- Email: [email protected]
The Validity of Fractional Excretion of Uric Acid in the Diagnosis of Acute Kidney Injury Due to Decreased Kidney Perfusion
Correspondence
ACKNOWLEDGEMENTS
1.00
1186
© 2009 by the National Kidney Foundation, Inc. doi:10.1053/j.ajkd.2009.09.015
THE VALIDITY OF FRACTIONAL EXCRETION OF URIC ACID IN THE DIAGNOSIS OF ACUTE KIDNEY INJURY DUE TO DECREASED KIDNEY PERFUSION To the Editor: The validity of the fractional excretion of sodium (FENa) for the diagnosis of acute kidney injury (AKI) caused by decreased kidney perfusion is limited in patients receiving diuretics. Fractional excretion of uric acid (FEU〈) may be useful in such cases.1-3 We studied the validity of FEU〈 in 44 patients, 22 (15 men and 7 women; mean age, 57.4 ⫾ 16.2 [SD] years) with AKI caused by decreased kidney perfusion and 22 (14 men and 9 women; mean age, 54.2 ⫾ 14.5 years) with AKI from other causes.
Sensitivity 0.50 0.25
FE Na ROC area: 0.98 FE Uric Acid ROC area: 0.90 Reference Line
0.00
REFERENCES 1. Ashman N. Efficacy of sodium citrate antimicrobial locks for reducing rates of catheter-related bacteremia [letter]. Am J Kidney Dis. 2009;54(6):1185. 2. Power A, Duncan N, Singh SK, et al. Sodium citrate versus heparin catheter locks for cuffed central venous catheters: a single-center randomized controlled trial. Am J Kidney Dis. 2009;53(6):1034-1041. 3. Winnett G, Nolan J, Miller M, Ashman N. Trisodium citrate 46.7% selectively and safely reduces staphylococcal catheter-related bacteraemia. Nephrol Dial Transplant. 2008; 23(11):3592-3598. 4. Rabindranath KS, Bansal T, Adams J, et al. Systematic review of antimicrobials for the prevention of haemodialysis catheter-related bacteraemia. Nephrol Dial Transplant. 2009; doi 10.1093/ndt/gfp327. 5. Bleyer AJ, Mason L, Russell G, et al. A randomised, controlled trial of a new vascular catheter flush solution (minocycline-EDTA) in temporary haemodialysis access. Infect Control Hosp Epidemiol. 2005;26(6):520-524. 6. Zhang P, Zhang A, Qiang H, et al. A randomized controlled study on the prevention of cuff-tunneled catheter related bacteremia with gentamicin-heparin locked solution [abstract]. J Am Soc Nephrol. 2006;17:592A. 7. Zhang P, Yuan J, Tan H, et al. Successful prevention of cuffed hemodialysis catheter-related infection using an antibiotic lock technique by strictly catheter-restricted antibiotic lock solution method. Blood Purif. 2009;27(2): 206-211. 8. Power A, Duncan N, Singh SK, et al. Long-term, high-adequacy haemodialysis can be delivered safely by Tesio-Caths [abstract]. J Am Soc Nephrol. 2008;19:905A.
0.75
Financial Disclosure: None.
0.00
0.25
0.50 1-Specificity
0.75
1.00
Figure 1. Area under the receiver operating characteristic (ROC) curve for fractional excretion of sodium (FENa; upper plot) and uric acid (FEUA; lower plot). P ⫽ 0.09.
We measured sodium (Na), creatinine (Cr), and uric acid (UA) in serum (S) and a spot urine sample (U) and calculated FENa and FEUA using the formulas (NaU · CrS/CrU · NaS) · 100 and (UAU · CrS/CrU · UAS) · 100, respectively. No patient had used diuretics. The diagnosis of AKI from decreased kidney perfusion was based on: (1) clinical manifestations of hypovolemia, oliguria, or significant decrease in urine output; (2) absence of urine findings indicating intrinsic renal injury; and (3) quick restitution of urine output, as well as renal function, after correction of the hemodynamic disturbances. FENa and FEU〈 were significantly lower in the patients with AKI caused by decreased kidney perfusion. For these patients, the limit of detection for FENa was 2.47% (with 91% sensitivity and specificity), and for FEUA, 23.79% (82% sensitivity/specificity). In the comparison of receiver operating characteristic curves, there was a trend (P ⫽ 0.085) toward greater accuracy of FENa than FEUA (Fig 1). In conclusion, calculation of FEUA may be a useful method for the diagnosis of AKI caused by decreased kidney perfusion. George Kosmadakis, MD1 Maria Viskaduraki, PhD2 Spyridon Michail, MD1 1 Laiko Hospital Athens, Greece 2 University of Leicester United Kingdom
ACKNOWLEDGEMENTS The corresponding author, Dr Kosmadakis, may be contacted at [email protected]. Support: None. Financial Disclosure: None.
