Idiopathic erythrocytosis in a patient on chronic hemodialysis

A 78-year-old man on hemodialysis presented to our hospital with erythrocytosis. He had started hemodialysis 4 years previously, with a hemoglobin level of 9.8 g/dL, and was administered erythropoiesis stimulating agents and ferrous sulfate. Two years previously, his hemoglobin level increased to 14.5 g/dL and the treatment for anemia was discontinued. He continued hemodialysis thrice weekly; however, the hemoglobin level had increased to 17.0 g/dL at the time of presenting to our hospital. His serum erythropoietin level was 31.4 mIU/mL (range, 3.7-31.5 mIU/mL), carboxyhemoglobin level was 0.6% (range, 0-1.5%), and oxygen saturation in ambient air was 95.4%. The JAK2 V617F mutation was not observed and other bone marrow abnormalities were not identified. The patient was diagnosed with bladder cancer and a transurethral resection was performed. Eight months after the treatment of bladder cancer, his hemoglobin level was 15.1 g/dL, and he was diagnosed with idiopathic erythrocytosis.

Two Cases of Fabry Disease in Women with Proteinuria Diagnosed by Molecular Analysis of the alpha-Galactosidase A Gene and Kidney Biopsy / 대한내과학회지

Fabry disease is an X-linked lysosomal storage disorder caused by alpha-galactosidase A deficiency, which results in the intracellular accumulation of globotriaosylceramide and leads to severe painful neuropathy with progressive renal, cardiovascular, and cerebrovascular dysfunction and early death. We report 52- and 55-year-old women with proteinuria and hematuria that were proven to be due to Fabry disease. A gene analysis using PCR direct sequencing confirmed a missense mutation of the GLA (alpha-galactosidase A) gene. Electron microscopy of a kidney biopsy showed lamella inclusion bodies, which are typical findings of Fabry disease. The patients were treated with enzyme replacement therapy as outpatients. They had a reduction in proteinuria and normal renal function.

Changes in serum magnesium concentration after use of a proton pump inhibitor in patients undergoing percutaneous coronary intervention

BACKGROUND: Although cross-sectional studies have suggested a relationship between proton pump inhibitor (PPI) use and hypomagnesemia, no large-scale cohort study has been conducted to date. Here, we examined the changes in serum magnesium levels in response to PPI use. We hypothesized that PPI use might change the serum magnesium concentration. METHODS: Of the 2,892 patients hospitalized for percutaneous coronary intervention between January 2007 and May 2012, 1,076 patients with normal baseline (1.6-2.5 mg/dL) and follow-up serum magnesium concentrations were enrolled. These patients were divided into two groups: the PPI group and the control group. RESULTS: The mean follow-up period was 9.51+/-2.94 months. The incidence of hypomagnesemia ( or =12 months, n = 71) and short-term PPI groups (duration of use <12 months, n = 763), and the control group (n = 242; P = 0.620). The effect of PPI use on change in serum magnesium concentration was affected by the use of multiple diuretics (-0.01+/-0.25 mg/dL; P = 0.025), although a single diuretic use with PPI did not alter the change in magnesium level (0.12+/-0.27 mg/dL). CONCLUSION: Changes in magnesium levels might be subtle after PPI use in patients with normal baseline magnesium values.

Urokinase, urokinase receptor, and plasminogen activator inhibitor-1 expression on podocytes in immunoglobulin A glomerulonephritis

BACKGROUND/AIMS: The purpose of this study was to investigate the expression of urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), and plasminogen activator inhibitor (PAI)-1 on podocytes in immunoglobulin A (IgA) glomerulonephritis (GN). METHODS: Renal biopsy specimens from 52 IgA GN patients were deparaffinized and subjected to immunohistochemical staining for uPA, PAI-1, and uPAR. The biopsies were classified into three groups according to the expression of uPA and uPAR on podocytes: uPA, uPAR, and a negative group. The prevalences of the variables of the Oxford classification for IgA GN were compared among the groups. RESULTS: On podocytes, uPA was positive in 11 cases and uPAR was positive in 38 cases; by contrast, PAI-1 was negative in all cases. Expression of both uPA and uPAR on podocytes was less frequently accompanied by tubulointerstitial fibrosis. CONCLUSIONS: Our results suggest a possible protective effect of podocyte uPA/uPAR expression against interstitial fibrosis.

