Incidence, risk factors, and clinical outcomes of acute kidney injury associated with acute pyelonephritis in patients attending a tertiary care referral center.

Acute kidney injury (AKI) associated with acute pyelonephritis (APN) rarely has been reported. The aim of this study was to evaluate the incidence and risk factors of AKI associated with APN. We retrospectively reviewed the medical records of 403 patients over 18-year old age hospitalized for APN management from October 2009 to September 2014 in tertiary care referral center. Demographic data, clinical symptoms and signs, and laboratory findings were gathered from the medical records and analyzed. The mean age of patients was 57 years and APN commonly occurred in female (87.6%). AKI occurred in 253 patients (62.8%). As per the RIFLE classification, renal injury was graded as 'Risk' (62.1%), 'Injury' (26.5%), and 'Failure' (11.4%). AKI patients were more likely a male gender and had complicated APN. The AKI group had a significantly higher tendency to present with shock. The prevalence of underlying chronic kidney disease (CKD) was significantly higher in the AKI group. There was no difference in mortality between the AKI and non-AKI groups. Multivariate analysis revealed that age over 65 (OR 1.93, 95% CI 1.18-3.13, p= .008), complicated (OR 2.13, 95% CI 1.35-3.34, p= .001) and bilateral APN (OR 1.71, 95% CI 1.01-2.88, p= .045), and initial shock (OR 2.44, 95% CI 1.05-5.71, p= .039) were independent risk factors for the occurrence of AKI in patients with APN. Physicians should attempt to prevent, detect, and manage AKI associated with APN in patients with above conditions.

The incidence, risk factors, and outcomes of acute kidney injury in patients with pyogenic liver abscesses.

BACKGROUND: Acute kidney injury (AKI) can occur in various infectious conditions. Liver abscess is relatively rare, but can lead to sepsis and/or other severe complications. Few studies of AKI in patients with a liver abscess have been conducted. Therefore, we analyzed the clinical and laboratory data of AKI in patients with a liver abscess. METHODS: We retrospectively reviewed the medical records of patients who were diagnosed with a liver abscess from January 2000 to March 2013. The study included 404 patients with a liver abscess confirmed by clinical presentation and computed tomography. RESULTS: AKI occurred in 137 patients (34 %). As per RIFLE classification, renal injury was graded as either at risk of renal dysfunction (35.8 %), renal injury (47.4 %), and renal failure (16.5 %). AKI occurred more frequently in males and patients with liver cirrhosis (P < 0.001 and P = 0.005). Patients with AKI had lower serum albumin and higher AST and ALT levels than did patients without AKI. Bacteria were frequently isolated in AKI patients from blood culture and liver abscess aspirates (P < 0.001 and P = 0.007). The occurrence of septic shock was positively correlated with AKI (P = 0.002) and AKI was more frequent in patients with chronic kidney disease (P = 0.04). Higher mortality was observed in CKD patients accompanied by AKI (P < 0.001). Three patients with AKI underwent hemodialysis; two patients who had initially normal renal function completely recovered whereas one CKD patient progressed to ESRD, requiring maintenance hemodialysis. CONCLUSION: AKI is relatively common in patients with liver abscess. Physicians should therefore attempt to prevent, detect, and manage AKI early in patients with liver abscess.

Macrophage depletion ameliorates glycerol-induced acute kidney injury in mice.

BACKGROUND: This study was conducted to elucidate the role of renal macrophages in the development of acute kidney injury (AKI) in a glycerol (Gly)-induced rhabdomyolysis mouse model. METHODS: The experimental model of rhabdomyolysis requires injecting 50% Gly (10 ml/kg) intramuscularly into mice. Control mice were injected into the tail vein with the liposomal vehicle. Liposome-encapsulated clodronate (LEC)-only mice were injected with LEC. Gly-only mice were injected with Gly into a hind limb. LEC+Gly-treated mice were injected intravenously with 100 µl of LEC 24 h prior to Gly injection. Mice were sacrificed 24 h after Gly injection. RESULTS: Gly injection increased the serum creatinine level, and induced tubular damage. Renal CD45(+)CD11b(+)Ly6c(+) or CD45(+)CD11b(+)Ly6c(+)F4/80(+) macrophages were decreased by pretreatment with LEC in both normal and injured kidneys. Macrophage depletion prevented Gly-induced apoptotic death of tubular epithelial cells by decreasing caspase-9, ERK and p53, while increasing Bcl-2 expression. Expression of the inflammatory mediators NF-κB, MCP-1, ICAM-1, iNOS and COX-2 were also decreased with LEC pretreatment of mice injected with Gly. CONCLUSION: These results support the hypothesis that depletion of macrophages prevents renal dysfunction by abrogating apoptosis and attenuating inflammation during AKI.

