Renal Physiology Guide: Glomerular Filtration, Tubular Transport Processes
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The document summarizes renal physiology concepts related to kidney tubular transport. It discusses the processes of glomerular filtration, tubular reabsorption, and secretion that produce urine. Key transport mechanisms and proteins involved in reabsorption and secretion in different segments of the nephron are described, including the proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting duct. Specific transporters, channels, and proteins involved in electrolyte transport and their roles in related kidney conditions are also outlined.
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Renal Physiology Guide: Glomerular Filtration, Tubular Transport Processes
- 1. Back to Basics: Renal Physiology Kidney Tubular Transport Mohammed Abdel Gawad Nephrology Consultant - Alexandria MD Nephrology - Mansoura University drgawad@gmail.com
- 2. To download the lecture with full animations contact me drgawad@gmail.com For more Nephrology lectures visit www.NephroTube.com
- 4. Urine Glomerular Filtration Tubular Reabsorption Tubular Secretion Excretion
- 6. Urine Glomerular Filtration Tubular Reabsorption Tubular Secretion Excretion Reabsorption Secretion
- 7. Urine Glomerular Filtration Tubular Reabsorption Tubular Secretion Excretion Reabsorption Secretion Luminal border (brush border) Basolateral border
- 8. Urine Glomerular Filtration Tubular Reabsorption Tubular Secretion Excretion Reabsorption Secretion Luminal border (brush border) Basolateral border Paracellular reabsorption Transcellular reabsorption Transcellular secretion
- 9. Luminal border (brush border) Paracellular reabsorption Transcellular reabsorption Transcellular secretion NHE SGLT PO4 Active transport Primary Active Secondary Active Counter Co Passive transport (Diffusion) Protein channel Facilitated (carrier protein) Passive transport Osmosis
- 10. PCT
- 11. K, Ca Cl, H2O PCT (early part) PO4 SGLT NHE K+ PO4 K+
- 12. PCT (early part) PO4 SGLT NHE K, Ca Cl, H2O K+ PO4 K+
- 13. PCT (early part) PO4 H+ PCT (late part) SGLT NHE NHE K, Ca Cl, H2O K+ K+ PO4 K+
- 14. PCT (early part) PO4 Cl H+ Base H+ Cl K+ e.g. formate, HCO3, oxalate PCT (late part) SGLT NHE NHE K, Ca Cl, H2O K+ K+ PO4 K+
- 15. PCT (early part) PO4PO4 Cl H+ Base H+ Cl K+ e.g. formate, HCO3, oxalate PCT (late part) isotonic SGLT NHE NHE K, Ca Cl, H2O ? K+ K+ PO4 K+
- 16. PCT (early part) PO4PO4 Cl H+ Base H+ Cl K+ e.g. formate, HCO3, oxalate PCT (late part) isotonic SGLT NHE NHE bile salts, oxalate, urate, and catecholamines drugs or toxins Ca, PO4 K, Ca Cl, H2O K+ K+ K+
- 22. NCCT K+
- 28. principal cells of the late distal tubules and cortical collecting tubules ENaC K+
- 29. principal cells of the late distal tubules and cortical collecting tubules K+ Aldosterone ENaC ADH ANP Locally produced PGE 2
- 30. principal cells of the late distal tubules and cortical collecting tubules K+ Aldosterone ENaC ADH ANP Locally produced PGE 2
- 32. Type A and type B intercalated cells of the collecting tubule Cl- Cl- AE1 protein pendrin Metabolic acidosis AldosteroneAldosterone
- 33. Type A and type B intercalated cells of the collecting tubule Cl- AE1 protein Aldosterone
- 37. 37 ADH - Action – H2O V2 Vasopressin binds V 2 receptors located on the basolateral membrane of principal cells in the collecting duct
- 38. 38 ADH - Action – H2O V2 Vasopressin binds V 2 receptors located on the basolateral membrane of principal cells in the collecting duct Defects in aquaporin-2 structure and function underlie X-linked nephrogenic diabetes insipidus Hypercalcaemia → ↑ intraluminal Ca 2+ → interferes with aquaporin-2 membrane insertion → defective urinary concentrating ability, polyuria, and dehydration
- 39. Already water- permeable with no need for ADH
- 40. ADH - Action – Urea
- 41. 41ADH - Action – Urea
- 42. Thank You
Editor's Notes
- • In addition, K + re-enters the lumen through a luminal K + channel (ROMK channel): - a recycling process that is necessary to prevent K + availability from becoming a limiting factor for the operation of NKCC. - This movement of K + back to the lumen also keeps it electrically net positive, which facilitates the passive paracellular reabsorption of Na + (as well as K + , Ca 2+ , NH 4 + , and Mg 2+ ).
