Renal PhysiologyReview

1 Arcuate artery2 Interlobular artery3 Afferent arteriole4 Efferent arteriole

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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

ElectrolytesWithin 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 receptors on 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

Phosphate and CalciumPTH inhibits phosphate reabsorption in the

proximal tubulePTH 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

Substance Proximal tubule Loop of Henle Distal tubule Collecting duct

GlucoseSLGT-2 (Apical) and GLUT-2

(basolateral)

Ureareabsorption (50%) via passive transport (solvent drag)

Secretion (urea transporter)

Reabsorption (urea transporter) in medullary collecting ducts

Sodiumreabsorption (65%) via Na-H antiporter & Na-Glucose symporter

reabsorption (25%, thick ascending, Na-K-2Cl symporter)

reabsorption (5%, Na-Cl symporter – aldosterone

reabsorption (5%, principal cells), stimulated by aldosterone via ENaC

Chloride reabsorption

reabsorption (passive by thin ascending, thick ascending, Na-K-2Cl symporter)

reabsorption (sodium-chloride symporter)

Waterabsorbed osmotically along with solutes

reabsorption (descending tubule)

reabsorption (regulated by ADH activating aquaporin channels

Bicarbonate

reabsorption (80-90%) via intra/extracellular carbonic anhydrase + denovo synthesis using glutamine -> ammonium

DeNovo synthesis by intercalated cells secreting H+

PotassiumPassive reabsorption (65%) due to concentrating effect

reabsorption (20%, thick ascending, Na-K-2Cl symporter)

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secretion (common, via Na+/K+-ATPase, increased by aldosterone), or reabsorption (rare, hydrogen potassium ATPase)

Calcium

Reabsorption via basolateral calcium ATPase, Na-Ca exchanger & apical Ca channels

reabsorption (thick ascending) via passive transport

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Magnesium

Reabsorption: Ca & magnesium compete, an excess of one can lead to excretion of the other

reabsorption (thick ascending)

reabsorption

Phosphatereabsorption (85%) via Na-phosphate cotransporter Inhibited by PTH

Carboxylatereabsorption (100%) via carboxylate transporters.

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

Acid Base Balance

De-Novo bicarbonate is producedwithin the proximal tubules via theexcretion of NH4+ originating from circulating glutamine. Failure of thisoccurs in Addison’s disease resultingin a mild Type 4 RTA

De-Novo bicarbonate is producedwithin alpha intercalated cells of the cortical collecting duct via theexcretion of H+ which is buffered by phosphate. Failure results in Type 1 RTA

Bicarbonate is reabsorbed by this processin the proximal tubule. Failure of this process in Falconi’s syndrome causesrenal tubular acidosis (Type 2 RTA)