A retrospective study of short- and long-term effects on renal function after acute renal infarction.

PURPOSE: Acute renal infarction is often missed or diagnosed late due to its rarity and non-specific clinical manifestations. This study analyzed the clinical and laboratory findings of patients diagnosed with renal infarction to determine whether it affects short- or long-term renal prognosis. METHODS: We retrospectively reviewed the medical records of 100 patients diagnosed as acute renal infarction from January 1995 to September 2012 at Gyeongsang National University Hospital, Jinju, South Korea. RESULTS: Acute kidney injury (AKI) occurred in 30 patients. Infarct size was positively correlated with the occurrence of AKI (p = 0.004). Compared with non-AKI patients, AKI occurrence was significantly correlated with degree of proteinuria (p < 0.001) and the presence of microscopic hematuria (p = 0.035). AKI patients had higher levels of aspartate transaminase (p < 0.001), alanine transaminase (p < 0.001), and lactated dehydrogenase (p = 0.027). AKI after acute renal infarction was more common in patients with chronic renal failure (CRF) (eGFR < 60 mL/min), compared with non-CRF patients, whose baseline eGFR was >60 mL/min (p = 0.003). Most patients recovered from AKI, except for seven patients (7%) who developed persistent renal impairment (chronic kidney disease progression) closely correlated with magnitude of infarct size (p = 0.015). Six AKI patients died due to combined comorbidity. CONCLUSIONS: AKI is often associated with acute renal infarction. Although most AKI recovers spontaneously, renal impairment following acute renal infarction can persist. Thus, early diagnosis and intervention are needed to preserve renal function.

Severe hypokalemic paralysis and rhabdomyolysis occurring after binge eating in a young bodybuilder: Case report.

RATIONALE: Severe hypokalemia can be a potentially life-threatening disorder and is associated with variable degrees of skeletal muscle weakness. PATIENT CONCERNS: We report a case of severe hypokalemic paralysis and rhabdomyolysis in a 28-year-old bodybuilder. He was admitted to the emergency room due to progressive paralysis in both lower extremities, which had begun 12 hours earlier. He was a bodybuilder trainer and had participated in a regional competition 5 days earlier. He went on a binge, consuming large amounts of carbohydrates over 4 days, resulting in a gain of 10 kg in weight. DIAGNOSES: He had no family history of paralysis and this was his first attack. He strongly denied drug abuse, such as anabolic steroids, thyroid and growth hormone, and diuretics. Neurological examinations revealed symmetrical flaccid paralysis in his lower extremities, but the patient was alert and his sensory system was intact. His initial serum potassium and phosphate level was 1.8 mmol/L and 1.4 mg/dL, respectively. The calculated transtubular potassium gradient (TTKG) was 2.02. His thyroid function was normal. INTERVENTIONS AND OUTCOMES: Serum potassium levels increased to 3.8 mmol/L with intravenous infusion of about 50 mmol of potassium chloride over 20 hours. OUTCOMES: His muscular symptoms improved progressively and he was discharged from the hospital 7 days after admission on foot. He was followed in our outpatient clinic, without recurrence. LESSONS: Physicians should keep in mind that large intakes of food during short periods can provoke hypokalemic paralysis and rhabdomyolysis, especially in bodybuilders.

Clinical features of hepatitis B and C virus infections, with high α-fetoprotein levels but not hepatocellular carcinoma.

The appropriate α-fetoprotein (AFP) level to confirm hepatocellular carcinoma (HCC) could be 100 ng/mL; however, the clinical significance of falsely elevated AFP in patients without HCC has not been fully studied. We investigated the clinical features and outcome of patients without HCC but with high AFP levels (100 ng/mL), especially with chronic hepatitis B (CHB) or C (CHC).The sample included 124 consecutive patients with CHB (n = 97) or CHC (n = 27), with AFP levels >100 ng/mL and without HCC at baseline. Multivariate Cox proportional regression analysis was performed to determine the factors associated with AFP normalization and HCC development.During the mean 52-month follow-up, the proportion of patients with CHB with AFP normalization (90.7%) was significantly higher than the proportion of patients with CHC (59.3%, P < 0.001). Initial aspartate aminotransferase levels (hazard ratio [HR] = 1.02 per 10 U/L increase, P = 0.021) and antiviral therapy (HR = 2.89, P < 0.001) were significantly associated with AFP normalization. Of the 16 (12.9%) patients who developed HCC, hepatitis B virus infection (HR = 10.82, P = 0.001), initiation of antiviral treatment postenrollment (HR = 0.23, P = 0.030), and AFP normalization within 12 months (HR = 0.13, P = 0.011) were associated with HCC development.CHB and CHC were the most common causes of falsely elevated AFP (>100 ng/mL). With either CHB or CHC, persistent AFP elevation (>12 months), regardless of antiviral treatment, might be an important marker of HCC development.

