WCIM 2014 SEOUL KOREA 167
Poster Session
The Korean Journal of Internal Medicine Vol. 29, No. 5 (Suppl. 1)
PS 0468 Nephrology
Is it Possible to Estimate the Correct Amount of Sodi- um Intake Using Spot Urine Sample?
Sung-Joon SHIN1, Moo-Yong RHEE2
Nephrology, Dongguk University Ilsan Hospital, Korea1, Cardiovascular Center, Dongguk University Ilsan Hospital, Korea2
Background: Because measurement of sodium intake by 24-hour urine collection is labor intensive, a more convenient method of sodium intake assessment has been required. The present study evaluated the reliability of equations using spot urine (SU) samples in the estimation of 24-hour urine sodium excretion (24HUNa), which were developed by us and other investigators.
Methods: Participants were recruited by list-assisted random-digit dialing (LARDD) in four cities. Equations estimating 24HUNa from SU samples were derived from morning fi rst SU of 101 participants (52.4±11.1 years). Equations developed by us and other investigators were validated with SU samples from a separate group of participants (n=224, 51.0±10.9 years). The equation was based upon the following hypothesis.
(1) 24HUCr ˜ predicted 24-hour urine creatinine excretion (PrUCr) (2) 24-HUNa/24HUCr 8 SU sodium (SUNa)/SU creatinine (SUCr) (3) 24-HUNa 8 SUNa/SUCr × PrUCr
Results: We developed the linear, quadratic, and cubic equations from morning fi rst SU samples because morning fi rst SU sodium/creatinine ratio had the highest corre- lation coeffi cient for 24HUNa/creatinine ratio (r=0.728, p<0.001). In the validation group, the estimated 24HUNa by Kawasaki’s, Tanaka’s, linear, quadratic, and cubic equation showed signifi cant correlations with measured 24HUNa values. The estimat- ed 24HUNa by the linear, quadratic, and cubic equations developed from our study were not signifi cantly different from measured 24HUNa, while estimated 24HUNa by Kawasaki and Tanaka equations were signifi cantly different from measured 24HUNa values. The limits of agreement between measured and estimated 24HUNa obtained by 5 equations were more than 100 mmol/24-hour in the Bland-Altman analysis. All equations showed tendency of under- or over-estimation of 24HUNa, depending on the level of measured 24HUNa.
Conclusions: The result of this present study suggests that estimation of 24HUNa from single SU could not be used for the estimation of 24HUNa.
PS 0469 Nephrology
Ability of Nafamostat Mesilate to Prolong Filter Pa- tency during Continuous Renal Replacement Therapy in Patients with a High Risk of Bleeding: A Randomized Controlled Study
Yong Kyu LEE1, Hae Won LEE2, Kyu Hun CHOI2, Beom Seok KIM2
National Health Insurance Corp. Ilsan Hospital, Korea1, Severance Hospital, Yonsei University College of Medicine, Korea2
Background: Continuous renal replacement therapy (CRRT) is considered as an ef- fective modality for renal replacement therapy in hemodynamically unstable patients within intensive care units (ICUs). However, role of heparin anticoagulation, which is used to maintain circuit patency, is equivocal due to the risk of bleeding and morbidity.
Among the various alternative anticoagulants, nafamostat mesilate is as an effective anticoagulant for patients prone to bleeding. Hence, we conducted a prospective, randomized controlled study investigating the effect of nafamostat mesilate on CRRT fi lter life span and the adverse events in the patients prone to bleeding.
Methods: Seventy three Patients were randomized into either the futhan or no-an- ticoagulation group. The thirty six subjects in futhan group received nafamostat mesilate, while the thirty seven subjects in no-anticoagulation group received no anti- coagulation medication. Baseline characteristics and appropriate laboratory tests were taken from each group.
Results: Seventy three Patients were randomized into either the futhan or no-antico- agulation group. The thirty six subjects in futhan group received nafamostat mesilate, while the thirty seven subjects in no-anticoagulation group received no anticoagula- tion medication. Baseline characteristics and appropriate laboratory tests were taken from each group.
Conclusions: nafamostat mesilate may be used as an effective and safe anticoagula- tion treatment, without increasing major bleeding complications, in patients prone to bleeding.
PS 0470 Nephrology
Acute Toluene Intoxication: Prospective Observational Study
RENE RODRIGUEZ-GUTIERREZ1, ROBERTO MONREAL-ROBLES1, CARLOS R.