A case of scrub typhus requiring maintenance hemodialysis

Renal failure caused by scrub typhus is known to be reversible. In most cases, renal function is almost fully restored after appropriate antibiotic treatment. A 71-year-old man was diagnosed with scrub typhus complicated by renal failure. A renal biopsy revealed histopathologic findings consistent with acute tubulointerstitial nephritis. Renal function did not improve 18 months after discharge and the patient required continuous hemodialysis. Although severe renal failure requiring dialysis is a rare complication of scrub typhus, we describe a case of scrub typhus requiring maintenance hemodialysis. To the best of our knowledge, this is the first such report.

Incidence, Etiology, and Outcomes of Rhabdomyolysis in a Single Tertiary Referral Center

We have encountered numerous cases of rhabdomyolysis associated with acute pesticide intoxication; however, the cause, incidence, and treatment outcomes of rhabdomyolysis have not been studied. The current study involved 2,125 patients hospitalized with acute chemical poisoning. Based on clinical and laboratory parameters and treatment outcomes, we found that overall incidence of rhabdomyolysis in our hospital was 0.06% (93 of 143,830 patients admitted), but the incidence associated with acute pesticide intoxication was 1.8% (33 of 1,793 cases). The incidence of rhabdomyolysis after pesticide intoxication was significantly higher in men than in women (P = 0.010). The amount of pesticide ingested was significantly higher in rhabdomyolysis patients than that in those who did not develop rhabdomyolysis (mean +/- SD, 114.1 +/- 79.5 mL vs 74.1 +/- 94.2 mL, P = 0.010). Our results show that pesticide intoxication is a frequent cause of rhabdomyolysis and is more common among men than women. The volume of pesticide ingested, and not the degree of human toxicity, is the main factor influencing the incidence of rhabdomyolysis.

Hyperuricemia as a marker for progression of immunoglobulin A nephropathy

BACKGROUND: The variable clinical and histopathological manifestations of immunoglobulin A nephropathy (IgAN) make it difficult to predict disease progression. A recent study showed that hyperuricemia, a condition common in hypertension and vascular disease, may contribute to renal dysfunction and histological changes including renal arteriosclerosis, tubular atrophy, and interstitial fibrosis. Herein, we investigated the clinical significance of uric acid level at the time of biopsy, as a marker of IgAN progression. METHODS: We included 193 patients with biopsy-proven IgAN. Renal disease progression was defined as serum creatinine elevation above 1.2mg/dL or over 20% elevation from baseline. Hyperuricemia was defined as a serum uric acid level > or =7.3mg/dL in men and > or =5.3mg/dL in women, which were 1 standard deviation above the mean value in the normal subjects. RESULTS: The hyperuricemia group (n=50) had higher blood pressure, body mass index, and serum creatinine, and a greater amount of proteinuria and a lower glomerular filtration rate than the nonhyperuricemia group (n=143). Hyperuricemia increased the risk of IgAN progression (odds ratio, 4.53; 95% confidence interval, 1.31-15.66). The disease progression group (n=26) had a greater frequency of hyperuricemia, hypertension, and nephrotic range proteinuria than the nonprogression group (n=119). The renal survival analysis showed that the hyperuricemia group had a higher rate of IgAN disease progression. CONCLUSION: Hyperuricemia at the time of diagnosis is an important marker for IgAN progression.

Erratum: A Case of Green Urine after Ingestion of Herbicides

In this article, Table 1's data was given incorrectly. Metodopramide should be corrected as Metoclopramide.

Acute Oral Poisoning Due to Chloracetanilide Herbicides

Chloracetanilide herbicides (alachlor, butachlor, metachlor) are used widely. Although there are much data about chronic low dose exposure to chloracetanilide in humans and animals, there are few data about acute chloracetanilide poisoning in humans. This study investigated the clinical feature of patients following acute oral exposure to chloracetanilide. We retrospectively reviewed the data on the patients who were admitted to two university hospitals from January 2006 to December 2010. Thirty-five patients were enrolled. Among them, 28, 5, and 2 cases of acute alachlor, metachlor, butachlor poisoning were included. The mean age was 49.8 +/- 15.4 yr. The poison severity score (PSS) was 17 (48.6%), 10 (28.6%), 5 (14.3%), 2 (5.7%), and 1 (2.9%) patients with a PSS of 0, 1, 2, 3, and 4, respectively. The age was higher for the symptomatic patients (1-4 PSS) than that for the asymptomatic patients (0 PSS) (43.6 +/- 15.2 vs 55.7 +/- 13.5). The arterial blood HCO3 was lower in the symptomatic patients (1-4 PSS) than that in the asymptomatic patients (0 PSS). Three patients were a comatous. One patient died 24 hr after the exposure. In conclusion, although chloracetanilide poisoning is usually of low toxicity, elder patients with central nervous system symptoms should be closely monitored and cared after oral exposure.