REFERENCES 1. Steiner RW. Interpreting the fractional excretion of sodium. Am J Med. 1984;77(4):699-702. 2. Quarantino CP, Di Sciascio N, Rucci C, Ciaglia P, Giacomello A. The normal range of serum urate levels and of fractional urate excretion. Adv Exp Med Biol. 1994;370: 91-93.
Correspondence
1187
3. Cappuccio FP, Strazzyllo P, Farinaro E, Trevisan M. Uric acid metabolism and tubular sodium handling. Results from a population-based study. JAMA. 1993;270(3):354359. © 2009 by the National Kidney Foundation, Inc. doi:10.1053/j.ajkd.2009.09.008
HYPERTENSION SECONDARY TO BILATERAL HYDRONEPHROSIS CAUSED BY A LARGE UTERINE MYOMA To the Editor: Individuals with secondary hypertension constitute 5%10% of the hypertensive population, with most cases of secondary hypertension attributable to kidney disease.1 Only rarely has secondary hypertension been linked to hydronephrosis.2-4 We report the case of 26-year-old woman with secondary hypertension due to bilateral hydronephrosis caused by uterine myoma. This patient first noticed an abdominal mass ⬃3 months before presentation. At the initial evaluation, she presented with abdominal distension, nausea, and blood pressure of 220/120 mm Hg. Laboratory results included urea nitrogen level of 12 mg/dL (4.28 mmol/L) and serum creatinine level of 1.21 mg/dL (107 mol/L). Thyroid function test results and 24-hour urine catecholamine levels were within normal limits. Urine dipstick was negative for blood or protein, and sediment was bland. Computed tomography of the abdomen showed a heterogeneous enhancing mass (26 ⫻ 25 ⫻ 30 cm) with bilateral hydronephrosis attributed to compression (Fig 1). Exploratory laparotomy and myomectomy were performed. At 1 and 6 months after laparotomy, blood pressure was normal in the absence of antihypertensive medications, and hydronephrosis was absent on renal ultrasonography. The effects of hydronephrosis on blood pressure in humans are unclear. Possible mechanisms of hypertension secondary to hydronephrosis include increased intrarenal pressure and/or compression of intrarenal veins against the renal capsule. This could result in a decreased glomerular filtration rate with compensatory increased proximal reabsorption of filtered volume and sodium associated with tubuloglomerular feedback and increased plasma rennin activity.4,5 However, further study is needed to elucidate the mechanism relating hypertension to hydronephrosis in this setting. Chih-Cheng Lai, MD Cheng-Kun Chang, MD
Figure 1. Computed tomography of the abdomen shows a heterogeneous enhanced mass with bilateral hydronephrosis caused by mass compression.
Jen-Yu Wang, MD Cardinal Tien Hospital, Fu-Jen Catholic University Hsintien, Taipei Hsien, Taiwan
ACKNOWLEDGEMENTS Support: None. Financial Disclosure: None.
