CME: Kidney - Anatomy & Physiology

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CME: Kidney - Anatomy & Physiology

  1. 1. Prof.Dr.P.Vijayaraghavan’s unit Dr.B.Elavazhagan THE KIDNEY ANATOMY AND PHYSIOLOGY
  2. 2. EMBRYOLOGY <ul><li>Development starts at 4 th week </li></ul><ul><li>intermediate mesoderm </li></ul><ul><li>primordial components ----pronephros ,mesonephros,metanephros </li></ul><ul><li>pronephros :appear as solid cell groups in cervical region ,which then regresses </li></ul><ul><li>mesonephros : forms glomerulus bowman’s capsule, which opens into </li></ul><ul><li>mesonephric duct </li></ul><ul><li>except mesonephric duct rest of these structures regresses </li></ul><ul><li>mesonephric duct forms internal genitalia in males , an out growth </li></ul><ul><li>from it forms ureteric bud </li></ul>
  3. 3. <ul><li>metanephros forms excretory part of definitive kidney upto </li></ul><ul><li>DCT </li></ul><ul><li>ureteric bud forms the rest, from collecting tubules upto </li></ul><ul><li>trigone of the bladder </li></ul><ul><li>interaction between metanephros and ureteric bud initiates development of kidney </li></ul><ul><li>growth factors :metanephros ----WT1,GDNF,HGF </li></ul><ul><li>ureteric bud-----FGF2,BMP7 </li></ul>
  4. 5. CLINICAL CORRELATES <ul><li>persistant fetal lobulations [DROMEDARY HUMP] </li></ul><ul><li>-----a normal variant </li></ul><ul><li>Ureteric bud branches normally and metanephric differentiation faulty </li></ul><ul><li>-----multicystic dysplastic kidney </li></ul><ul><li>Failure of ureteric bud branching (GDNF)-----renal agenesis </li></ul><ul><li>B/L renal agenesis ----POTTER’S SEQUENCE </li></ul><ul><li>(anuria ,oligohydramnios,hypoplastic lung) </li></ul><ul><li>POTTER’S FACIES ----(flattened facies,beak nose,club foot) </li></ul>
  5. 6. <ul><li>ARPKD ----cyst arises from collecting duct only </li></ul><ul><li>ADPKD-----cyst arises from all segments of nephrons </li></ul><ul><li>WILM’S TUMOUR ---- due toWT1 mutation </li></ul><ul><li>premature termination of ureteric bud branching causes low nephron mass ----preterm babies </li></ul><ul><li>Normal –1 million nephrons at birth </li></ul><ul><li>Pre term babies –2.25 lakh nephrons at bith , hence </li></ul><ul><li>prone for CKD </li></ul>
  6. 8. GROSS ANATOMY <ul><li>position : T12 - L3. </li></ul><ul><li>Rt kidney -lower ,Lt kidney- medial </li></ul><ul><li>size: 11×6×3 </li></ul><ul><li>consists of 1) cortex (renal arches ,renal columns ) </li></ul><ul><li>2) medulla (pyramids,papillae,major calyx,minor calyx) </li></ul><ul><li>3) renal sinus (pelvis,renal vessels and lymphatics ) </li></ul><ul><li>Blood supply : abdominal aorta at the level of L2 </li></ul><ul><li>renal veins drains into IVC </li></ul>
  7. 11. Vascular anatomy <ul><li>Aorta </li></ul><ul><li>renal artery </li></ul><ul><li>segmental artery </li></ul><ul><li>inter lobar artery </li></ul><ul><li>arcuate artery </li></ul><ul><li>inter lobular artery </li></ul><ul><li>afferent arteriole </li></ul><ul><li>glomerular capillary </li></ul><ul><li>efferent arteriole </li></ul><ul><li>peritubular capillary </li></ul><ul><li>Inter lobular vein </li></ul><ul><li>arcuate vein </li></ul><ul><li>inter lobar vein </li></ul><ul><li>segmental vein </li></ul><ul><li>renal vein </li></ul><ul><li>ivc </li></ul>
