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Renal Physiology

Renal Physiology

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Renal Physiology

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  1. Renal Physiology Review

  2. 1 Arcuate artery 2 Interlobular artery 3 Afferent arteriole 4 Efferent arteriole 5 6 7 7

  3. What is this process called? • Describe the mechanism when MAP drops from 160mm to 80mm • Interlobular arteries and afferent arterioles dilate while efferent arterioles constrict • What happens when MAP falls below 80mm Hg • Acute renal failure

  4. Electrolytes • Within the proximal tubule sodium is reabsorbed by active transport, which is regulated by angiotensin II • The reabsorption of sodium in the collecting ducts is increased by the action of aldosterone which activates ENaC channels in principal cells • ADH binds to V2 receptorson the basolateral surface of the cells of the collecting ducts causing insertion of aquaporins causing urine to become more concentrated Abnormally low levels of this hormone or defective V2 receptors results in diabetes insipidus

  5. Phosphate and Calcium • PTH inhibits phosphate reabsorption in the proximal tubule • PTH increases reabsorption of calcium and magnesium from the distal tubule. • The net increase in the ratio of serum calcium to serum phosphate means PTH greatly increases the concentration of free calcium

  6. Where and by which transporters are the following substances reabsorbed or excreted:

  7. Acid Base Balance Bicarbonate is reabsorbed by this process in the proximal tubule. Failure of this process in Falconi’s syndrome causesrenal tubular acidosis (Type 2 RTA) De-Novo bicarbonate is produced within alpha intercalated cells of the cortical collecting duct via the excretion of H+ which is buffered by phosphate. Failure results in Type 1 RTA De-Novo bicarbonate is produced within the proximal tubules via the excretion of NH4+ originating from circulating glutamine. Failure of this occurs in Addison’s disease resultingin a mild Type 4 RTA