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.

Effects of neutral pH and low-glucose degradation product-containing peritoneal dialysis fluid on systemic markers of inflammation and endothelial dysfunction: a randomized controlled 1-year follow-up study.

BACKGROUND: The local peritoneal effects of low-glucose degradation product (GDP)-containing peritoneal dialysis fluid (PDF) have been extensively described. However, the systemic effects of prolonged prescription of these solutions are unknown. This study aimed to evaluate the effects of neutral pH and low-GDP PDF on systemic inflammation and endothelial dysfunction markers in peritoneal dialysis (PD) patients. METHODS: This is a multicenter, open labeled, randomized controlled trial including one hundred fifty-two patients initiating continuous ambulatory peritoneal dialysis for end-stage renal disease from seven centers in Korea. Participants were randomly allocated to conventional PDF (Stay safe®; Fresenius Medical Care, Bad Homburg, Germany) or low-GDP PDF (Balance®; Fresenius Medical Care) and were followed for 1 year. Primary outcome variable was the inflammation and endothelial dysfunction index (IEDI), a composite score derived from serum levels of soluble intercellular adhesion molecule (sICAM)-1, soluble vascular cellular adhesion molecule (sVCAM)-1 and high-sensitivity C-reactive protein (hs-CRP). sICAM-1, sVCAM-1, residual renal function (RRF), peritoneal membrane transport characteristics, ultrafiltration volume and nutritional parameters were measured as secondary outcome variables. RESULTS: Of 152 patients randomized, 146 (low-GDP: conventional PDF, 79:67) patients entered the trial (46% male, 53% with diabetes mellitus). At 12-month follow-up, the low-GDP group had significantly lower levels of IEDI, sICAM-1 and sVCAM-1 compared to the conventional group; hs-CRP was not different between groups. Peritoneal transport characteristics, RRF, nutritional parameters, incidence of peritonitis and death-censored technique survival were not different between groups. CONCLUSION: Neutral pH and low-GDP PDF likely produce fewer changes in markers of endothelial dysfunction compared to conventional PDF in incident PD patients.

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 µM and 100 µM in a dose-dependent manner. However, the toxicity graph of concentration vs toxicity had a point of inflection at 25 µM. The slope of the toxicity graph was gentle when the concentration was below 25 µM and steep when the concentration was greater than 25 µM. In conclusion, our results suggest that the toxicity of surfactants be taken care of pertinent treatment of acute herbicide intoxication.

Serum uric acid level as a marker for mortality and acute kidney injury in patients with acute paraquat intoxication.

BACKGROUND: Paraquat (PQ) is a non-selective herbicide that generates reactive oxygen species (ROS) in vivo. Uric acid emerged as a marker of oxidative stress and may enhance ROS-mediated injury in acute PQ intoxication. Therefore, we investigated the association between uric acid levels and mortality and acute kidney injury (AKI) in the present study. METHODS: From January 2007 to December 2008, patients who arrived at our hospital with acute PQ intoxication (n = 513) were included in the study. Patients were divided into two groups (hyperuricaemia vs non-hyperuricaemia) based on uric acid levels. Mortality and AKI were analysed in reference to uric acid level. RESULTS: Patient mortality was higher in the hyperuricaemia group than the non-hyperuricaemia group (68.4% vs 38.3%, P < 0.05). The incidence of AKI and kidney failure was 64% and 43.3%, respectively. Hyperuricaemia increased the risk of mortality and kidney failure to 3.7- and 3.3-fold after adjustments for age, sex and the estimated amounts of PQ ingestion. Mean serum uric acid level was higher in death group than survival group and higher in kidney failure group than non-AKI group and non-failure group. CONCLUSIONS: Baseline serum uric acid level might be a good clinical marker for patients at risk of mortality and AKI after acute PQ intoxication.

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, pCO(2), HCO(3) (-), 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.

Clinical outcome of hemoperfusion in poisoned patients.