REFERENCES 1. Victor RG, Kaplan NM. Systemic hypertension: mechanisms and diagnosis. In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, PA: Saunders; 2008. 2. Wise HM. Hypertension resulting from hydronephrosis [abstr]. JAMA. 1975;231(5):491-492. 3. Mizuiri S, Amagasaki Y, Hosaka H, et al. Hypertension in unilateral atrophic kidney secondary to ureteropelvic junction obstruction. Nephron. 1992;61(2):217-219. 4. Chakrabartty PK. Hypertension secondary to bilateral hydronephrosis. CMAJ. 1977;116(7):716-718. 5. Carlström M, Wåhlin N, Sällström J, Skøtt O, Brown R, Persson AE. Hydronephrosis causes salt-sensitive hypertension in rats. J Hypertens. 2006;24(7):1437-1443. © 2009 by the National Kidney Foundation, Inc. doi:10.1053/j.ajkd.2009.10.002
ACKNOWLEDGEMENTS
1.00
1186
© 2009 by the National Kidney Foundation, Inc. doi:10.1053/j.ajkd.2009.09.015
THE VALIDITY OF FRACTIONAL EXCRETION OF URIC ACID IN THE DIAGNOSIS OF ACUTE KIDNEY INJURY DUE TO DECREASED KIDNEY PERFUSION To the Editor: The validity of the fractional excretion of sodium (FENa) for the diagnosis of acute kidney injury (AKI) caused by decreased kidney perfusion is limited in patients receiving diuretics. Fractional excretion of uric acid (FEU〈) may be useful in such cases.1-3 We studied the validity of FEU〈 in 44 patients, 22 (15 men and 7 women; mean age, 57.4 ⫾ 16.2 [SD] years) with AKI caused by decreased kidney perfusion and 22 (14 men and 9 women; mean age, 54.2 ⫾ 14.5 years) with AKI from other causes.
Sensitivity 0.50 0.25
FE Na ROC area: 0.98 FE Uric Acid ROC area: 0.90 Reference Line
0.00
REFERENCES 1. Ashman N. Efficacy of sodium citrate antimicrobial locks for reducing rates of catheter-related bacteremia [letter]. Am J Kidney Dis. 2009;54(6):1185. 2. Power A, Duncan N, Singh SK, et al. Sodium citrate versus heparin catheter locks for cuffed central venous catheters: a single-center randomized controlled trial. Am J Kidney Dis. 2009;53(6):1034-1041. 3. Winnett G, Nolan J, Miller M, Ashman N. Trisodium citrate 46.7% selectively and safely reduces staphylococcal catheter-related bacteraemia. Nephrol Dial Transplant. 2008; 23(11):3592-3598. 4. Rabindranath KS, Bansal T, Adams J, et al. Systematic review of antimicrobials for the prevention of haemodialysis catheter-related bacteraemia. Nephrol Dial Transplant. 2009; doi 10.1093/ndt/gfp327. 5. Bleyer AJ, Mason L, Russell G, et al. A randomised, controlled trial of a new vascular catheter flush solution (minocycline-EDTA) in temporary haemodialysis access. Infect Control Hosp Epidemiol. 2005;26(6):520-524. 6. Zhang P, Zhang A, Qiang H, et al. A randomized controlled study on the prevention of cuff-tunneled catheter related bacteremia with gentamicin-heparin locked solution [abstract]. J Am Soc Nephrol. 2006;17:592A. 7. Zhang P, Yuan J, Tan H, et al. Successful prevention of cuffed hemodialysis catheter-related infection using an antibiotic lock technique by strictly catheter-restricted antibiotic lock solution method. Blood Purif. 2009;27(2): 206-211. 8. Power A, Duncan N, Singh SK, et al. Long-term, high-adequacy haemodialysis can be delivered safely by Tesio-Caths [abstract]. J Am Soc Nephrol. 2008;19:905A.
0.75
Financial Disclosure: None.
0.00
0.25
0.50 1-Specificity
0.75
1.00
Figure 1. Area under the receiver operating characteristic (ROC) curve for fractional excretion of sodium (FENa; upper plot) and uric acid (FEUA; lower plot). P ⫽ 0.09.
We measured sodium (Na), creatinine (Cr), and uric acid (UA) in serum (S) and a spot urine sample (U) and calculated FENa and FEUA using the formulas (NaU · CrS/CrU · NaS) · 100 and (UAU · CrS/CrU · UAS) · 100, respectively. No patient had used diuretics. The diagnosis of AKI from decreased kidney perfusion was based on: (1) clinical manifestations of hypovolemia, oliguria, or significant decrease in urine output; (2) absence of urine findings indicating intrinsic renal injury; and (3) quick restitution of urine output, as well as renal function, after correction of the hemodynamic disturbances. FENa and FEU〈 were significantly lower in the patients with AKI caused by decreased kidney perfusion. For these patients, the limit of detection for FENa was 2.47% (with 91% sensitivity and specificity), and for FEUA, 23.79% (82% sensitivity/specificity). In the comparison of receiver operating characteristic curves, there was a trend (P ⫽ 0.085) toward greater accuracy of FENa than FEUA (Fig 1). In conclusion, calculation of FEUA may be a useful method for the diagnosis of AKI caused by decreased kidney perfusion. George Kosmadakis, MD1 Maria Viskaduraki, PhD2 Spyridon Michail, MD1 1 Laiko Hospital Athens, Greece 2 University of Leicester United Kingdom
ACKNOWLEDGEMENTS The corresponding author, Dr Kosmadakis, may be contacted at [email protected]. Support: None. Financial Disclosure: None.
