Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Renal Physiology and Failure

1,928 views

Published on

  • Suffer from Kidney Disease? how his patients avoid dialysis? Aussie Naturopath tells all... click here to find out how  https://tinyurl.com/yy8pd5uf
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here

Renal Physiology and Failure

  1. 1. Renal Physiology CT1 Education Series (Intro) R McKee
  2. 2. Renal Physiology • Removal: fluid, electrolytes, metabolic waste (tight control) • Significant blood flow: 20% of CO = 400 ml/100g/min = 1-1.2 l/min
  3. 3. Renal Physiology • Nephron – Functional unit – From Bowman’s capsule to collecting duct – 2 types • Cortical (superficial) – Majority • Juxtamedullary – Longer LoH
  4. 4. Renal Physiology • Massive concentrating ability - GFR 120 ml/min => Urine 1 ml/min • 2 main processes – Filtration [Bowman’s capsule] – Reabsorption [Everywhere else] • Water tends to follow Na+ [Na transport central]
  5. 5. Renal Physiology • Proximal convuluted tubule – 70% filtered Na reabsorbed – Active & Iso-osmotic - Volume reduction only
  6. 6. Renal Physiology • Loop of Henle – Active Na reabsorption only in Thick ascending limb • Water impermeable • Rise in medullary osmolality
  7. 7. Renal Physiology • Loop of Henle – Descending limb can lose water and ions • Concentrated and dehydrated – Fluid in ascending limb becomes dilute • Na loss
  8. 8. Renal Physiology • Distal convuluted tubule – Remaining Na reabsorption • Aldosterone
  9. 9. Renal Physiology • DCT and Collecting Duct – Water reabsorption • Passage through medulla • Final urine concentration • ADH control
  10. 10. Renal Physiology • Glomerular blood supply – Afferent from renal artery – Efferent draining glomerular capillaries • Dual arterial system allows tight autoregulation across glomerulus – Afferent dilation following systemic hypotension allows blood flow to remain high – Filtration can continue
  11. 11. Renal Physiology • Renal blood supply – Peritubular capillary network (vasa recta) • From efferent arteriole • Surrounds tubules and LoH • Excellent concentrating ability • Significant tubular energy consumption
  12. 12. Renal Physiology • Renal blood supply – Glomerular filtration is not energy-intensive – Most energy (and O2) use in the kidney is for Na/K/ATPase active pumps: Na reabsorption • Mainly in thick ascending limb of LoH
  13. 13. Renal Physiology • Blood flow to nephron – Hairpin-bend arrangement – Highest O2 consumption in outer medulla • Blood leaving capillary bed hypoxic • O2 tends to leave capillaries on entering to diffuse across (close apposition) – Medulla therefore hypoxic • Of most concern in outer medulla
  14. 14. Renal Physiology • Problems – Highest energy consumption in area with relative hypoxia – Hypotension • Glomerular filtration hydrostatic pressure initially maintained: afferents dilate (flow remains) • Blood flow still relatively maintained to outer medulla – Allows concentration to continue • Feedback mechanism reduces glomerular filtration – Reduces energy expenditure by medulla – Reduces Na loss
  15. 15. Renal Physiology Glomerular blood flow • If autoregulation fails… – <70mmHg – Flow becomes pressure dependant – Filtration therefore falls… – And if GFR falls, then less can be excreted.
  16. 16. Renal Failure • So… – Renal failure often the effect of distant processes – “Innocent bystander” • But… – Early intervention can reduce likelihood
  17. 17. Renal Failure • What is it? – Sudden (usually) reversible failure of kidneys to excrete nitrogenous and other waste – Multiple definitions – Now: ADQI • Review evidence • Set research agenda • Make management recommendations In acute renal failure, and use of renal replacement
  18. 18. RIFLE Criteria
  19. 19. What causes acute renal failure? Silvester, Bellomo et al Crit Care Med 2001:29;10
  20. 20. Renal Failure • Vast majority: poor renal perfusion – Cardiac output/blood pressure • Hypovolaemia • Other low CO states (e.g. cardiogenic shock) • Low SVR (e.g. sepsis) – Large vessel obstruction • Aortic thrombus/dissection • Renal artery obstruction – Intra-renal haemodynamics (autoregulation) • Prolonged hypotension • Sepsis • Drugs • obstruction
  21. 21. Renal Failure • Co-morbidities leading to reduced reserve – CKD – Diabetes – Heart failure – Obstructive uropathy – Liver disease More vulnerable to insult
  22. 22. Renal Failure • In ICU… – Co-morbidities – Medications • Antihypertensives => Hypotension • Beta blockers => Hypotension • ACE inhibitors => Hypotension • Duiretics => Hypovolaemia • NSAIDs => loss of autoregulation
  23. 23. Renal Failure • Does renal failure matter? – Acceptable casualty?? – Another organ failure??
  24. 24. Renal Failure • Renal failure is an independent risk factor for mortality – Levy et al (1996): similar illness severity with renal failure-up to x6.5 risk of death – CCMed (2002): similar disease severity and renal failure x2 mortality of those without renal failure
  25. 25. Renal Failure • Balancing – Optimal support for all organ systems – Overall patient support Means kidneys sometimes do suffer Remember this is not benign!
  26. 26. Urine Acidification • PCT: Na-H exchange – Na-K-ATPase • Catalysed by Carbonic Anhydrase • DCT/CD: H loss independent of Na in tubular lumen – ATP driven proton pump • Stimulated by aldosterone
  27. 27. Urine Acidification • Maximum gradient against which transport mechanisms can secrete corresponds to urine pH 4.5 • Buffers allow more H secretion H+ + HCO3 - H2CO3 (C. Anhydrase: PCT only) H+ + HPO4 2- H2PO4 - (DCT / CD) H+ + NH3 NH4 + (PCT and DCT)
  28. 28. • Carbonic anhydrase is in PCT – Allows formation of CO2 and H2O in tubular fluid • CO2 diffuses across membranes, becoming available to form H2CO3 • Since most of H+ removed from tubule, pH of fluid changes little
  29. 29. Drug Effects • Alcohol: inhibits vasopressin • Caffeine: inhibits vasopressin • CA inhibitors: decrease H secretion; resultant rise in Na and K loss • Metolazone, thiazides: Inhibit Na-Cl cotransport in early DCT • Loops: inhibit Na-K-2Cl cotransporter in medullary thick ascending LoH • K-sparing naturietics: inhibit Na-K exchange in CD by inhibiting aldosterone

×