Extracorporeal removal techniques are effective methods for toxin removal from the body. To define the safety and clinical outcomes of hemoperfusion, we evaluated retrospectively clinical outcomes of hemoperfusion over a 3-year period in our clinical center. From January 2006 to December 2008, we analyzed 803 patients. Mortality, catheter-related bleeding, systemic bleeding, hypocalcemia, and thrombocytopenia were investigated. Medical drugs (n = 54) and pesticide toxins (n = 749) were represented. Pesticides included herbicides (n = 598), insecticides (n = 130), mixed herbicides and insecticides (n = 4), and unknown pesticides (n = 17). Among those with herbicide poisoning, 493 cases were caused by paraquat, and among those affected by insecticides, 67 cases were caused by organophosphate insecticides. After hemoperfusion, systemic bleeding complications were observed in 26 cases (3.0%). Systemic bleeding was a greater mortality risk factor than nonsystemic bleeding (OR 2.779, 95% CI 1.07-7.23). Hypocalcemia was observed in 69.1% and thrombocytopenia in 31.1%. Excess mortality was 44.4%. In hemoperfusion cases, systemic bleeding is a major factor to predict adverse outcome.

Sequential change of asymmetric dimethylarginine levels after initiation of peritoneal dialysis in patients with end-stage renal disease.

BACKGROUND: We hypothesized that the asymmetric dimethylarginine (ADMA) metabolism in end-stage renal disease may be linked to the rate of protein turnover and to the vast pool of amino acids. In order to determine a correlation between the plasma levels of ADMA and the protein catabolic rate, we measured the ADMA levels as well as nutritional markers such as the normalized protein catabolic rate (nPCR) in patients with newly initiated continuous ambulatory peritoneal dialysis (CAPD). METHODS: Twenty-four patients were recruited for this study. All patients were on the standard CAPD protocol, and followed for at least 1 year. Blood samples were collected at baseline before the initiation of peritoneal dialysis, and every 6 months for 1 year. The blood parameters studied included the serum albumin, total cholesterol, glucose, urea nitrogen, creatinine and ADMA. Peritoneal equilibrium test and measurements of weekly Kt/Vurea and nPCR were performed within 4 weeks of the blood sampling. RESULTS: The change of ADMA levels over 1 year was positively correlated with that of haemoglobin (r = 0.592, P = 0.002) and nPCR during the same period (r = 0.508, P = 0.026). CONCLUSION: The findings of our study suggest that nPCR might influence the change of ADMA levels after initiation of CAPD.

The clinical features of acute kidney injury in patients with acute paraquat intoxication.

BACKGROUND: Paraquat (PQ) is a non-selective herbicide that generates reactive oxygen species in vivo. We hypothesized that acute kidney injury (AKI) in patients with acute PQ poisoning would provide a model for the clinical features of ROS-induced AKI. METHODS: From January 2007 to December 2007, 278 patients with acute PQ intoxication were included in the study. AKI was defined based on the RIFLE classification. The serial changes of creatinine (Cr), the incidence of AKI and the mortality according to the RIFLE classification were analysed. RESULTS: An initial serum Cr >1.2 mg/dL was a significant predictor of mortality [odds ratio 9.00, 95% C.I. (4.747, 17.061), P < 0.01]. The incidence of AKI was 51.4% among the 173 patients who had an initial serum Cr < or =1.2 mg/dL. Among them, 34.7% were the failure group and oliguric AKI was observed in 10 patients. The average peak serum Cr level, among the 13 survivors in the failure group, was 4.38 mg/dL at the fifth day, after ingestion, and their Cr level normalized within 3 weeks. None of the 13 survivors had permanent loss of renal function. The estimated amount of PQ ingestion was a predictor of the incidence of AKI. The mortality risk was significantly higher in the failure group than in the group without failure. CONCLUSION: The clinical feature was characterized by fully developed AKI at the fifth day after PQ ingestion and normalized within 3 weeks without exception.

The area of ground glass opacities of the lungs as a predictive factor in acute paraquat intoxication.

