Clinical Features and Effects on Prognosis of ARF that Occurred after Liver Transplantation / 대한신장학회잡지

BACKGROUND: One of the major complications of liver transplantation is acute renal failure(ARF). The outcome in patients who develop postoperative renal failure has been dismal. But there are few reports on ARF after liver transplantation in Korea. The aim of this study was to determine the incidence, clinical characteristics, and prognosis of ARF in patients undergoing liver transplantation. METHODS: The records of 35 adult patients who received liver transplantation at the Seoul National University Hospital between october 1992 and June 2001 were reviewed retrospectively. RESULTS: 22 patients were male and 13 were female, with an age range of 15 years to 65 years(median, 49 years). The 35 recipients included 18 with liver cirrhosis, 10 with liver cirrhosis and hepatoma, 3 with hepatoma, 3 with fulminant hepatitis, and 1 with biliary atresia. Death occurred in 10 patients (29%) overall. ARF was developed in 25 cases(71%), and 8 cases(32%) expired. Among the 9 patients with peak serum creatinine level > or = 2.0 mg/dL, 7 patients expired. 2 patients required hemodialysis following liver transplantation and all of them expired. ARF was developed within 1day(0-39 days). Of 25 ARF cases, 21 cases of hypotension, 6 acute rejection, 10 spontaneous bacterial peritonitis(SBP), and 8 massive packed RBC transfusion were associated. Renal function at latest follow-up was improved in patients who were suffered with ARF. CONCLUSION: ARF is a frequent complication of liver transplantation, and the strategy of management and prevention of ARF needs to be developed.

The Effect of Uteroglobin Exon 1, 5' Untranslated Region Polymorphism on the Progression of IgA Nephropathy / 대한신장학회잡지

Uteroglobin(UG) is an anti-inflammatory/immunomodulatory protein secreted by the epithelial cells of vertebrates. Targeted disruption of UG rendered mouse glomerulonephritis resembling IgA nephropathy(IgAN). Sequence analysis on exon 1 of UG showed several putative binding sites for transcription factors, and genetic polymorphisms in this site might influence the expression level of UG as a competitive protein. We speculated that the single nucleotide polymorphism at the 38th nucleotide from the transcription initiation site of UG exon 1 would impact the progression of IgAN. PCR-RFLP was instituted to determine the genetic polymorphism in 60 patients with IgAN. Other measures like SSCP and direct sequencing were also adopted for the verification of polymorphic sites. Seventeen patients with IgAN(28%) were homozygous for adenine at position 38(38AA), 26 patients(43%) were heterozygous(38AG), and 17 patients(28%) were homozygous for the polymorphism(38GG), which was similar to the pattern obtained from the 60 normal controls. The amount of daily proteinuria, presence of hypertension, the level of IgA, and the amount of IgA-fibronectin(FN) complexes was similar between the genotypes. Serum IgA-FN level did not influence the progression of disease. However, 8 out of 17 patients (47%) with the AA genotype had progressive disease(PD), 10 of 26 patients(38%) with the AG genotype had PD, and only 1 of 17 patients(6%) with GG homozygocity had PD after 94+/-30.1 months of follow-up(mean+/-S.D.). The odds ratio for the progression of renal disease in patients with the AA genotype was 14.93(p=0.0355) and in patients with AG genotype was 12.94(p=0.0496) compared with patients have the GG genotype. Moreover, serum creatinine at the time of kidney biopsy was higher in patients with AA and AG genotypes than in patients with the GG genotype(1.5+/-0.69 : 1.3+/-0.53 : 1.0+/-0.31mg/dL; AA : AG : GG; p=0.0137 AA vs. GG; p=0.0269 AG vs. GG). Our results suggest that polymorphism at the 5' UTR region of UG exon 1 is an important marker for the progression of IgAN.

