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Tubular Function
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Glucose is reabsorbed in the proximal tubule by co-transport with sodium ions. The proximal tubule reabsorbs all of the glucose in the tubular fluid. However, the specific carrier mechanism for glucose can be overloaded as the proximal tubule has a transport maximum for glucose (and other nutrients). If the filtered load exceeds the proximal tubule transport maximum, as in diabetes mellitus, glucose appears in urine. In humans, at a normal GFR of 125 mL/min, glucose begins to appear in the urine at a threshold plasma glucose concentration of 10–12 mmol/L. At a plasma glucose concentration of 15 mmol/L, and with a normal GFR, the proximal tubular carrier mechanism is completely saturated, and the transport maximum is reached at a filtered glucose load of 125 mL/min × 15 mmol/L = 1.88 mmol/min (Figure 43.8).
Urinary Excretion
Published in John G. Wagner, Pharmacokinetics for the Pharmaceutical Scientist, 2018
Tubular secretion. Some drugs are excreted from the capillaries surrounding the renal tubuli into the tubular fluid by a carrier-mediated and active process. This process is saturable and there is a transport maximum value for each drug which is actively secreted.
Renal Handling of Glucose, Sodium and Inulin
Published in Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod, The Primary FRCA Structured Oral Examination Study Guide 1, 2017
Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod
How much glucose is filtered by the kidney, and how much can be reabsorbed?100% of plasma glucose is filtered.Active transport mechanisms become saturated at higher concentrations of solute and their maximum rate of transport (reabsorption) is reached. This is known as the transport maximum (Tm) for a given solute.Glucose reabsorption is proportional to the amount filtered, and hence to its plasma concentration multiplied by the GFR, up to the transport maximum, which is about 180 g/dL or 10 mmol/L of glucose in venous plasma.Once the renal threshold for glucose is reached, not all the filtered glucose is reabsorbed and glucose starts to appear in the urine.
Euglycaemic diabetic ketoacidosis as a complication of SGLT-2 inhibitors: epidemiology, pathophysiology, and treatment
Published in Expert Opinion on Drug Safety, 2020
Erasmia Sampani, Pantelis Sarafidis, Aikaterini Papagianni
SGLT-2 is a high-capacity/low-affinity glucose transporter located in the apical surface of renal proximal tubular cells of the S1 segment at the kidneys. It is responsible for 90% of renal glucose reabsorption [10]. The co-transportation of glucose and sodium is active in a 1:1 ratio [11]. The remaining 10% of glucose is reabsorbed in the S2/S3 segment of proximal tubules by SGLT-1 protein. In this way, the SGLTs family proteins reabsorb almost all of the glucose that is freely filtered at the glomeruli, up to a maximum of around 375 mg/min (2.08 mmoL/min) (glucose transport maximum) [12]. In the setting of acute hyperglycemia, the increased amount of filtered glucose leads to saturation of the SGLTs, resulting in excretion of the excessive glucose. However, in diabetic patients, the kidneys increase up to threefold the expression of SGLT-2, which from an evolutionary perspective can be seen as an adaptive response of the body to preserve glucose, i.e. the precious fuel; thus, their glucose reabsorption capacity is increase by at least by ~20%, compared to healthy individuals [13]. The consequence of this adaptation is the minimization of glucosuria which further enhances hyperglycemia, representing one of the multiple pathophysiological mechanisms for glucose increase in T2DM2. SGLT-2 inhibitors reach their target from the luminal side through glomerular filtration and result in excretion of 50–60% of the filtered glucose, instead of 90% because of a partial compensation by an upregulation of SGLT-1 co-transporters [13].