Even though plasma paraquat (PQ) levels have known to be an informative predictor, many patients succumb at low PQ levels in acute PQ intoxication. This study was designed to see whether the high resolution computerized tomography (HRCT) of the lungs would be a predictive measure in acute PQ intoxication. HRCT of the lungs was obtained from 119 patients with acute PQ intoxication on 7 days after PQ ingestion. The areas with ground glass opacities (GGOs) were evaluated at five levels with the area measurement tool of the picture archiving and communication systems. Among 119 patients, 102 survived and 17 died. The plasma PQ levels were significantly higher in the non-survivors than in the survivors (2.6+/-4.0 microg/mL vs. 0.2+/-0.4 microg/mL, P=0.02). The area with GGOs was 2.0+/-6.4% in the survivors and 73.0+/- 29.9% in the non-survivors (P<0.001). No patients survived when the area with GGOs was more than 40% but all of the patients survived when the area affected by GGOs was less than 20%. In conclusion, the area of GGOs is a useful predictor of survival in acute PQ intoxication, especially in patients with low plasma PQ levels.

Total and high molecular weight adiponectin concentrations in plasma of patients with end-stage renal disease before and after peritoneal dialysis.

BACKGROUND: Adiponectin is an antiatherogenic adipocyte-derived proteins. The level of plasma adiponectin is inversely correlated to cardiovascular risk in patients with end-stage renal disease (ESRD). The aim of this study was to elucidate the changes of adiponectin concentrations in newly diagnosed ESRD patients after peritoneal dialysis. METHODS: In 16 newly diagnosed ESRD patients, total concentrations of adiponectin and high molecular weight (HMW) adiponectin, the HMW ratio (HMWR; ratio of the plasma level of HMW adiponectin to that of total adiponectin), the body mass index (BMI), insulin concentrations, blood glucose and estimation of the insulin sensitivity index by the homeostasis model assessment (HOMR(IR)) were compared before and after 1 year of peritoneal dialysis. RESULTS: Plasma total adiponectin was decreased from 15.52 +/- 9.35 microg/mL to 11.80 +/- 6.84 microg/mL (P = 0.046), HMW adiponectin was decreased from 9.05 +/- 6.48 microg/mL to 4.83 +/- 4.15 microg/mL (P = 0.009), and HMWR was decreased from 0.51 +/- 0.18 to 0.35 +/- 0.20 (P = 0.008). Total and HMW adiponectin/BMI ratio was decreased. The BMI was increased from 25.2 +/- 5.7 to 25.8 +/- 6.2 (P = 0.036). The HOMR(IR), insulin level and lipid profile were not changed. CONCLUSION: Total adiponectin, HMW adiponectin and HMWR were decreased in newly diagnosed ESRD patients after 1 year of peritoneal dialysis. The factors that influence the decrease of the level of adiponectin should be studied in a larger prospective study.

Pesticide-initiated idiopathic environmental intolerance in South Korean farmers.

This study was designed to study patients with intolerance to pesticide smells. Ten subjects chosen were complaining of vague symptoms such as headache, dizziness, fatigue, nausea, vomiting, abdominal pain, myalgia, flu-like symptoms, etc., whenever exposed to the pesticide smells even at low intensity. To determine whether the etiology of this kind of pesticide hypersensitivity was of organic or psychiatric nature, all the subjects underwent tests as follows: complete blood cell count, urinalysis, and blood chemistry as routine tests; esophogastroduodenoscopy and abdomen ultrasonography for the gastrointestinal symptoms; chest x-ray, pulmonary function tests, and electrocardiography for the respiratory and/or cardiac symptoms; nerve conduction velocity and brain magnetic resonance imaging (MRI) for peripheral and central nerve system symptoms; and K-WAIS, Rey-Kim memory test, Rorschach, Mini Mental State Examination (MMSE), and Minnesota Multiphasic Personality Inventory (MMPI) for psychoanalysis. Of the 10 cases in which the chief complaint was headache, symptoms of two cases were caused by maxillary sinusitis. Another two showed typical multiple chemical sensitivity (MCS) or idiopathic environmental intolerance (IEI). Six out of the 10 cases, whose symptoms closely resembled the others, did not conclusively meet the criteria of classic MCS or IEI. The subjects of this case shared vague fears, both fear of pesticides and hypochondriasis. Some subjects faced financial insecurity and social uncertainty; others felt uneasy about the future of their farming life. Thus, to help verify the causes of MCS or IEI, which is strongly suggestive of pesticide smells, diagnosis needs a dual approach: on the anima and soma. Psychoanalysis can delve into the mental status of the patients to see whether the patients are aware of their symptoms. Clinical tests can see through the physical structure and functions of the organs on which patients' complaints are centered.

