
⬇️ PG - reduced arterial pressure
⬇️ resistance efferent (⬇️PG) - ⬇️angiotensin II (antagonists)
⬆️ resistance afferent (⬇️PG) - sympathetic activity, vasoconstrictor hormones (norad)
Effects of renal sympathetic activation
Constriction of afferent and efferent arterioles and reduced renal blood flow and GFR
Structure of juxtaglomerular complex
Macula densa cells in initial portion of distal tubule
Juxtaglomerular cells in walls of afferent and efferent arterioles
Function and mechanism of macula densa
Decreased GFR leads to decreased NaCl conc in distal tubule.
Macula densa senses decreased conc and initiates signals:
1. Afferent arteriole dilation. Decreased afferent resistance. Increased renal flow. Increased PG. Increase GFR.
2. Signals release of renin from juxtaglomerular cells. (RAS cycle). Constricts efferent, increasing resistance. Increased PG. Increase GFR.
Urinary excretion =
Glomerular filtration
- tubular reabsorption
+ Tubular secretion
Substances reabsorbed/secreted in Proximal convoluted tubule
Reabsorbed: Na+, Cl-, K+, H2O, HCO3-, Glucose, amino acids
Secreted: H+, organic acids & bases (bile salts, oxalate, urate, catecholamines)
Mechanisms of Na reabsorption in PCT
Primary active transport: Na-K ATPase pumps Na out of tubular epithelial cells: generates conc gradient favouring Na reabsorption and negative charge attracting positive Na from lumen.
Secondary active transport (Co-transport): SGLT2 & 1 (sodium-glucose CO-transporters). SGLT2 (early part, 90% of glucose), SGLT1 (later part, 10%).
Secondary active secretion (counter-transport): Na-H exchanger extruded H+ from the cell coupled with Na+ entry.
Water reabsorption in the kidney
Proximal parts of nephron are highly permeable to H2O.
By osmosis through tight junctions between epithelial cells in permeable parts (PCT).
By aquaporins in distal parts and collecting duct (caused by ADH)
Substances reabsorbed/secreted in descending loop of Henle
Water reabsorbed
Substances reabsorbed/secreted in thick ascending loop of Henle
Reabsorbed: Na+, Cl-, K+, Ca2+, HCO3-, Mg2+
Secreted: H+
Mechanisms of reabsorption in thick ascending loop of Henle
Na-K ATPase creates low intercellular Na conc.
Na/2-Cl/K Co-transporter, moves K/Cl with Na as it follows conc gradient.
High intracellular K means backleak into the lumen, creating positive charge (+8mV).
Positive charge drives cations (Mg2+, Ca2+, Na+, K+) diffusion into interstitium
Na-H counter-transporter.
No absorption of water, creating very dilute fluid in lumen.
Substances reabsorbed/secreted in distal tubule
Early distal tubule:
Reabsorbed: Na, Cl, Ca, Mg
Late distal tubule:
Reabsorbed: Na, Cl, H2O, HCO3-, K
Secreted: H+
Mechanisms of reabsorption/secretion in distal tubule/collecting tubule
Proximal part:
Na- K ATPase pumps Na into interstitial fluid. Na-Cl co-transporter moves NaCl from lumen into cell.
Distal part:
Na-K ATPase creates gradients. Na moves down gradient into cell. K moves down gradients into lumen.
Type A intercalated cells in collecting tubule:
Secretion of H+ by K/H ATPase transporter and H+ ATPase transporter.
Carbonic anhydrase works in cells turning CO2 + H2O to H+ + HCO3-. For each H+ ion secreted a HCO3- is available to reabsorb across basement.
Type B intercalated cells:
Opposite action to type A. Can absorb H+ and secrete HCO3- in alkalosis.