  8. 13. <ul><li>Glomerulus </li></ul><ul><li>1) Vasculature : afferent arteriole , glomerular </li></ul><ul><li>capillary,efferent arteriole </li></ul><ul><li>2) Bowman’s capsule : visceral epithelium , </li></ul><ul><li>parietal epithelium </li></ul><ul><li>3) Filtration barrier : formed by podocytes of visceral epithelium ,basement membrane , capillary endothelium </li></ul><ul><li>4) Mesangial cells : between capillary endothelium </li></ul><ul><li>and basal lamina, contractile in nature </li></ul>
  9. 17. Diagram illustrating hypothetical assembly of nephrin forming the filter of the podocyte slit diaphragm. Nephrin molecules from adjacent interdigitating foot processes are shown in different shades of purple. X indicates proteins interacting with nephrin and connecting with the plasma membrane
  10. 18. <ul><li>Tubules : 1) PCT---Brush border cells,tight epithelial </li></ul><ul><li>junctions ,lateral inter cellular spaces </li></ul><ul><li>2) LOOP OF HENLE ---descending </li></ul><ul><li>ascending (thin,thick) </li></ul><ul><li>3) DCT </li></ul><ul><li>4) COLLECTING DUCT --- P-cells </li></ul><ul><li>I-cells </li></ul>
  11. 21. RENAL PHYSIOLOGY <ul><li>Excretory function : 1)glomerular filtration </li></ul><ul><li>2)tubular reabsorption </li></ul><ul><li>3)tubular secretion </li></ul><ul><li>Endocrine function :1) erythropoitein </li></ul><ul><li>2) ca2+ & po4 metabolism </li></ul><ul><li>3) RAAS </li></ul><ul><li>4) Kinins </li></ul>
  12. 22. GLOMERULAR FILTRATION <ul><li>Normal GFR: 125ml/min </li></ul><ul><li>Factors : A) Favouring :1)capillary hydrostatic pressure </li></ul><ul><li>2)tubular oncotic pressure </li></ul><ul><li>B) Opposing :1) capillary oncotic pressure </li></ul><ul><li>2) tubular hydrostatic pressure </li></ul><ul><li>Permeability : Neutral substances < 4nm </li></ul><ul><li>4-8nm </li></ul><ul><li>>8nm </li></ul><ul><li>Anionic & cationic substances </li></ul>
  13. 23. <ul><li>What is GFR? </li></ul><ul><li>What is CLEARANCE? </li></ul><ul><li>What is EXTRACTION RATIO? </li></ul><ul><li>What is FILTRATION FRACTION? </li></ul><ul><li>Clearance of a substance=U x.VP x </li></ul><ul><li>=GFR + tubular secretion – tubular </li></ul><ul><li>absorption </li></ul><ul><li>Extraction ratio depends on tubular absorption and secretion </li></ul><ul><li>Filtration fraction = GFR </li></ul><ul><li>RPF </li></ul>
  14. 24. MEASUREMENT OF GFR <ul><li>Methods used :1) inulin clearance (gold standard) </li></ul><ul><li>2) creatinine clearance (clinically used) </li></ul><ul><li>3) cr51 ,EDTA ( most sensitive ) </li></ul><ul><li>4) cystatin C ( endogenous ,not affected by </li></ul><ul><li>age ,muscle mass,sex) </li></ul>
  15. 25. AUTOREGULATION <ul><li>systemic arterial pressure increases </li></ul><ul><li>afferent arteriole constricts </li></ul><ul><li>systemic arterial pressure drops </li></ul><ul><li>efferent arteriole constricts </li></ul>