Plasma surfactant D in patients following acute paraquat intoxication.

Free radical-induced lung injury is a major problem that occurs because of paraquat intoxication. Serum surfactant protein D (SP-D) reflects the severity of various lung diseases. The purpose of this study is to investigate the changes in plasma SP-D concentrations and to correlate disease severity with SP-D concentrations in patients with acute paraqaut intoxication. Twelve paraquat-intoxicated patients participated in this study. Their paraquat exposure was assessed by their plasma's paraquat level. Serial plasma SP-Ds were measured by ELISA. SP-D was decreased two and three days after the initial measurement within 2 to 72 hours of ingestion. There was no difference in initial SP-D levels between survivors and non-survivors. The SP-D test revealed a significant positive correlation between the SP-D level and PaO(2) (r = 0.384, p = 0.003, N = 57). SP-D did not predict the likelihood of survival, but it was positively correlated with PaO(2). This finding suggests that low concentrations of plasma SP-D could reflect hypoxia due to free radical-induced injury.

Clinical implications of the ethane in exhaled breath in patients with acute paraquat intoxication.

STUDY OBJECTIVES: Pulmonary fibrosis due to lipid peroxidation is a major symptom of paraquat intoxication. Ethane in the expired breath (exEth) reflects lipid peroxidation and may be a measure of the damage effected by oxygen radicals in acute lung injury. The purpose of this study was to evaluate the clinical efficacy of exEth as a measure of exposure to paraquat and as an indicator of lung damage. DESIGN: Exposure levels were evaluated by the amount ingested, semiquantitative measurement of urine paraquat levels, and plasma paraquat concentration. End-tidal breath was collected for measurement of ethane 24 h after paraquat ingestion. Renal function and blood gas analyses were conducted on the same day as the breath collection, and the final clinical outcome was defined as either recovery or death. Associations between exEth and paraquat exposure profiles and clinical outcomes were assessed using linear regression models. PATIENTS: Twenty-one patients poisoned by paraquat were selected for the study during 2001 and 2002. RESULTS: exEth could not be used as a predictor of laboratory parameters such as Pa(O2), Pa(CO2), serum creatinine, and lung injury (as graded by high-resolution CT). A logistical analysis revealed that only the amount of paraquat ingested was a significant predictor of fatality (p = 0.021). The strength of the association between exEth and fatality was unaffected by the addition of potential confounders such as age, sex, and time interval and paraquat concentration. CONCLUSION: exEth cannot be used as either an independent predictor of survival or a specific marker of lung injury in patients with acute paraquat poisoning.

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.

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 (< 1.6 mg/dL) was 0.4% (3/834) in the PPI group and 0.4% (1/242) in the control group (P = 0.904). The change in magnesium levels did not differ between the two groups, and this result was maintained in the analysis of covariance after adjusting for confounding factors (P = 0.381). Moreover, magnesium levels did not significantly differ between the long-term (duration of use ≥ 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.

ARF requiring hemodialysis after accidental perchloroethylene ingestion.

Perchloroethylene (PCE) is an unsaturated chlorinated hydrocarbon in the form of a colorless, volatile liquid that is used as an industrial organic solvent for metal degreasing and for dry cleaning. The majority of cases of PCE intoxication have occurred by chronic inhalation, and PCE has been implicated previously in the development of mild renal dysfunction. However, the acute effects of PCE on the kidney are not well characterized, and the authors know of no reports of renal biopsy findings in the human. Here the case of a 32-year-old man who manifested by semicomatose state and oliguric acute renal failure requiring dialysis after accidental ingestion of 75 g of PCE is presented. A renal biopsy performed on the 19th day after ingestion showed features characteristic of severe acute tubular necrosis: aggregations of triangular or rhomboid crystals in the tubular lumens. A von Kossa stain showed that the crystal deposits were strongly positive for calcium. After 5 hemodialyses and conservative treatment, renal function gradually returned to normal.

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.

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 1.2 mg/dL or over 20% elevation from baseline. Hyperuricemia was defined as a serum uric acid level ≥7.3 mg/dL in men and ≥5.3 mg/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.