Rhabdomyolysis associated with single-dose intravenous esomeprazole administration: A case report.

BACKGROUND: Proton pump inhibitors are usually safe, although serious adverse effects can occur. We report the first case of rhabdomyolysis associated with single-dose intravenous esomeprozole administration. METHODS: A 45-year-old Korean male visited our emergency room because of persistent lower chest discomfort that started 10 hours before. He had been diagnosed with diabetes and coronary heart disease, but discontinued oral hypoglycemic agents 1 month earlier. He continued to take medications for coronary heart disease. There was no abnormality on an electrocardiogram or in cardiac enzymes. Initial laboratory findings did not show abnormalities for muscle enzymes. Esomeprozole 40 mg was administrated intravenously for the control of his ambiguous chest discomfort. Then, 12 hours later, he complained of abrupt severe right buttock pain. An area of tender muscle swelling 8 cm in diameter was seen on his right buttock area. Creatine kinase and lactate dehydrogenase were elevated to 40,538 and 1326 U/L, respectively. A bone scan using 20 mCi of Tc-hydroxymethylene diphosphonate was compatible with rhabdomyolysis. RESULTS: His muscular symptoms, signs, and laboratory findings improved markedly with conservative management, including hydration and urine alkalinization. He is being followed in the outpatient department with no evidence of recurrence. CONCLUSION: We should keep in mind that single-dose intravenous administration of esomeprazole can induce rhabdomyolysis.

Inappropriate antidiuretic hormone syndrome presenting as ectopic antidiuretic hormone-secreting gastric adenocarcinoma: a case report.

INTRODUCTION: Although the syndrome of inappropriate antidiuretic hormone has connection with various malignant tumors, there are few reports associated with advanced gastric cancer. CASE PRESENTATION: We describe the case of a 63-year-old Korean male with inappropriate antidiuretic hormone syndrome due to an ectopic antidiuretic hormone-producing advanced gastric adenocarcinoma manifested with overt serum hypo-osmolar hyponatremia and high urinary sodium concentrations. His adrenal, thyroidal, and renal functioning were normal, and the hyponatremia improved following removal of the tumor. The cancer cells were immunostained and found to be positive for the antidiuretic hormone. To our knowledge, this is the first report of an antidiuretic hormone-secreting advanced gastric adenocarcinoma associated with the syndrome of inappropriate antidiuretic hormone, showing cancer cells immunostained for the antidiuretic hormone. CONCLUSIONS: Although a strong relationship between gastric cancer and the syndrome of inappropriate antidiuretic hormone remains to be established, we suggest that gastric cancer could be included as a differential diagnosis of cancer that is associated with the syndrome of antidiuretic hormone.

Initial serum sodium concentration determines the decrease in sodium level after terlipressin administration in patients with liver cirrhosis.

BACKGROUND: Terlipressin, as a prodrug of vasopressin, has agonistic effects on the V1 receptor and partial agonistic effects on renal vasopressin V2 receptors. However, its effects on serum sodium concentration are controversial. METHODS: This study retrospectively investigated 127 patients with liver cirrhosis to examine the incidence and risk factors for the decrease in serum sodium level following terlipressin administration. RESULTS: Terlipressin was prescribed for bleeding control (99) and management of hepatorenal syndrome (28). Serum sodium level decreased from 134.0 ± 6.5 mmol/L to 130.4 ± 6.2 mmol/L during or after terlipressin treatment (P < 0.001) in all patients. In 45 patients (35.4%), the serum sodium concentration decreased by > 5 mmol/L, in 29 patients (22.8%); by 5-10 mmol/L; and in 16 patients (12.6%), by > 10 mmol/L. Five patients in the latter group showed neurological manifestations. In the univariate analysis, several factors including age, purpose of use, serum creatinine, and Model for End-Stage Liver Disease score, representing liver function, were significantly associated with the decrease in serum sodium after terlipressin administration. However, a multivariate analysis revealed that only initial sodium level was the most powerful predictor of terlipressin-induced reduction in serum sodium. CONCLUSION: An acute reduction in serum sodium concentration was not uncommon during terlipressin treatment, and the baseline serum sodium level was closely related to the reduction in serum sodium concentration.