Increases of cAMP Production and Urinary cAMP Excretion by Oxytocin in the Inner Medullary Collecting Duct(IMCD) / 대한신장학회잡지

Oxytocin, like vasopressin, has been known to act in the IMCD by the activation of adenylyl cyclase through V2 receptor, but the exact mechanism of its action remains to be elucidated. To prove whether oxytocin is involved in the activation of adenylyl cyclase in the renal collecting duct, we measured the cAMP production and urinary cAMP excretion rate. After single IMCD segments of Sprague-Dawley rats were microdissected and treated with different con- centrations of vasopressin(10pM, 10nM) and oxytocin (10pM, 10nM), cAMP production was measured. Urinary cAMP excretion rate was measured after dehydration and intraperitoneal injection of vasopressin and oxytocin. The results are as follows. 1) cAMP production in single IMCD was significantly increased in vasopressin group(10pM: 48,9+/-4.7(mean+/-SE), 10nM:94.6+/-5.3fmol/mm) and oxy-tocin group(10pM: 11.3+/-2.9, 10nM: 65.7+/-6.1fmol/mm) compared with that in the control(3.2+/-0.2fmol/ mm). 2) Urine volume was significantly decreased in dehydration group(40+/-7Ml/hour) and vasopressin group(420+/-120Ml/hour), but urine volume of oxytocin group(1,480+/-230Ml/hour) was not different from that of control(1,550+/-120Ml/hour). Urine osmolality was significantly increased in all experimental groups(control: 737.0+/-132.6, dehydration group : 2,463.9+/- 412.5, vasopressin group : 1,702+/-412.5, oxytocin group 1,293.4+/-117.9mOsm/kg). Urinary cAMP excretion rate was significantly increased in dehydration group(4,149.5+/-1,072.3pmol/hour) and oxytocin group(4,843.3+/-2,341.8pmol/hour), but not in vasopressin group(1,358.1+/-690.2pmol/hour), compared with that in control(49+/-10.7pmoVhour). These results suggest that oxytacin has anti-diuretic effect by the activation of adenylyl cyclase through V2 receptor.

Effect of Mineralocorticoid on Serum Potassium Regulation and Urine Ammonium Excretion in Chronic Renal Patients / 대한신장학회잡지

Mineralocorticoids influences on acid-base homeostasis by the regulation of urine acidification. But its mechanism of acion is not well known in human. This study compared the acid-base status and the indices of urine acidification before and after mineralocorticoid administration in human, and analyzed the effect of mineralocorticoids on human acid-base homeostasis. We administered 9a-fludrocortisone in 6 chronic renal failure patients and 6 normal controls 0.5mg daily for 7 days. The results were as following: 1) After administration of 9a-fludrocortisone in patients group, serum aldosterone level changed from 120.2+/-71.0pg/mL to 44.8+/-32.2pg/mL(mean+/-SD, p< 0.05). Serum HCO- level was not changed. Urine ammonium excretion was incresed from 24.6+/-12.3 mmol/day to 43.7+/-19.0 (p<0.05), but there were no change in urine pH and urine anion gap, Serum potassium level decreased from 5.5+/-0.7mBq/L to 4.1+/-0.5mEq/L (p<0.05), and TTKG increased from 3.9 to 8.9(p<0.05). 2) After administration of 9a-fludrocortisone in control group, serum aldosterone level changed from 99.7+/-44.5pg/mL to 25.1+/-3 mL(p<0.05). Serum HCO- level was not changed. Urine ammonium excretion was incresed from 44.3+/-21.6mmoVday to 76.3+/-19.6(p<0.05), but there were no change in urine pH and urine anion gap. Serum potassium level decreased from 4.8+/-0.5mEq/L to 3.9+/-0.2mHq/L(p< 0.05), but there was no change in TTKG. 3) No patient or control showed any discomfort after 9-fludrocortisone administration, and there was no elevation in diastolic blood pressure, increase in body weight, electrolyte abnormality. In summary, after 9alpha-fludrocortisane administration, urinary ammonium excretion increased in both patients and control group, and this phenomenon occured with correction of hyperkalemia without urine pH change. This result implies urinary ammonium excretion increase by mineralocorticoid. In human increase in renal distal acidification by mineralocorticoid is due to increase in renal ammoniagenesis rather than stimulation on proton excretion.