Renal Physiology and Renal Function

28/04/2013 by admin | Renal

Renal physiology and renal function

  1. 1 x kidney = 1 x million nephrons
  2. Each nephron: glomerulus located in cortex – filters into renal tubule and LoH (main site of water and electrolytes reabsorption). Urine drains to collecting duct. Further water reabsorption. Drains to renal pyramids.
  3. Thick ascending limb of LoH attaches to extra-glomerular mesangium and afferent arteriole = ‘juxtaglomerular apparatus’ (site of renin secretion – regulating GFR).
  4. Kidneys receive 20% of CO, filter 7L fluid/h, and produce 50-100ml urine/h.
  5. Functions: excrete/secrete wasteful products of metabolism, whilst conserving useful constituents of blood. Plus key endocrine functions.

 

Functions:

  1. Waste product elimination: based on GFR. Can show efficacy of elimination based on amount of creatinine (waste product of skeletal muscle breakdown) eliminated. Most accurate measure = creatinine clearance measures.
  2. Conservation of normal blood constituents: glomerular function may be disturbed = so that plasma is not conserved and leaked (can be a marker of mild diseasesevere = profound hypoalbuminaemia and oedema). Proteinuria may reflect = defected tubular function, overflow (MM, Ig kappa/lambd, acute leukaemia, lyzomuria).
  3. Ability to concentrate urine: in LoH via countercurrent mechanism, controlled by ADH. Disturbed in intrinsic renal diseases (especially in tubulointerstitial disease) and ADH deficiencies (diabetes insipidus). Test concentrating power using osmolality of early morning urine.
  4. Amino acid conserving function: AAs filtered at glomerulus and reabsorbed at proximal tubule. Diffuse proximal tubular damage = aminoaciduria. Detect by two-dimensional chromatography.
  5. Renal acid-base control: function of proximal and distal tubules. Advanced renal disease = retention of metabolic acids (exacerbating renal bone disease and myocardial depression).
  1. Electrolyte control: control of potassium by secretion of K into tubular fluid in exchange for sodium or hydrogen ions. Therefore central in regulating urinary pH. In advanced renal disease = distal tubule cannot exchange plasma K/H for Na = hyperkalaemia = cardiac arrest.
  2. Hormonal function: produce renin and erythropoietin, and the 1-alpha-hydroxylation of Vit D from inactiveactive form. Renal deficiet = hormone production diminished = anaemia (due to reduced EPO)! Also dysregulate RAA system (therefore renal ischemia/RAS/GN = HTN).

 

Change in urine profile based on pathology:

  1. Glomerulonephritis: proteinuria, nephrotic syndrome may be present, dipstick positive for protein, no kappa/lambda chains.
  2. Tubular disease: proteinuria, no nephrotic syndrome, dipstick negative for protein, kappa/lambda chain positive.
  3. Overflow proteinuria: proteinuria, nephrotic syndrome may be present, amyloid in multiple myeloma, dipstick negative for protein, monoclonal Ig kappa/lambda chain positive. 
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