  16. 26. GLOMERULO TUBULAR BALANCE <ul><li>When GFR increases ---more solutes and water reabsorbed </li></ul><ul><li>from tubules </li></ul><ul><li>% of solute reabsorption is constant </li></ul><ul><li>Mech : Increase in oncotic pressure in peritubular capillaries </li></ul>
  17. 27. TUBULO GLOMERULAR FEEDBACK <ul><li>Increased solute delivery to the distal tubule </li></ul><ul><li>sensed by macula densa </li></ul><ul><li>increased ATPase & formation of adenosine </li></ul><ul><li>Constriction of afferent arteriole </li></ul>
  18. 28. TRANSPORTERS OF RENAL TUBULE <ul><li>PCT : co-transporters ----Na/glucose,Na/po4,Na/A Na/lactate </li></ul><ul><li>exchangers ----Na/H+,Cl/base </li></ul><ul><li>Thick ascending limb :Na +K+2CL- Na+H+ exchanger </li></ul><ul><li>DCT : Na- cl co transporter </li></ul><ul><li>COLLECTING DUCT :ENaC </li></ul>
  19. 29. Na-Cl reabsorption <ul><li>Except thin portions of loop of Henle ,Na is actively transported out of all parts </li></ul><ul><li>PCT -60% </li></ul><ul><li>TALH-30% </li></ul><ul><li>DCT -7% </li></ul><ul><li>CD-3% </li></ul><ul><li>Glucose ,amino acids ,bicarbonate ---reabsorb along with Na </li></ul><ul><li>in early PCT </li></ul><ul><li>Chloride reabsorbed along with Na in distal PCT ,TALH,DCT </li></ul>
  20. 30. Water reabsorption <ul><li>60 – 70 % in PCT;15% in descending loop of henle ;5 % in DCT 15 % in collecting duct; </li></ul><ul><li>Absorption in collecting duct is solely dependent on ‘vasopressin ‘; </li></ul><ul><li>Plasma osmolality </li></ul><ul><li>vasopressin release </li></ul><ul><li>V 2 receptor– aquaporin 2 </li></ul><ul><li>water absorption </li></ul><ul><li>Water diuresis / osmotic diuresis </li></ul><ul><li>Vaptans- V 2 receptor antagonist; </li></ul>
  21. 31. H + /HCO 3 –SECRETION / ABSORPTION <ul><li>PCT-- Na + /H + transporter--Na dependent; </li></ul><ul><li>DCT & collecting duct –H+/ATPase –Na independent ; </li></ul><ul><li>Buffers :- </li></ul><ul><li>1.HCO3¯ –in PCT </li></ul><ul><li>2.HPO4 ²¯-in DCT & collecting duct </li></ul><ul><li>3.NH3 – in PCT & DCT ,non ionic diffusion </li></ul><ul><li>H + secretion depends on pCO2 ,K,CA, & aldosterone ; </li></ul><ul><li>CKD & RTA – defective H + secretion </li></ul>
  22. 32. COUNTER CURRENT MECHANISM <ul><li>CC mutiplier: loop of henle makes the medullary interstium more hypertonic more towards tip of pyramid. </li></ul><ul><li>CC exchanger: vasarecta keeps hypertonic interstium stable. it is a passive process. </li></ul>
  23. 33. JUXTA GLOMERULAR APPARATUS <ul><li>Macula densa in distal tubule. </li></ul><ul><li>Juxta glomerular cells in AA </li></ul><ul><li>(renin secreting) </li></ul><ul><li>Lacis cells. </li></ul>
  24. 34. RENIN ANGIOTENSIN SYSTEM <ul><li>RENIN by </li></ul><ul><li>sympathetic activity </li></ul><ul><li>prostaglandins </li></ul><ul><li>hypotension </li></ul><ul><li>cirrhosis </li></ul><ul><li>cardiac failure </li></ul><ul><li>Angiotensin 2 – </li></ul><ul><li>vasoconstriction </li></ul><ul><li>aldosterone secretion </li></ul><ul><li>Na reabsorption </li></ul>
  25. 35. THANK YOU

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