Min Jee Kim

Relation Between Transient or Persistent Acute Kidney Injury and Long-Term Mortality in Patients With Myocardial Infarction

Limited information is available regarding the impact of acute kidney injury (AKI) during hospitalization on clinical outcomes after myocardial infarction (MI), and the effect of transient kidney injury (KI) on long-term mortality has not been validated. We retrospectively analyzed 2,289 patients diagnosed with MI. AKI patients were classified into a transient KI group and a persistent KI group based on serum creatinine levels at discharge. The end point of the study was 3-year mortality after MI. We included 2,110 patients of whom 237 patients (11%) developed AKI during hospitalization. Of these 237 patients, 154 (65%) had transient KI, and 83 (35%) had persistent KI. Multivariate analysis showed that age, left ventricular ejection fraction, estimated glomerular filtration rate on admission, and Killip class were significantly associated with developing AKI during hospitalization. The adjusted hazard ratios for 3-year mortality were 1.71 (95% confidence interval: 1.08-2.70) for AKI patients with transient KI and 2.21 (95% confidence interval: 1.34-3.64) for AKI patients with persistent KI, compared with no AKI. In conclusion, AKI was associated with an increased risk of death for patients who experienced MIs and survived during hospitalization. Although renal function had completely recovered in many AKI patients at discharge, these transient KI patients are also at a great risk of death after MI.

Impact of Acute Kidney Injury on Clinical Outcomes after ST Elevation Acute Myocardial Infarction.

Purpose This study aimed to compare the incidence and clinical significance of transient versus persistent acute kidney injury (AKI) on acute ST elevation myocardial infarction (STEMI). Materials and Methods The study was a retrospective cohort of 855 patients with STEMI. AKI was defined as an increase of ≥0.3 mg/dL in creatinine level at any point during hospital stay. The study population was classified into 5 groups: 1) patients without AKI; 2) patients with mild AKI that was resolved by discharge (creatinine change less than 0.5mg/dL compared with admission creatinine during hospital stay, transient mild AKI); 3) patients with mild AKI that did not resolve by discharge (persistent mild AKI); 4) patients with moderate/severe AKI that was resolved by discharge (creatinine change more than 0.5 mg/dL compared with admission creatinine, transient moderate/severe AKI); 5) patients with moderate/severe AKI that did not resolve by discharge (persistent moderate/severe AKI). We investigated 1-year all-cause mortality after hospital discharge for the primary outcome of the study. The relation between AKI and 1-year mortality after STEMI was analyzed. Results AKI occurred in 74 (8.7%) patients during hospital stay. Adjusted hazard ratio for mortality was 3.139 (95% CI 0.764 to 12.897, p=0.113) in patients with transient, mild AKI, and 8.885 (95% CI 2.710 to 29.128, p<0.001) in patients with transient, moderate/severe AKI compared to patients without AKI. Persistent moderate/severe AKI was also independent predictor of 1 year mortality (hazard ratio, 5.885; 95% CI 1.079 to 32.101, p=0.041). Conclusion Transient and persistent moderate/severe AKI during acute myocardial infarction is strongly related to 1-year all cause mortality after STEMI.

Prevalence and associations for abnormal bleeding times in patients with renal insufficiency.