CAMARA-LEMARROY1, JOSE G GONZALEZ-GONZALEZ1
Endocrinology Division and Internal Medicine Department, University Hospital, Mexico1
Background: Toluene is one of the most widely abused inhaled drugs and dangerous metabolic abnormalities are associated to its acute intoxication. It has been previously reported that rhabdomyolysis and acute hepatorenal injury could be hallmarks of the disease, and could constitute risk factors for poor outcomes. The objective was to describe the clinical presentation, to characterize the renal and liver abnormalities, the management and prognosis associated to acute toluene intoxication.
Methods: We prospectively assessed 20 patients that were admitted to a single center’s emergency department from 2007-2014 with clinical and metabolic altera- tions due to acute toluene intoxication.
Results: Patients were severely acidotic on admission (mean pH: 7.14 ± 0.09) with a mean anion gap of 16 ± 6.9 mmol/L and mean potassium level of 2.19 mmol/L ± 1.32. The main clinical presentation consisted of weakness associated to severe hy- pokalemia and acidosis. Renal glomerular injury (proteinuria) was ubiquitous. Serum creatine-phosphokinase levels were elevated in 16 cases, with a mean elevation of 6 times the upper normal limit (1,544 ± 1,864 U/L). Liver function tests were normal, except for ALP, which was elevated in 15 patients. Gamma-glutamyl transpeptidase was elevated in all patients, with a mean of 103.9 ± 66.9. Rhabdomyolysis occurred in 80% of patients, probably due to hypokalemia and hypophosphatemia. There were three deaths, all associated with altered mental status, severe acidosis, hypokalemia and acute oliguric renal failure. The causes of death were cardiac rhythm abnormalities.
Conclusions: The hallmarks of acute toluene intoxication are hypokalemic paralysis and metabolic acidosis. Liver injury and rhabdomyolysis are common. Altered mental state on admission, renal failure, severe acidemia and female gender could be associ- ated with a poor outcome, and patients with these characteristics should be treated in an intensive care unit.
PS 0471 Nephrology
A Case of Interstitial Nephritis Caused by Psychogenic Anorexia
Hwa Rim KANG1, Jee Hyun KIM1, Jin Yong PARK1, Soon Kil KWON1, Hye-Young KIM1, Sun Moon KIM1, Ho-Chang LEE2
Internal Medicine, Chungbuk National University Hospital, Korea1, Pathology, Chungbuk National Univer- sity Hospital, Korea2
Introduction: Anorexia nervosa can affect almost every organ system, resulting severe medical complications such as energy metabolism abnormality, fl uid and electrolyte imbalances, hypotension, amenorrhea, and sometimes can make acute kidney injury.
However, repeated vomiting induced interstitial nephritis is rarely reported, pathophys- iology is unknown either. We report an tubulo-interstitial nephritis developed in young male with psychogenic eating disorder and hypokalemia.
Case: A 26-year-old male was admitted because of known hypokalemia. He had nausea, vomiting, and diffuse muscle weakness for 3 years. His appetite was normal, but he frequently vomited especially after large meal. He had diagnosed hypokalemia and been treated with potassium supplement in the outside hospital. There was no remarkable past medical history including diuretics. Serum electrolytes were sodium 137 mEq/L, potassium 2.2 mEq/L, chloride 63 mEq/L, total CO2 61 mEq/L. Calcium/
phosphorus were 9.3/4.6 mg/dL, blood urea nitrogen/creatinine were 10/1.52 mg/dL, serum magnesium was 2.0 mg/dL. Arterial blood gas analysis showed pH 7.532, PCO2 35.5 mmHg, PaO2 128 mmHg, and HCO3 was 29.7 mEq/L. Urine Na/K/Cl/Cr were 96/81.5/12/111.12 mEq/L and mg/dL. Allele test for Gitelman syndrome was negative.
Renal biopsy revealed acute tubular necrosis and tubulo-interstitial nephritis. There were nonspecifi c calcifi cation in the renal tubules below the epithelial cells. Several glomeruli showed ischemic damage without other defi nite abnormality. The patient showed improvement of vomiting after treatment with mirtazapine. Serum potassium was increased up to 3.5-4.4 mmol/L.
Conclusion: Psychogenic vomiting and hypokalemia can be a risk for acute kidney injury. We report a pathology of repeated vomiting induced acute kidney injury. We suggest that the mechanism of renal damage is caused by tubular necrosis and inter- stitial infl ammation.