Cellular Toxicity of Surfactants Used as Herbicide Additives

The cellular toxicities of surfactants, a solvent, and an antifreeze that are included in herbicide formulations were assessed by measuring their effects on membrane integrity, metabolic activity, mitochondrial activity, and total protein synthesis rate in a cell culture. Polyethylene glycol, propylene glycol, and monoethylene glycol exhibited no cellular toxicity even at a high concentration of 100 mM. Sodium lauryl ether sulfate and polyoxyethylene lauryl ether significantly damaged the membrane, disturbed cellular metabolic activity, and decreased mitochondrial activity and the protein synthesis rate; however, their toxicity was far below those of the severely toxic chemicals at comparable concentrations. The severely toxic category included polyoxypropylene glycol block copolymer, polyoxyethylene tallow amine, and polyoxyethylene lauryl amine ether. These surfactants were cytotoxic between 3.125 microM and 100 microM in a dose-dependent manner. However, the toxicity graph of concentration vs toxicity had a point of inflection at 25 microM. The slope of the toxicity graph was gentle when the concentration was below 25 microM and steep when the concentration was greater than 25 microM. In conclusion, our results suggest that the toxicity of surfactants be taken care of pertinent treatment of acute herbicide intoxication.

A Case of Acute Respiratory Failure After Trichloroethylene Inhalation

Trichloroethylene (TCE, C2HCl3), which was introduced as a gas for general anesthesia and analgesia in early 1900's has been widely used in industry as an organic solvent. Occupational exposure to TCE is an important medical problem. Manifestations of acute exposure to TCE include mucocutaneous irritation, hepatotoxicity, cognitive impairment, sleep, headache, respiratory insufficiency and death. We report a 38-year-old man who was admitted to a department of emergency medicine after occupational inhalation exposure to TCE. He rapidly developed semicoma and respiratory depression. After mechanical ventilation, hypercapnea and hypoxemia disappeared and his mental state again became alert. Careful evaluation and proper respiratory support are important for respiratory failure after occupational TCE inhalation.

Association of Blood and Bone Lead with a Decrease in Renal Function Indices in Patients with Chronic Kidney Disease / 대한신장학회지

PURPOSE: This study assessed the environmental lead exposure in patients with chronic kidney disease (CKD) and the relationship between lead exposure and renal function indices. METHODS: Seventy-one patients with CKD and 40 control subjects without known renal disease were included. Blood lead was measured by atomic absorption spectrophotometry and tibial lead was measured via 109Cd-based K-shell X-ray fluorescence. Blood urea nitrogen (BUN), serum creatinine, urine creatinine and urine N-acetyl-beta glucosaminidase (NAG) were also measured. Blood lead was corrected with hematocrit (female: 35%, male: 42%) to adjust for differences in anemic status of patients compared with control subjects. RESULTS: The mean level of hematocrit-adjusted blood lead was significantly higher in patients with CKD (4.18+/-1.74 microg/dL) compared with that in control subjects (3.00+/-0.92 microg/dL); the mean tibial lead level tended to be higher in patients with CKD (3.38+/-9.93 microg/g) than that in control subjects (1.28+/-7.92 microg/g), but no statistical significance was observed. In a multivariate regression analysis after adjusting for gender, age, and drinking and smoking status, adjusted blood lead was a significant predictor of increases in BUN and serum creatinine, but not of the level of urine NAG or creatinine. In contrast, no significant association between tibial lead and renal indices was observed in the multivariate regression analysis. CONCLUSION: These results suggest that environmental lead exposure may compromise renal function.

Tissue Plasminogen Activator and Plasminogen Activator Inhibitor-1 Levels in Patients with Acute Paraquat Intoxication

To investigate the effects of reactive oxygen species (ROS) on tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) plasma levels, and their possible implications on clinical outcome, we measured tPA and PAI-1 levels in 101 patients with acute paraquat (PQ) intoxication. The control group consisted of patients who ingested non-PQ pesticides during the same period. tPA and PAI-1 levels were higher in the PQ group than in the controls. PQ levels were significantly correlated with ingested amount, timelag to hospital, tPA level, and hospitalization duration. tPA levels were correlated with PAI-1, fibrin degradation product (FDP), and D-dimer. D-dimer levels were lower in the PQ group than in the controls. Univariate analysis indicated the following significant determinants of death: age, ingested amount, PQ level, timelag to hospital, serum creatinine, lipase, pH, pCO2, HCO3-, WBC, FDP, PAI-1, and tPA. However, multivariate analysis indicated that only PQ level was significant independent factor predicting death. In conclusion, tPA and PAI-1 levels were higher, while D-dimer levels were lower in the PQ group than in the controls, implying that ROS stimulate tPA and PAI-1, but PAI-1 activity overrides tPA activity in this setting. Decreased fibrinolytic activity appears to be one of the clinical characteristics of acute PQ intoxication.