- The energy for the action of the NCCT co-transporter is again derived from Na + K + -ATPase, as the resulting electrochemical gradient permits Na + reabsorption into the cell.
- Thiazide diuretics enhance Ca 2+ absorption (exact mechanisms unknown) Hypokalaemia occurs, as there will be an increase in Na + delivery to the collecting ducts and additional uptake via ENaCs. This will increase activity of the basolateral Na + K + -ATPase, and the resulting intracellular K + will then move into the lumen and be lost in the urine.
- Thiazide diuretics enhance Ca 2+ absorption (exact mechanisms unknown) Hypokalaemia occurs, as there will be an increase in Na + delivery to the collecting ducts and additional uptake via ENaCs. This will increase activity of the basolateral Na + K + -ATPase, and the resulting intracellular K + will then move into the lumen and be lost in the urine.
- Thiazide diuretics enhance Ca 2+ absorption (exact mechanisms unknown) Hypokalaemia occurs, as there will be an increase in Na + delivery to the collecting ducts and additional uptake via ENaCs. This will increase activity of the basolateral Na + K + -ATPase, and the resulting intracellular K + will then move into the lumen and be lost in the urine.
- Thiazide diuretics enhance Ca 2+ absorption (exact mechanisms unknown) Hypokalaemia occurs, as there will be an increase in Na + delivery to the collecting ducts and additional uptake via ENaCs. This will increase activity of the basolateral Na + K + -ATPase, and the resulting intracellular K + will then move into the lumen and be lost in the urine.
- Amiloride and triamterene block ENaC, thus reducing both Na + reabsorption and K + excretion. Spironolactone inhibits the effect of aldosterone on its receptor, with similar effects on Na + and K + .
- Principal cells ( approximately 65% of cells) are responsible for Na + (and water) reabsorption and K + excretion. Intercalated cells secrete H + ( A -intercalated cells) or HCO 3 – ( B -intercalated cells). Metabolic acidosis converts the collecting tubule from a state of HCO 3 secretion to HCO 3 absorption (and then H + secretion) that involves a phenotypic shift of B -intercalated cells to A -intercalated cells. In circumstances of severe acidosis or d K + , intercalated cells also express an H + /K + ATPase, similar to that responsible for gastric acid secretion. This allows additional H + secretion in exchange for K + .
- Principal cells ( approximately 65% of cells) are responsible for Na + (and water) reabsorption and K + excretion. Intercalated cells secrete H + ( A -intercalated cells) or HCO 3 – ( B -intercalated cells). Metabolic acidosis converts the collecting tubule from a state of HCO 3 secretion to HCO 3 absorption (and then H + secretion) that involves a phenotypic shift of B -intercalated cells to A -intercalated cells. In circumstances of severe acidosis or d K + , intercalated cells also express an H + /K + ATPase, similar to that responsible for gastric acid secretion. This allows additional H + secretion in exchange for K + .
- Aquaporin-2 is stored in intracellular vesicles ready for membrane insertion (the basolateral membrane is already water-permeable by virtue of aquaporin-3 and -4).