Platelet dysfunction and associated hemorrhagic complications are often encountered in patients with chronic kidney disease. This study aimed to evaluate the prevalence and associations for abnormal bleeding time (BT) in patients with renal dysfunction. Hemoglobin, hematocrit, platelet, blood urea nitrogen, creatinine, and parathyroid hormone levels were determined in 1716 patients (55.18 ± 17.19 years, men 50.8%). For these patients, BTs were estimated using a platelet function analyzer-100. Glomerular filtration rates (GFRs) were estimated using the Chronic Kidney Disease Epidemiology Collaboration equation. The study population was divided into six groups according to the estimated GFR (eGRF): group I, eGFR ≥ 90 ml/min/1.73 m2; group II, 60 ≤ eGFR < 90 ml/min/1.73 m2; group III, 30 ≤ eGFR < 60 ml/min/1.73 m2; group IV, 15 ≤ eGFR < 30 ml/min/1.73 m2; group V, eGFR < 15 ml/min/1.73 m2; and group VI, undergoing regular hemodialysis. Renal insufficiency was defined as eGFR < 60 ml/min/1.73 m2. To further investigate the role of inflammatory cytokines, nitric oxide (NO) and tumor necrosis factor alpha (TNF-α) were measured in a 327-patient subset of the total patient population (52.82 ± 18.3 years, men 60.9%). Abnormal BT occurred in 11.8% of group I, 15.3% of group II, 29.1% of group III, 37.5% of group IV, 35.0% of group V, and 32.1% of group VI. By Pearson correlation coefficient, eGFR (r = −0.089), hemoglobin (r = −0.127), platelet (r = −0.054) were correlated with BT. Multivariate analysis revealed that age [odds ratio (OR), 1.013; 95% CI, 1.004–1.022], renal insufficiency (eGFR < 60 ml/min/1.73 m2; OR, 2.271; 95% CI, 1.672–3.083), anemia (hemoglobin < 120 g/l; OR, 1.486; 95% CI, 1.089–2.027), and thrombocytopenia (platelet < 150 × 109/l; OR, 1.445; 95% CI, 1.089–1.918) were independently associated with prolonged BT. Plasma levels of NO and TNF-α were increased in patients with renal insufficiency (eGFR < 60 ml/min/1.73 m2). Plasma levels of NO in renal insufficiency group were higher in prolonged BT than those in normal BT. A significant positive correlation was noted between BTs and NO levels (r = 0.152, p = 0.009) but not with TNF-α levels. The prevalence of abnormal BTs was higher as eGFR declined. Old age, renal insufficiency, anemia, and thrombocytopenia were independent associations for abnormal BT.

Association of Age and CKD with Prognosis of Myocardial Infarction

BACKGROUND AND OBJECTIVES CKD is a well known poor prognostic factor in myocardial infarction (MI). This study evaluated the prognostic significance of CKD, particularly in association with increasing age, in MI patients. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS This study was based on a retrospective cohort, the Korean Acute Myocardial Infarction Registry. Patients with a discharge diagnosis of MI were analyzed to investigate the association of CKD with mortality risk according to age. A total of 11,268 patients (mean age 63.0±12.6 years) were included and followed for 1 year. RESULTS In the full cohort, 26% of patients had CKD (n=2929). The prevalence of CKD was higher with advancing age. Eight hundred sixty-one patients (7.6%) died and the interaction for 1-year mortality between age strata and estimated GFR (eGFR) strata was significant (P<0.001). Within each age category, the absolute 1-year mortality was higher in patients with a low eGFR. However, the adjusted relative mortality risk for a low eGFR was lower with increasing age (adjusted hazard ratio [95% confidence interval] for 1-year mortality at eGFR <30 ml/min per 1.73 m(2): 4.84 [1.93-12.15], 4.53 [2.42-8.47], 3.51 [2.42-5.09], and 3.30 [2.41-4.52] for patients aged <55, 55-64, 65-74, and ≥75 years compared with those with eGFR ≥60 ml/min per 1.73 m(2), respectively). CONCLUSIONS For all age categories, the overall mortality was significantly higher as eGFR declined. The association of a lower eGFR with mortality was weaker with increasing age, indicating that the prognostic significance of CKD in MI patients is age dependent.

Concomitant impact of high-sensitivity C-reactive protein and renal dysfunction in patients with acute myocardial infarction.