A Case of Licorice-Induced Hypokalemic Rhabdomyolysis in a Patient Using a Diuretic Drug / 대한내과학회지

Glycyrrhizic acid is a component of licorice. It can cause hypokalemia through the inhibition of 11beta-hydroxysteroid dehydrogenase. The severity of symptoms depends on the dose and duration of licorice intake, as well as the individual susceptibility. The safe dose of licorice is 10 mg per day. Even a small amount of licorice can cause side effects, including hypokalemia in patients taking diuretics, with diarrhea, or congestive heart failure. We experienced a 59-year-old male with muscle weakness. He had ingested losartan and indapamide due to hypertension. At presentation, he had ingested 8 mg of licorice daily for the previous 17 days. The patient presented with severe hypokalemia (1.8 mEq/L) and rhabdomyolysis. His renin activity was 0.44 ng/mL/h, and his aldosterone level was 6.0 pg/mL. After cessation of licorice and indapamide, his potassium level recovered. In conclusion, even a small amount of licorice can induce hypokalemia in patients who are taking diuretics.

Two Cases of Metformin-Induced Lactic Acidosis Successfully Treated by Hemodialysis / 대한내과학회지

Metformin-induced lactic acidosis is a rare life-threatening complication associated with metformin treatment and has a high mortality rate. Here, two cases of metformin-induced lactic acidosis are reported. A 22-year-old woman was admitted to our hospital with a metformin overdose (25 g) and lactic acidosis. Hemodialysis was initiated to correct the acidemia, and the patient showed full recovery. Her serum creatinine level returned to normal. A 50-year-old man presented with a 5-day history of muscle weakness. His medical history included diabetes mellitus for 6 years treated with metformin at 3,000 mg/day and hypertension. An arterial blood sample showed metabolic acidosis, with a venous lactate level of 31.1 mg/dL. The patient recovered fully after treatment with bicarbonate dialysis. These cases illustrate that the presence of clinical conditions such as renal failure increase the risk of metformin-induced lactic acidosis. Prompt recognition of lactic acidosis and early treatment with bicarbonate dialysis can result in a successful clinical outcome.

Clinical Course in Patients with an Intentional Amlodipine Overdose / 대한내과학회지

BACKGROUND/AIMS: Calcium channel blockers (CCBs) are anti-hypertensive medications that are used worldwide. CCB overdose has increased in proportion to the use of these drugs. Although amlodipine is the most widely used CCB, many physicians are not familiar with amlodipine overdose. We report the clinical outcome in patients with an intentional amlodipine overdose. METHODS: We retrospectively reviewed the medical records of the patients who visited Soonchunhyang University Cheonan Hospital with an amlodipine overdose from January 2002 through December 2010. We recorded the initial vital signs, blood chemistry, electrocardiography, and estimated amount of amlodipine ingested. RESULTS: Nine patients were enrolled, of whom two patients died. Both patients who died had ingested more than 200 mg/m2 of amlodipine, while all of the patients who ingested less than 200 mg/m2 of amlodipine survived. Three patients had blood sugar levels exceeding 200 mg/dL and two of these died despite high-dose insulin therapy in combination with glucose infusion (hyperinsulinemia/euglycemia therapy). Although three patients also took a glimepiride overdose, none had hypoglycemia. The amount of amlodipine ingested relative to the body surfaced area (BSA) was 197.1 +/- 92.3 mg/m2 in patients with an abnormal ECG and 58.5 +/- 27.1 mg/m2 in patients with a normal ECG. CONCLUSIONS: Amlodipine overdose can induce hyperglycemia, resulting in lethal cardiogenic shock owing to the decreased calcium influx, inappropriate energy production, and weakened inotropic effect. Therefore, amlodipine-induced hyperglycemia indicates a poor prognosis.

