High uric acid, reduced glomerular filtration rate and non-alcoholic fatty liver in young people with obesity

Abstract Background and Aims Recent evidences showed an association between NAFLD and extrahepatic manifestations such as chronic kidney disease (CKD) although the result is still inconclusive. This study aims to measure the association of microalbuminuria and estimated glomerular filtration rate (eGFR) decline as CKD risks in NAFLD patients. Method Comprehensive searching using predefined queries was done through online databases Pubmed, EMBASE, ScienceDirect, and The Cochrane Library to include all relevant literature until November 2020. We included all cohort studies of NAFLD patients diagnosed by ultrasonography (USG), commutated tomography (CT), or scoring system fatty liver index (FLI) that reports microalbuminuria and eGFR decline below 60 ml/min/1.73m2. Bias risk was assessed by The Newcastle-Ottawa Scale for cohort studies. Analysis of this study was performed to provide pooled hazard ratio (HR) with 95% confidence interval (CI) using random-effect heterogeneity test. Results We included 10 cohort studies met our criteria. Analysis of 6 NAFLD cohort studies diagnosed by USG is significantly associated with eGFR decline (pooled HR = 1.54, 95% CI 1.13 to 2.11, p=0.006, I2=88%), while NAFLD patients diagnosed by FLI also showed significant association with eGFR decline (pooled HR = 1.58, 95% CI 1.52 to 1.64, p<0.0001, I2=0%), thus overall analysis combined with CT diagnostic modalities showed significant association between NAFLD and eGFR decline (pooled HR=1.53 95%CI 1.29-1.80 p<0.00001 I2=82%). Microalbuminuria risk is significantly increased in NAFLD patients (pooled HR = 1.93, 95% CI 1.39 to 2.67, p<0.0001, I2=0%). Surprisingly, NAFLD patients whose increased gamma-glutamyltransferase (GGT) has higher eGFR decline risk (pooled HR = 1.73, 95% CI 1.02 to 2.92, p=0.04, I2=78%). Conclusion Microalbuminuria and eGFR decline are associated as CKD risks in NAFLD patients. However, further studies are still needed to establish the causality.

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P0035URINARY CITRATE AS A MARKER OF RENAL FUNCTION IN PATIENTS WITH AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa142.p0035 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Francisco-Jose Borrego-Utiel ◽

Isidoro Herrera ◽

Enoc Merino Garcia ◽

Clara Moriana Dominguez ◽

Victoria Camacho Reina ◽

...

Keyword(s):

Uric Acid ◽

Glomerular Filtration Rate ◽

Kidney Disease ◽

Glomerular Filtration ◽

Filtration Rate ◽

Autosomal Dominant ◽

Urinary Calcium ◽

Polycystic Kidney ◽

Autosomal Dominant Polycystic Kidney ◽

Urinary Citrate

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.

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