Search

Background: In autosomal dominant polycystic kidney disease (ADPKD) it is frequently found a reduction in urinary citrate of unknown origin. It has been suggested that it could be a marker of acid retention in chronic kidney disease. Our aim was to compare urinary citrate in ADPKD with other nephropathies and to show its relation with serum bicarbonate. Methods: We determined urinary citrate in patients with several nephropathies and varied renal function. We included 291 patients, 119 with glomerular diseases, 116 with ADPKD, 21 with other nephropathies, and 35 patients with normal renal function. Results: Urinary citrate was higher in women and in patients with normal renal function. ADPKD patients showed similar values of urinary citrate to patients with glomerular diseases and with other nephropathies. We observed a progressive reduction in urinary citrate with renal impairment, in a comparable way among patients with ADPKD and glomerular diseases. We did not observe a relationship with serum bicarbonate. Serum uric acid levels were significantly higher in patients with glomerular diseases than in ADPKD patients, even after correction with the degree of renal function. Conclusions: Hypocitraturia is not specific of ADPKD but it is also present in all tested nephropathies and is related with renal impairment and not with serum bicarbonate. It could be interesting to study urinary citrate as a marker of renal function and as a prognostic factor. [ABSTRACT FROM AUTHOR]

Introduction: 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 in chronic kidney disease. Objective: Our aim was to analyze relationship between urinary citrate levels, renal function, and serum bicarbonate in ADPKD patients. Methods: We determined citrate in 24-h collected urine from ADPKD patients and correlated with glomerular filtration rate (CKD-EPI equation) and serum bicarbonate concentration. Results: We included 120 patients, 60% men, eGFR was 71 ± 32 mL/min/1.73 m2. Urinary citrate/creatinine ratio was 195 ± 152 mg/gCr (range 1.2–689) with levels significantly higher in females. Urinary citrate lower than 300 mg/gCr was present in 75% of patients and when considering chronic kidney stages (CKD), we observed reduced levels in 48.8% in CKD1 stage, in 79.4% in CKD2 stage, in 96.2% in CKD3 stage, and in 94.7% of patients in CKD4 stage. Urinary citrate was correlated with serum creatinine (r = − 0.61, p < 0.001) and eGFR (r = 0.55, p < 0.001) in both gender. We did not find any correlation with serum bicarbonate. Using a general linear modeling analysis, we found as predictors of urinary citrate/creatinine ratio to glomerular filtration rate, gender, and age. Lower levels of urinary citrate were accompanied by a decline in urinary osmolality and in renal excretion of calcium and uric acid. In a subgroup of patients, we measured total kidney volume and we found an inverse correlation with urinary citrate levels that disappeared when it was corrected with glomerular filtration rate. Conclusions: Urinary citrate is very frequently reduced in ADPKD patients being present from very early CKD stages. Their levels in urine are inversely correlated with glomerular filtration rate and it is not related with serum bicarbonate concentration. We think that it would be interesting to study urinary citrate as a marker of chronic kidney disease in ADPKD patients. [ABSTRACT FROM AUTHOR]

Introduction: Mayo clinic classification (MCC) has been proposed in patients with autosomal dominant polycystic kidney disease (ADPKD) to identify who may experience a rapid decline of renal function. Our aim was to validate this predictive model in a population from southern Spain. Methods: ADPKD patients with measurements of height-adjusted total kidney volume (HtTKV) and baseline estimated glomerular filtration rate (eGFR) >30 mL/min/1.73 m2 were selected. Last eGFR was estimated with Mayo Clinic (MC) equation and bias and accuracy were studied. We also analyzed predictive capacity of MCC classes using survival analysis and Cox regression models. Results: We included 134 patients with a mean follow-up of 82 months. While baseline eGFR was not different between classes, last eGFR decreased significantly with them. eGFR variation rate was different according to the MCC class with a more rapid decline in 1C, 1D, and 1E classes. Final eGFR predicted was not significantly different from the real one, with an absolute bias of 0.6 ± 17.0 mL/min/1.73 m2. P10 accuracy was low ranging from 37.5 to 59.5% in classes 1C, 1D, and 1E. Using MC equation, the rate of eGFR decline was underestimated in 1C, 1D, and 1E classes. Cox regression analysis showed that MCC class is a predictor of renal survival after adjusting with baseline eGFR, age, sex, and HtTKV, with 1D and 1E classes having the worst prognosis. Conclusion: MCC classification is able to identify patients who will undergo a more rapid decline of renal function in a Spanish population. Prediction of future eGFR with MC equation is acceptable as a group, although it shows a loss of accuracy considering individual values. The rate of eGFR decline calculated using MC equation can underestimate the real rate presented by patients of 1C, 1D, and 1E classes. [ABSTRACT FROM AUTHOR]