A Case of Acute Renal Failure Induced by Acetaminophen Intoxication / 대한내과학회지

Acetaminophen is a widely used analgesic and antipyretic. Acetaminophen-induced kidney injury is poorly described. Hepatorenal syndrome, prerenal failure, and direct toxicity of acetaminophen metabolites could be involved in the development of acute renal failure with acetaminophen intoxication. We treated a 58-year-old female who was found stuporous and brought to the emergency room by ambulance. She had ingested acetaminophen 4~5 g per day for a chronic headache for over 10 years. At presentation, she had ingested about 8 g of acetaminophen. She presented in non-oliguric acute renal failure with hepatic injury. Hemoperfusion, hemodialysis, and N-acetylcysteine infusion were applied. The creatinine peaked on the sixth day. Subsequently, her renal function recovered. After 34 days, she was discharged in relatively good condition. In conclusion, supportive care and proper extracorporeal therapy can improve the survival in acute renal failure after acetaminophen intoxication.

Association of the Superoxide Dismutase (V16A) and Catalase (C262T) Genetic Polymorphisms with the Clinical Outcome of Patients with Acute Paraquat Intoxication

BACKGROUND/AIMS: Many patients with acute paraquat (PQ) intoxication die even at low PQ concentrations, whereas others with similar concentrations recover. Therefore, it is possible that individual differences in antioxidant capacity are responsible for the variable clinical outcome in patients with acute PQ intoxication. METHODS: We investigated whether there was a relationship between the genetic polymorphisms of SOD (V16A), catalase (C262T), and GPX1 (C593T) in 62 patients with acute PQ intoxication and the clinical outcomes of these patients. RESULTS: The frequency of the Mn-SOD V/V, V/A, and A/A genotypes were 56.3, 43.5, and 0% in survivors and 86.9, 13.1, and 0% in non-survivors (p > 0.05). The GPX1 C/C, C/T, and T/T genotypes were present in 100, 0, and 0% of all subjects. The catalase C/C, C/T, and T/T genotypes were present in 100, 0, and 0% of survivors, and in 82.6, 17.4, and 0% of non-survivors. Neither erythrocyte SOD activity nor catalase activity were significantly different between survivors and non-survivors. CONCLUSIONS: No association was found between clinical outcome of acute PQ intoxication and the genetic polymorphism of GPX1 (C593T) or the genetic polymorphisms or enzyme activity of superoxide dismutase (V16A) or catalase (C262T).

A Case of Acute Kidney injury After Seawater Immersion / 대한신장학회지

Acute renal failure (ARF) secondary to immersion and near-drowning has rarely been described and it is poorly understood. ARF associated with immersion and near-drowning might be involved with systemic tissue hypoxia, hypovolemia and hypothermia. Some reports have shown that rhabdomyolysis could be involved. We report here on a 52 year old seaman who developed ARF after cold sea-water immersion. He had been swimming for one hour in cold sea-water because his ship became stuck on a rock. After 2 days, his serum creatinine level was increased to 7.8 mg/dL, and pulmonary edema was developed. The serum myoglobin level was 495.1 ng/mL. He was diagnosed as oliguric ARF and treated with hemodialysis. Thereafter, renal function was gradually recovered. We presumed that hypothermia-induced vasoconstriction, hypovolemia and rhabdomyolysis were involved in ARF in the patient. It should be considered that cold sea-water immersion for a long time could evoke ARF in healthy men.

Effect of Glutathione Administration on Serum Levels of Reactive Oxygen Metabolites in Patients with Paraquat Intoxication: A Pilot Study

BACKGROUND/AIMS: Based on preliminary in vitro data from a previous study, we proposed that 50 mg/kg glutathione (GSH) would be adequate for suppressing reactive oxygen species in patients with acute paraquat (PQ) intoxication. METHODS: Serum levels of reactive oxygen metabolites (ROM) were measured before and after the administration of 50 mg/kg GSH to each of five patients with acute PQ intoxication. RESULTS: In one patient, extremely high pretreatment ROM levels began to decrease prior to GSH administration. However, in the remaining four cases, ROM levels did not change significantly prior to GSH administration. ROM levels decreased significantly after GSH administration in all cases. In two cases, ROM levels decreased below that observed in the general population; one of these patients died after a cardiac arrest at 3 hours after PQ ingestion, while the other represented the sole survivor of PQ intoxication observed in this study. In the survivor, ROM levels decreased during the first 8 hours of GSH treatment, and finally dropped below the mean ROM level observed in the general population. CONCLUSIONS: Treatment with 50 mg/kg GSH significantly suppressed serum ROM levels in PQ-intoxicated patients. However, this dose was not sufficient to suppress ROM levels when the PQ concentration was extremely high.