P0234LOW URINARY CITRATE LEVELS ARE NOT SPECIFIC OF AUTOSOMAL POLYCYSTIC KIDNEY DISEASE (ADPKD) AND ARE PRESENT WHEN RENAL FUNCTION IS IMPAIRED IN ALL NEPHROPATIES

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Francisco-Jose Borrego-Utiel ◽  
Enoc Merino Garcia ◽  
Isidoro Herrera ◽  
Clara Moriana Dominguez ◽  
Victoria Camacho Reina ◽  
...  
Keyword(s):  
Renal Function ◽  
Uric Acid ◽  
Kidney Disease ◽  
Renal Impairment ◽  
Polycystic Kidney Disease ◽  
Normal Renal Function ◽  
Serum Bicarbonate ◽  
Polycystic Kidney ◽  
Glomerular Diseases ◽  
Urinary Citrate

Abstract Background and Aims In polycystic kidney disease (PKD) it is frequently found a reduction in urinary citrate that is related with degree of renal impairment but it is unknown if this alteration is specific or if it is also present in other nephropathies. Recently it has been suggested that urinary citrate could be a marker of covert metabolic acidosis and reflects acid retention in chronic kidney disease (CKD). Our aim was to compare urinary citrate in PKD with other renal diseases and to show its relation with serum bicarbonate and excretion of uric acid and calcium. Method We determined citrate, calcium and uric acid in 24-hour urine in patients with PKD and with other nephropathies with varied degree of renal impairment followed in a outpatient clinic of nephrology. Results We included 291 patients, 119 with glomerular diseases, 116 with PKD, 21 with other nephropathies, and 35 patients with normal renal function. Urinary citrate was higher in women (Females 309±251 mg/gCr vs. males 181±145 mg/gCr, p<0.001) and in patients with normal renal function (normal 380±210 mg/gCr; PKD 203±166 mg/gCr; glomerular 279±282 mg/gCr; p<0,001). PKD patients showed similar values of urinary citrate to patients with glomerular diseases and with other nephropathies. We observed a progressive reduction in urinary citrate parallel to degree of renal impairment, in a comparable way among patients with PKD and glomerular diseases. We did not observe a relationship between urinary citrate and serum bicarbonate levels. Calcium and uric acid elimination in ADPKD patients was similar to other nephropathies and lower to patients with normal renal function. However, serum uric acid was significantly higher in glomerular patients than other nephropathies after adjust with glomerular filtration rate and sex. Conclusion Hypocitraturia is not specific of PKD but it is also present in all nephropathies. Urinary citrate are related to degree of renal impairment and it is not related with serum bicarbonate. We think that it could be interesting to study urinary citrate as a marker of renal function and its role as prognostic factor of renal deterioration.

Urinary citrate as a marker of renal function in patients with autosomal dominant polycystic kidney disease

2021 ◽  
Author(s):  
Francisco José Borrego Utiel ◽  
Isidoro Herrera Contreras ◽  
Enoc Merino García ◽  
Maria Victoria Camacho Reina ◽  
Clara Moriana Domínguez ◽  
...  
Keyword(s):  
Renal Function ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney ◽  
Urinary Citrate

Individual Renal Function in Polycystic Kidney Disease

2001 ◽  
Vol 26 (6) ◽  
pp. 518-524 ◽  
Author(s):  
ANDREAS D. FOTOPOULOS ◽  
KOSTAS KATOPODIS ◽  
OLGA BALAFA ◽  
AFRODITI KATSARAKI ◽  
RIGAS KALAITZIDIS ◽  
...  
Keyword(s):  
Renal Function ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Polycystic Kidney

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

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.

Genotype-Clinical Correlations in Polycystic Kidney Disease with No Apparent Family History

2019 ◽  
Vol 49 (3) ◽  
pp. 233-240
Author(s):  
Akinari Sekine ◽  
Takuya Fujimaru ◽  
Junichi Hoshino ◽  
Tatsuya Suwabe ◽  
Masahiko Oguro ◽  
...  
Keyword(s):  
Renal Function ◽  
Family History ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Clinical Course ◽  
The Other ◽  
Renal Outcome ◽  
Polycystic Kidney ◽  
Annual Decline ◽  
Pkd2 Mutation

Background: Genetic characteristics of polycystic kidney disease (PKD) patients without apparent family history were reported to be different from those with a positive family history. However, the clinical course of PKD patients with no apparent family history is not well documented in the literature. Methods: We evaluated the relationship between genotype and the clinical course of 62 PKD patients with no apparent family history. Results: The annual decline of renal function was faster in the patients with PKD1/PKD2 mutation (PKD1 truncating [–3.08; 95% CI –5.30 to –0.87, p = 0.007], PKD1 nontruncating [–2.10; –3.82 to –0.38, p = 0.02], and PKD2 [–2.31; –4.40 to –0.23, p = 0.03]) than in the other patients without PKD1/PKD2 mutation. Similar results were obtained after adjustment for gender, age, estimated glomerular filtration rate (eGFR), height-adjusted total kidney volume (TKV), and mean arterial pressure (MAP). There was no significant difference in the annual decline of renal function among the different PKD1/PKD2 groups, but Kaplan-Meier analysis showed that progression to eGFR < 15 mL/min/1.73 m2 was significantly faster in PKD1 truncating group (p = 0.05). The annual rate of TKV increase was larger in the patients with PKD1/PKD2 mutation (PKD1 truncating [4.63; 95% CI 0.62–8.64, p = 0.03], PKD1 nontruncating [3.79; 0.55–7.03, p = 0.02], and PKD2 [2.11; –1.90 to 6.12, p = 0.29]) than in the other patients without PKD1/PKD2 mutation. Similar results were obtained after adjustment for gender, age, eGFR, and MAP. Conclusion: Detection of PKD1/PKD2 mutation, especially PKD1 truncating, is useful for predicting the renal outcome and rate of TKV increase in PKD patients with no apparent family history.

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