REFERENCES 1. Steiner RW. Interpreting the fractional excretion of sodium. Am J Med. 1984;77(4):699-702. 2. Quarantino CP, Di Sciascio N, Rucci C, Ciaglia P, Giacomello A. The normal range of serum urate levels and of fractional urate excretion. Adv Exp Med Biol. 1994;370: 91-93.
Correspondence
1187
3. Cappuccio FP, Strazzyllo P, Farinaro E, Trevisan M. Uric acid metabolism and tubular sodium handling. Results from a population-based study. JAMA. 1993;270(3):354359. © 2009 by the National Kidney Foundation, Inc. doi:10.1053/j.ajkd.2009.09.008
HYPERTENSION SECONDARY TO BILATERAL HYDRONEPHROSIS CAUSED BY A LARGE UTERINE MYOMA To the Editor: Individuals with secondary hypertension constitute 5%10% of the hypertensive population, with most cases of secondary hypertension attributable to kidney disease.1 Only rarely has secondary hypertension been linked to hydronephrosis.2-4 We report the case of 26-year-old woman with secondary hypertension due to bilateral hydronephrosis caused by uterine myoma. This patient first noticed an abdominal mass ⬃3 months before presentation. At the initial evaluation, she presented with abdominal distension, nausea, and blood pressure of 220/120 mm Hg. Laboratory results included urea nitrogen level of 12 mg/dL (4.28 mmol/L) and serum creatinine level of 1.21 mg/dL (107 mol/L). Thyroid function test results and 24-hour urine catecholamine levels were within normal limits. Urine dipstick was negative for blood or protein, and sediment was bland. Computed tomography of the abdomen showed a heterogeneous enhancing mass (26 ⫻ 25 ⫻ 30 cm) with bilateral hydronephrosis attributed to compression (Fig 1). Exploratory laparotomy and myomectomy were performed. At 1 and 6 months after laparotomy, blood pressure was normal in the absence of antihypertensive medications, and hydronephrosis was absent on renal ultrasonography. The effects of hydronephrosis on blood pressure in humans are unclear. Possible mechanisms of hypertension secondary to hydronephrosis include increased intrarenal pressure and/or compression of intrarenal veins against the renal capsule. This could result in a decreased glomerular filtration rate with compensatory increased proximal reabsorption of filtered volume and sodium associated with tubuloglomerular feedback and increased plasma rennin activity.4,5 However, further study is needed to elucidate the mechanism relating hypertension to hydronephrosis in this setting. Chih-Cheng Lai, MD Cheng-Kun Chang, MD
Figure 1. Computed tomography of the abdomen shows a heterogeneous enhanced mass with bilateral hydronephrosis caused by mass compression.
Jen-Yu Wang, MD Cardinal Tien Hospital, Fu-Jen Catholic University Hsintien, Taipei Hsien, Taiwan
ACKNOWLEDGEMENTS Support: None. Financial Disclosure: None.
REFERENCES 1. Victor RG, Kaplan NM. Systemic hypertension: mechanisms and diagnosis. In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, PA: Saunders; 2008. 2. Wise HM. Hypertension resulting from hydronephrosis [abstr]. JAMA. 1975;231(5):491-492. 3. Mizuiri S, Amagasaki Y, Hosaka H, et al. Hypertension in unilateral atrophic kidney secondary to ureteropelvic junction obstruction. Nephron. 1992;61(2):217-219. 4. Chakrabartty PK. Hypertension secondary to bilateral hydronephrosis. CMAJ. 1977;116(7):716-718. 5. Carlström M, Wåhlin N, Sällström J, Skøtt O, Brown R, Persson AE. Hydronephrosis causes salt-sensitive hypertension in rats. J Hypertens. 2006;24(7):1437-1443. © 2009 by the National Kidney Foundation, Inc. doi:10.1053/j.ajkd.2009.10.002