Potassium-sparing diuretics inhibit sodium
reabsorption in the latter parts of the distal tubule and the early collecting duct (Figure 3, F).
Weak expression of AQP1 in the thick descending limb and descending thin limb of Henle's loop also produced a urinary concentrating defect, thereby resulting in an impaired renal water
reabsorption.
The majority promotes a rise in sodium renal excretion, conditioning a decreased concentration of it and therefore the activation of a compensatory mechanism of increased sodium tubular
reabsorption and, as explained, also of lithium.
Diuretics decrease sodium
reabsorption, increasing FeNa and so interfering with the performance of FeNa in differentiating between T-AKI and P-AKI [35].
In fact, hypokalemia is typically associated with decreased AQP2 expression, hypercalciuria affects renal concentrating ability via activation of the calcium-sensing receptor, and nephrocalcinosis may impair water
reabsorption.
Because glucose and sodium are co-transported in the proximal tubules, inhibition of SGLT2 also decreases sodium
reabsorption (Wanner, 2017).
Selective SGLT-2 inhibitors reduce renal glucose
reabsorption by inhibiting SGLT-2 in the kidney, thus reducing the maximum glucose transport capacity in the proximal renal tubule and increasing renal glucose excretion.
The aim of our prospective cross-sectional study was to analyse glomerular and tubular renal function in patients with CF treated with repeated courses of once-daily tobramycin evaluating estimated GFR and tubular amino acid
reabsorption. We hypothesized that repeated courses of once-daily tobramycin result in hyperaminoaciduria.
[Na.sup.+]
reabsorption is mediated via the amiloride-sensitive epithelial sodium channel (ENaC), which exhibits high selectivity for sodium [15] and is a central requirement for [Na.sup.+]
reabsorption across renal epithelia.
In the coronal sections a hypodense image was observed in the body of the mandible region, left side, associated with the left permanent mandibular second molar, with radicular
reabsorption of the left permanent mandibular first molar (Figure 2).
In contrast to these studies [4-6, 17], PRTD and impaired phosphate renal tubular
reabsorption were seen in 15-48% of CHB patients receiving long-term ADV and TDF therapy as in real world clinical experience [8, 10,18-20].
"I was born with rare genetic bone condition osteopetrosis where the remodelling and
reabsorption of old bone and new bone is impaired, essentially leaving me with thick dense bones - but they are extremely brittle and prone to non-impact fractures.