Background Zinc deficiency is commonly encountered in chronic kidney disease (CKD). The aims of this study were to assess whether zinc deficiency was related to increased renal excretion of zinc and to the progression of CKD. Methods Plasma and 24-h urinary zinc levels, urinary electrolytes and uromodulin were measured in 108 CKD patients and 81 individuals without CKD. Serum creatinine values were collected for 3 years to calculate the yearly change in estimated glomerular filtration rate (eGFR). Multivariable regression analysis was performed to assess the association between baseline zinc levels and yearly change in eGFR. Results CKD patients had lower circulating zinc levels and higher 24-h urinary zinc excretion than non-CKD participants (612.4 ± 425.9 versus 479.2 ± 293.0 µg/day; P = 0.02). Fractional excretion (FE) of zinc was higher and it significantly increased at more advanced CKD stages. Zinc FE was correlated negatively with 24-h urinary uromodulin excretion (r=−0.29; P < 0.01). Lower baseline plasma zinc levels were associated with a faster yearly decline of renal function in age, gender, diabetes and hypertension adjusted models, but this relationship was no longer significant when baseline eGFR or proteinuria were included. Conclusions Zinc levels are lower in CKD, and not compensated by reduced renal zinc excretion. The inverse association between urinary zinc excretion and uromodulin possibly points to an impaired tubular activity, which could partly account for zinc imbalance in CKD. These data suggest that zinc status is associated with renal function decline, but further studies elucidating the underlying mechanisms and the potential role of zinc supplements in CKD are needed.

Screening for and treating asymptomatic bacteriuria are common in KTRs despite uncertainties around the benefits and harms. In an era of antimicrobial resistance, further studies are needed to address the diagnosis and management of asymptomatic bacteriuria in these patients.

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A precise maintenance of sodium and fluid balance is an essential step in the regulation of blood pressure and alterations of this balance may lead to the development of hypertension. In recent years, several new advances were made in our understanding of the interaction between sodium and blood pressure regulation. The first is the discovery made possible with by new technology, such as 23Na-MRI, that sodium can be stored non-osmotically in tissues including the skin and muscles particularly when subjects are on a high sodium diet or have a reduced renal capacity to excrete sodium. These observations prompted the refinement of the original model of regulation of sodium balance from a two-compartment model comprising the extracellular fluid within the intravascular and interstitial spaces to a three-compartment model that includes the intracellular space of some tissues, most prominently the skin. In this new model, the immune system plays a role, thereby supporting many previous studies indicating that the immune system is a crucial co-contributor to the maintenance of hypertension through pro-hypertensive effects in the kidney, vasculature, and brain. Lastly, there is now evidence that sodium can affect the gut microbiome, and induce pro-inflammatory and immune responses, which might contribute to the development of salt-sensitive hypertension.

Background Renal length, volume, and parenchymal thickness are important clinical parameters, yet data concerning the accuracy and reproducibility of ultrasound (US)-based renal length and volume assessment in patients with chronic kidney disease (CKD) are scarce. Purpose To establish whether renal length, volume, and parenchymal thickness can be reliably measured with renal US in patients with CKD. Material and Methods All participants underwent renal US, immediately followed by 3-T magnetic resonance imaging (MRI). Renal length, width, transverse diameter, and parenchyma thickness were measured with both methods; renal volume was calculated using the ellipsoid formula. A total of 45 patients with CKD (eGFR [mean ± SD] 57.4 ± 4.4 mL/min/1.73 m2) and 46 participants without CKD (eGFR 97.0 ± 2.4 mL/min/1.73 m2) were included. Results US-measured renal length correlated strongly with MRI-measured renal length in no-CKD patients (Spearman’s r = 0.83 and 0.85 for the right and left kidney, respectively; P < 0.005) and CKD patients (r = 0.89 and 0.92 for the right and left kidney, respectively; P < 0.005). There was a significant but weaker correlation between MRI- and US-measured right and left renal volume (r = 0.72, P < 0.005) in no-CKD (r = 0.74 and r = 0.72, respectively; for both: P < 0.005) and CKD patients (r = 0.83 and 0.85, P < 0.005). Weak to moderate correlations were found for parenchyma thickness for the right (CKD group: r = 0.29, no-CKD: r = 0.23; for both: P < 0.05) and left kidney (CKD: r = 0.52, no-CKD group: r = 0.37, P < 0.05). Both intra-observer (Pearson’s correlations of 0.82 for the right and 0.89 for the left kidney) and inter-observer (Lin’s correlation coefficient of 0.90 for the right and 0.82 for the left kidney) reproducibility of US-assessed renal length was high. Conclusions US-based assessment of renal length in CKD patients is comparable to MRI measures. Both intra- and inter-observer reproducibility of US-assessed renal length in CKD patients are high. Measurements of US renal volume and parenchymal thickness should, however, be interpreted with caution.