scholarly journals Glomerular filtration rate is the main predictor of urine volume in autosomal dominant polycystic kidney disease patients treated with tolvaptan when daily osmolar excretion is expressed as urinary osmolality/creatinine ratio

2020 ◽  
Author(s):  
Francisco José Borrego Utiel ◽  
Enoc Merino García
2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Francisco-Jose Borrego-Utiel ◽  
Isidoro Herrera ◽  
Enoc Merino Garcia ◽  
Clara Moriana Dominguez ◽  
Victoria Camacho Reina ◽  
...  

Abstract Background and Aims In autosomal dominant polycystic kidney disease (ADPKD) is frequent to find low urinary citrate levels. Recently it has been suggested that urinary citrate could be a marker of covert metabolic acidosis. Our aim was to analyze relationship between urinary citrate levels and renal functionality in ADPKD patients. Method We determined citrate, calcium and uric acid in 24-hour collected urine from 91 ADPKD patients Results Urinary citrate/creatinine ratio was 214±158 (range 5.3-678) mg/g Cr with levels significantly higher in females. When considering chronic kidney disease (CKD) stages we observed a progressive decrease in urinary osmolality and in urinary citrate, calcium and uric acid elimination. Low levels of citrate (<300 mg/g Cr) were present in 40% in CKD-1 stage, in 69.7% in CKD-2 stage, 92% in CKD-3 stage and 100% in CKD-4 + 5 stages. Urinary citrate was correlated with serum creatinine (r= -0.66, p<0.001) and eGFR (r= 0.56, p<0.001). Urinary citrate significantly correlated with urinary calcium but correlation with urinary uric acid was weaker. We did not find any correlation with serum bicarbonate. Using multiple lineal regression analysis we found as predictors of urinary citrate to glomerular filtration rate, female gender and urinary calcium levels. In a subgroup of patients we measured total kidney volume and we found an inverse correlation with urinary citrate levels that dissappeared when it was corrected with glomerular filtration rate. We did not also find a relationship between urinary elimination of calcium or uric acid and TKV after adjusting with eGFR. Conclusion Urinary citrate is very frequently reduced in ADPKD patients being present from very early CKD stages. Their levels are inversely correlated with glomerular filtration rate and directly with urinary calcium excretion. We did not found a relathionship with serum bicarbonate. We think that it would be interesting to study urinary citrate in other nephropathies and verify if it could be a marker of covert metabolic acidosis.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Francisco-Jose Borrego-Utiel ◽  
Enoc Merino Garcia ◽  
Maria Luisa Garnica Alvarez ◽  
Clara Moriana Dominguez

Abstract Background and Aims Tolvaptan was approved to treat autosomal dominant polycystic kidney disease (ADPKD) to slow the rate of kidney growth and renal function decline. Tolvaptan blocks the V2 vasopressin receptor in renal collecting ducts and distal nephron causing intense polyuria. Few authors have analyzed what factors influence the volume of diuresis in patients taking tolvaptan. Method We have analyzed the influence of solute excretion and glomerular filtration rate, besides age and gender as predictors of urine output, using multivariable analysis. In concret, we have searched the importance of osmolar excretion as predictor of volume of diuresis. Results We studied 24 h-urine samples from 18 ADPKD patients on treatment with tolvaptan, who had received the three doses: 45/15, 60/30 and 90/30 mg. Each patient was represented once per dose, for a total of 54 urine samples (Table 1). Tolvaptan increased urine volume, which was roughly doubled, and roughly halved urine solute concentrations expressed by volume and calculated osmolality. By contrast, solute concentrations expressed as ratios with creatinine remained constant as did osmolality corrected with urinary creatinine, indicating that there was no change in solute excretion after tolvaptan. Urine volume was correlated with serum creatinine (Rho= -0.36, p= 0.008), urinary creatinine (Rho = -0.29, p = 0.034) and GFR-MDRD4 (Rho = 0.44, p= 0.001). Urine volume was correlated with calculated daily osmolar excretion in Osm/day (Rho = 0.76, p <0.001). Urine volume was not correlated with calculated urinary osmolality in mOsm/Kg (Rho= -0.04, p= 0.77) or as urinary osmolality/creatinine ratio (Rho= 0.23, p= 0.1). Correlation of urine volume with osmolar excretion was lost when urine volume was removed from the predictor variable. Urine volume was additionally not correlated with urinary urea o sodium concentrations nor their solute/creatinine ratios, and although it was correlated with urinary potassium concentration (Rho = -0.33, p=0.014), it was not correlated with potassium/creatinine ratio. We also performed a linear regression analysis searching predictors of urine volume. Only GFR and the osmolality/creatinine ratio were significant predictors of urine volume (urine volume= 55.35 x GFR + 4.74 x Osmolality/Cr; r2= 0.41, p<0.001) but individual solute assessments or tolvaptan dose did not predict urine volume. Conclusions Therefore, urine volume after initiating tolvaptan in patients with ADPKD is influenced mainly by the degree of renal function. There might also be a contribution of urinary solute load but it can not be studied using total solute excretion due to collinearity. We propose that the urinary solute/creatinine ratio and osmolality/creatinine ratio should be used to search for predictors of urine output in patients on tolvaptan.


Nutrients ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 1051
Author(s):  
Carly Mannix ◽  
Anna Rangan ◽  
Annette Wong ◽  
Jennifer Zhang ◽  
Margaret Allman-Farinelli ◽  
...  

Maintaining hydration sufficient to reduce levels of arginine vasopressin has been hypothesised to slow kidney cyst growth in autosomal dominant polycystic kidney disease (ADPKD). The semi-quantitative beverage frequency questionnaire (BFQ) was designed to measure usual fluid intake over the past month. The aim of this study was to assess the validity and reliability of the BFQ compared with the 24-h urine biomarkers. Participants with ADPKD (18–67 years; estimated glomerular filtration rate (eGFR) ≥ 30 mL/min1.73 m2) completed the BFQ. Serum creatinine, eGFR, 24-h urine volume, and osmolality were measured. Pearson correlation coefficients, paired t test, and Bland–Altman plots were used to evaluate agreement between the methods. A subset repeated the BFQ to assess reliability. A total of 121 participants (54% male, 43 ± 11 years; mean ± SD) completed the BFQ and at least one 24-h urine collection. The correlation between the BFQ and the 24-h urine volume was moderate (r = 0.580) and weaker with the 24-h urine osmolality (r = −0.276). The Bland–Altman plots revealed good agreement between the BFQ and the 24-h urine volume with no obvious bias; however, the limits of agreement were wide (−1517–1943 mL). The BFQ1 and BFQ2 were strongly correlated (r = 0.799, p < 0.001) and were not significantly different (p = 0.598). The BFQ is a valid and reliable tool to assess the usual fluid intake of the ADPKD population.


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