Renal phys

• Paracellular transport means through tight junctions
• Transcellular transport means through the renal tubular epithelial cells
• Passive diffusion is simple diffusion, channel mediated, carrier mediated, osmosis
• Active transport has two types, primary or secondary
• The reabsorption of sodium is mainly an active process so most renal energy utilisation goes to accomplishing this
• The reabsorption of water is by osmosis and is secondary to reabsorption of sodium
• In the proximal tubule, 65% of both water and sodium are reabsorbed
• In the descending limb of Henle, 10% of water is reabsorbed
• In the ascending limb of Henle, 25% of sodium is reabsorbed
• In the distal convoluted tubule 5% of sodium us reabsorbed
• In the collecting duct, 4-5% of sodium and 5% of water is reabsorbed
• The collecting duct is the only point at which the body can modulate the amount of sodium and water being reabsorbed
• Transport maximum is the limit to the rate the solute can be actively reabsorbed
• Transport maximum is due to saturation of available carrier proteins, and the excess is excreted in urine
• Normal GFR is 125ml/min
• The glomerular filtration rate (GFR) is the volume of filtrate formed by the kidney each minute(ml/min)
• Reabsorption of glucose is proportional to the plasma concentration until the transport maximum is reached
• Glucosuria occurs when blood glucose levels exceed the transport maximum
• Transport maximum for glucos is 375mg/min
• Glucose excretion is zero until the last renal threshold is reached
• Transcellular tubular reabsorption is through the cells using separate transport steps in the apical and basolateral membranes whilst paracellular tubular reabsorption is around (para = next to/alongside) the cells through tight junctions.
• There are upper limits to the rate at which any given solute can be reabsorbed or secreted, either because the substance leaks back into the lumen (gradient-limited systems), or because the transporters become saturated (Tm; maximum glucose transport capacity).
• To be reabsorbed(move from flitrate to the plasma), a substance first needs to traverse the apical or luminal membrane before moving through the cytosol of the luminal cell. It then exits the luminal cell via the basolateral membrane into the interstitial space before passing through the capillary or endothelial membrane to enter the plasma.
• Glycosuria refers to the presence of glucose in the urine. This can occur in diabetes mellitus where the glucose filtered load is greater than the glucose transport maximum. In order words, if all glucose transporters are being used to reabsorb glucose from the lumen back into the plasma, in situations with a high glomerular filtration rate (GFR) and increased blood glucose levels, not all glucose is able to be reabsorbed, resulting in glycosuria.
• Autoregulation of vascular resistances keeps glomerular filtration rate within limits in the face of large variations in arterial pressure.
• Autoregulation is achieved by the myogenic mechanism and tubuloglomerular feedback
• The myogenic response (which is the contraction or relaxation of arteriolar smooth muscle in response to changes in vascular pressures) is very fast-acting and protects the glomeruli from short-term variations in blood pressure whilst tubuloglomerular feedback helps maintain the appropriate filtered load of sodium and waste products.
• Constriction of the efferent renal arteriole will increase GFR whilst dilation of the afferent renal arteriole will also increase GFR. Constricting both afferent and efferent renal arterioles actually leads to maintaining a constant GFR (not an increase in GFR). When GFR increases, it is true that there is inadequate time for reabsorption but this means that more substances are lost in the urine (not reduced waste excretion).
• An increase in hydrostatic pressure against the afferent arteriole walls activates stretch receptors which initiate vasoconstriction to return GFR to normal. These stretch receptors open calcium channels in the vascular smooth muscle cell membrane, leading to calcium influx and vascular smooth muscle cell contraction. This then leads to vasoconstriction of the afferent arterioles, which therefore reduces GFR, returning GFR to normal levels.
• Glomerular capillary pressure(PGC) is determined by arterial pressure, afferent and efferent pressure
• Increase in GFR means flow along tubules increase so inadequate time for reabsorption so substances lost in urine
• Decrease in GFR means reabsorption increased so wastes are not excreted
• Urine flow is not autoregulated

  it is directly proportional to arterial pressure

  process is pressure-natriiuriesis
• The kidney CANNOT correct for inadequate sodium and water intake.
•  High levels of extracellular sodium results in an increase in plasma osmolarity. This leads to water movement into the plasma, which therefore increases plasma (ECF) volume and results in a greater force being exerted against the arterial walls (higher blood pressure).
• A decrease in total body sodium reduces plasma osmolarity, leading to a decrease in plasma volume. As a result, there is a decrease in hydrostatic pressure in the glomerular capillaries which leads to a decrease in GFR and results in an increase in sodium reabsorption.
• Despite aldosterone acting on the late distal convoluted tubules and collecting ducts to increase reabsorption, the majority of sodium reabsorption still occurs in the proximal convoluted tubules.
• Aldosterone is a steroid hormone that diffuses through the cell membrane and combines with a mineralocorticoid receptor.
• The aldosterone-receptor complex migrates to the nucleus, inducing gene transcription and translation of proteins involved in Na+ reabsorption.
• Aldosterone increases the synthesis of K+ channels in the apical/luminal membrane and the synthesis of ATP.