Purpose The present study aimed to investigate the impact of high-sensitivity C-reactive protein (hs-CRP) and renal dysfunction on clinical outcomes in acute myocardial infarction (AMI) patients. Materials and Methods The study involved a retrospective cohort of 8332 patients admitted with AMI. The participants were divided into 4 groups according to the levels of estimated glomerular filtration rate (eGFR) and hs-CRP: group I, no renal dysfunction (eGFR ≥60 mL·min-1·1.73 m-2) with low hs-CRP (≤2.0 mg/dL); group II, no renal dysfunction with high hs-CRP; group III, renal dysfunction with low hs-CRP; and group IV, renal dysfunction with high hs-CRP. We compared major adverse cardiac events (MACE) over a 1-year follow-up period. Results The 4 groups demonstrated a graded association with increased MACE rates (group I, 8.8%; group II, 13.8%; group III, 18.6%; group IV, 30.1%; p<0.001). In a Cox proportional hazards model, mortality at 12 months increased in groups II, III, and IV compared with group I [hazard ratio (HR) 2.038, 95% confidence interval (CI) 1.450-2.863, p<0.001; HR 3.003, 95% CI 2.269-3.974, p<0.001; HR 5.087, 95% CI 3.755-6.891, p<0.001]. Conclusion High hs-CRP, especially in association with renal dysfunction, is related to the occurrence of composite MACE, and indicates poor prognosis in AMI patients.

Hypercalcemia in a patient with polycythemia vera.

A 59-year-old female with diabetes mellitus presented with hypercalcemia and polycythemia. Her serum calcium and intact parathyroid hormone (iPTH) levels were increased, and Tc-99m sesta-MIBI scanning showed hot uptake in the lower portion of the left thyroid lobe. After parathyroidectomy, her calcium, iPTH, and polycythemia were normalized. In conclusion, the differential diagnosis of polycythemia and hypercalcemia should also include the possibility of a parathyroid tumor in addition to other neoplasms.

Proteinuria as a Risk Factor for Mortality in Patients with Colorectal Cancer

Purpose We investigated the effects of proteinuria and renal insufficiency on all-cause mortality in patients with colorectal cancer, with special emphasis on cancer staging and cancer-related deaths. Materials and Methods We retrospectively studied a cohort of patients with colorectal cancer. In protocol 1, patients were classified into four groups based on the operability of cancer and proteinuria: group 1, early-stage cancer patients (colorectal cancer stage ≤3) without proteinuria; group 2, early-stage cancer patients with proteinuria; group 3, advanced-stage cancer patients without proteinuria (colorectal cancer stage=4); and group 4, advanced-stage cancer patients with proteinuria. In protocol 2, patients were classified into four similar groups based on cancer staging and renal insufficiency (eGFR <60 mL/min/1.73 m2). Between January 1, 1998 and December 31, 2009, 3379 patients were enrolled in this cohort and followed until May 1, 2012 or until death. Results The number of patients with proteinuria was 495 (14.6%). The prevalence of proteinuria was higher in advanced-stage cancer (n=151, 22.3%) than in early-stage cancer patients (n=344, 12.7%). After adjusting for age, gender and other clinical variables, the proteinuric, early-stage cancer group was shown to be associated with an adjusted hazard ratio of 1.67 and a 95% confidence interval of 1.38-2.01, compared with non-proteinuric early-stage cancer patients. However, renal insufficiency was not associated with colorectal cancer mortality. Conclusion Proteinuria is an important risk factor for cancer mortality, especially in relatively early colorectal cancer.

