Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Renal Oxygen Demand and Nephron Function: Is Glucose a Friend or Foe?

Version 1 : Received: 27 April 2023 / Approved: 28 April 2023 / Online: 28 April 2023 (03:08:47 CEST)

A peer-reviewed article of this Preprint also exists.

Gronda, E.; Palazzuoli, A.; Iacoviello, M.; Benevenuto, M.; Gabrielli, D.; Arduini, A. Renal Oxygen Demand and Nephron Function: Is Glucose a Friend or Foe? Int. J. Mol. Sci. 2023, 24, 9957. Gronda, E.; Palazzuoli, A.; Iacoviello, M.; Benevenuto, M.; Gabrielli, D.; Arduini, A. Renal Oxygen Demand and Nephron Function: Is Glucose a Friend or Foe? Int. J. Mol. Sci. 2023, 24, 9957.

Abstract

The kidney and the heart work together in balancing the body circulation and although their physiology is based on strict inter dependence, their performance fulfills different aims. While the heart can rapidly increase its own oxygen consumption to comply with the wide changes in metabolic demand linked to body function, the kidney physiology is primarily designed to maintain a stable metabolic rate and has limited capacity to cope with any steep increase in renal metabolism. In the kidneys the glomerular population filters a large amount of blood and the tubular system has been programmed to reabsorb 99% of filtrate by reabsorbing sodium together with other filtered substances including all glucose molecules. Glucose reabsorption involves the sodium-glucose cotransporters SGLT2 and SGLT1 on the apical membrane in the proximal tubular section; it also enhances bicarbonate formation so as to preserve the acid-base balance. The complex work of reabsorption in the kidney is the main factor in renal oxygen consumption; analysis of renal glucose transport in disease states is providing better understanding of the renal physiology changes that occur when clinical conditions alter the neurohormonal response leading to an increase in glomerular filtration pressure. In this circumstance glomerular hyperfiltration occurs, imposing a higher metabolic demand on kidney physiology and causing progressive renal impairment. Albumin urination is the warning signal of renal engagement over-exertion and most frequently heralds heart failure development, regardless of disease etiology. The review analyzes the mechanisms linked to renal oxygen consumption, focusing on sodium-glucose management.

Keywords

glucose transport; SGLT2 inhibitor; diabetic nephropathy; heart failure; chronic kidney disease

Subject

Medicine and Pharmacology, Endocrinology and Metabolism

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