Renal physiology and renal function
- 1 x kidney = 1 x million nephrons
- 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.
- Thick ascending limb of LoH attaches to extra-glomerular mesangium and afferent arteriole = ‘juxtaglomerular apparatus’ (site of renin secretion – regulating GFR).
- Kidneys receive 20% of CO, filter 7L fluid/h, and produce 50-100ml urine/h.
- Functions: excrete/secrete wasteful products of metabolism, whilst conserving useful constituents of blood. Plus key endocrine functions.
- 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.
- 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).
- 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.
- Amino acid conserving function: AAs filtered at glomerulus and reabsorbed at proximal tubule. Diffuse proximal tubular damage = aminoaciduria. Detect by two-dimensional chromatography.
- Renal acid-base control: function of proximal and distal tubules. Advanced renal disease = retention of metabolic acids (exacerbating renal bone disease and myocardial depression).
- 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.
- 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:
- Glomerulonephritis: proteinuria, nephrotic syndrome may be present, dipstick positive for protein, no kappa/lambda chains.
- Tubular disease: proteinuria, no nephrotic syndrome, dipstick negative for protein, kappa/lambda chain positive.
- Overflow proteinuria: proteinuria, nephrotic syndrome may be present, amyloid in multiple myeloma, dipstick negative for protein, monoclonal Ig kappa/lambda chain positive.