Acute kidney injury associated with nafronyl oxalate overdose

A 19-year-old woman presented to the emergency department with lower abdominal pain and oliguria. Laboratory studies were notable for a creatinine level of 5.4 mg/dL, a blood urea nitrogen level of 30.2 mg/dL, a HCO3 level of 18.8 mM (22–29 mM), a phosphorus level of 3.1 mg/dL (normal 2.5–8.5 mg/dL) and a calcium level of 8.4 mg/dL (normal 8.4–10.2 mg/dL). Her leukocyte count was normal without eosinophilia. Urine dipstick showed traces of protein and urine pH was 5.0 at admission. Immunologic tests were unremarkable and viral serologies were negative. Microscopic urine examination displayed 30–49 red cells/ high-power field and 4 white cells with 3 % of eosinophils. Kidney ultrasound showed both enlarged kidney and the presence of increased cortical echogenecity. In her medication history, she had received oral nafronyl oxalate (Nafril capsule , Hanall Biopharma, Seoul, Korea) 7000 mg because of toothache and otalgia over the past 2 days. Hydration was undertaken, but her creatinine level increased during the first 3 days of admission. We performed a renal biopsy to make a definite diagnosis. Glomeruli displayed no abnormalities. Acute interstitial inflammation with mononuclear cells and large refractile acellular deposits in the tubular lumens were seen (Fig. 1a). Polarizing light revealed large intratubular birefringent crystals (Fig. 1b). Immunofluoresence studies were negative. Infrared analysis of the biopsy confirmed the presence of whewellite, a rare form of crystallization of monohydrated calcium oxalate. Urine output increased throughout the hospital stay (\500 mL/day on day 1, 3300 mL on day 11). Serum creatinine peaked at 7.7 mg/ dL and decreased subsequently to 1.1 mg/dL over the following week. The 24-h urine oxalate excretion averaged 95.9 mg during the recovery phase. The patient’s renal function gradually improved and complete recovery was obtained after 1 month. With regard to the pathogenesis of acute kidney injury we assume that the high oxalate load (7000 mg nafronyl oxalate over 2 days) was responsible. According to clinical observations by Moesch et al. [1], intravenously administered naftidrofuryl oxalate may induce intratubular crystallization of calcium oxalate followed by interstitial nephritis and diffuse interstitial sclerosis. In our patient, the observation of calcium oxalate deposits within the tubules by renal biopsy strongly suggests that nafronyl oxalate toxicity was related to an acute oxalate overload with an attendant hyperoxaluria and intrarenal obstruction. Nafronyl oxalate is an oxalate salt containing 19 mg of oxalate by 100 mg of Nafril capsule . As oxalate is excreted solely through the kidneys by glomerular filtration and tubular excretion [2], a massive oxaluria is to be expected. Nafronyl oxalate, a vasodilator agent with antiaggregant properties, has been used for many years to treat peripheral and cerebrovascular diseases. Dosing regimens recommended by the manufacturer range from 200–400 mg of nafronyl oxalate, once or twice a day, infused over a period of 3 h for 7–10 days [3]. Nafronyl oxalate overload is an example of the nephrotoxicity of oxalate. M. J. Kim S. W. Kim (&) Department of Internal Medicine, Chonnam National University Medical School, 42 Jebongro, Gwangju 501-757, Korea e-mail: skimw@chonnam.ac.kr

Perirenal Fluid Collection after Kidney Transplantation

A 30-year-old male presented with pitting edema. He had received a kidney transplantation 3 months previously. His serum creatinine level was increased, and a renal ultrasound showed hypoechoic fluid collection in the perirenal space and pelvic cavity. We conducted sono-guided percutaneous drainage of the fluid collected in the pelvic cavity. The chemistry of the peritoneal fluid was more equivalent to serum chemistry values than to urinary values. Simple aspiration and treatment with antibiotics were performed. We have presented a case of lymphocele after kidney transplantation. This case suggests that physicians should remember how to differentiate the pelvic cavity fluid collection in patients who have received a kidney transplant.

Serratia marcescens Peritonitis in a Diabetic Patient Receiving Continuous Ambulatory Peritoneal Dialysis

We report a case of Serratia marcescens peritonitis in a 45-year-old man with insulin-dependent diabetes mellitus undergoing continuous ambulatory peritoneal dialysis (CAPD). The patient presented with abdominal pain and cloudy dialysate. Empiric antibiotic therapy was initiated intraperitoneally with cefazolin and ceftazidime for 5 days. Cultures of the dialysate revealed S. marcescens, and the treatment was subsequently changed to gentamicin and ceftazidime. Oral ciprofloxacin was also added. The patients abdominal pain and the dialysate white blood cell (WBC) count, however, did not improve. The indwelling CAPD catheter was therefore removed. This is an unusual case report in the Korean literature of S. marcescens peritonitis in a patient receiving CAPD.