Two additional cases of metformin-associated encephalopathy in patients with end-stage renal disease undergoing hemodialysis.

We report on two additional cases of metformin-associated encephalopathy in patients with end-stage renal disease (ESRD) undergoing hemodialysis. Two patients were seen at our hospital with abnormal neurological signs and symptoms. Magnetic resonance imaging (MRI) revealed the same pattern of high signal intensity in both basal ganglia in T2-weighted images in the two patients. The two patients had started taking metformin 5 and 6 weeks earlier at the same dose of 1000 mg per day. Metformin was immediately stopped, and regular hemodialysis was conducted. Their signs and symptoms resolved completely after these measures. The high signal intensity in both ganglia in T2-weighted MRI also disappeared. We should suspect metformin-induced encephalopathy and withdraw the drug when presented with diabetic patients with chronic kidney disease and neurological signs and symptoms of unknown cause.

Renal involvement of mantle cell lymphona leading to end stage renal disease.

Mantle cell lymphoma (MCL), owing to its insensitivity to chemotherapy, has a poor prognosis, with a median survival of 3 years to 4 years. MCL frequently infiltrates other organs. However, reports involving kidney in living patients are rare. Here, we report a case of MCL with renal involvement leading to end stage renal disease that required renal replacement therapy. A 69-year-old man diagnosed with MCL 3 years earlier was admitted to our emergency room due to uremic symptoms. After eight cycles of chemotherapy, he had displayed complete remission, but experienced a recurrence 1.5 years later; after refusing chemotherapy, the patient was lost on follow-up in the final 10 months. On presentation at the emergency room, the patient's serum blood urea nitrogen was 109.5 mg/dL, and creatinine was 11.1 mg/dL. All serological markers for secondary glomerulonephritis were negative. Renal biopsy revealed 50% sclerosis of the glomerulus and small dense lymphocyte infiltration of the tubulo-interstitium. Similar cells were found on the gastric mucosa. Despite our recommendation for chemotherapy, he refused all treatments except for hemodialysis, which was maintained for 12 months until his death. This patient represents the first case report of the renal involvement of MCL leading to end stage renal disease.

A case of end-stage renal disease initially manifested with visual loss caused by uremic optic neuropathy.

Uremic optic neuropathy (UON) is extremely rare, although sporadic cases have been reported. UON is sometimes regarded as a manifestation of uremic neuropathy. Here, we report a case of end-stage renal disease presenting as UON. A 22-year-old male was transferred to our nephrology department due to azotemia. Sudden deterioration of his vision occurred 3 days before his transfer. The patient's blood pressure was 150/90 mmHg, and he had no symptoms or signs of uremia, except for the visual disturbance. Blood tests showed an elevated serum creatinine of 6.0 mg/dL and serum BUN of 53.6 mg/dL. Both kidneys were decreased in size on ultrasound. His best-corrected vision was 20/62.5 in both the eyes. Ophthalmoscopy revealed hyperemia, swelling of both optic nerve heads, and blurred margins of both optic disks. These findings are compatible with UON. The patient's visual acuity and visual field improved following hemodialysis and corticosteroid treatment. The swelling of the patient's optic disks was also resolved. The patient is currently undergoing hemodialysis with the goal of vision restoration. Uremic optic neuropathy should be considered when patients with advanced chronic kidney disease complain of deterioration of their vision.

Bowel perforation after erlotinib treatment in a patient with non-small cell lung cancer.

Erlotinib is accepted as a standard second-line chemotherapeutic agent in patients with non-small cell lung cancer who are refractory or resistant to first-line platinum- based chemotherapy. There has been no previous report of bowel perforation with or without gastrointestinal metastases related to erlotinib in patients with non-small cell lung cancer. The exact mechanism of bowel perforation in patients who received erlotinib remains unclear. In this report, we report the first case of enterocutaneous fistula in a female patient with metastatic non-small cell lung cancer 9 months, following medication with erlotinib as second-line chemotherapy.

A case of Hughes-Stovin syndrome associated with hyperhomocysteinemia.

We report a case of Hughes-Stovin syndrome (HSS) associated with hyperhomocysteinemia. A 24-year-old man who has no clinical features suggestive of Behcet's disease was admitted for hemoptysis and dyspnea. Radiological and laboratory evaluation revealed multifocal pulmonary artery aneurysms involving bilateral segmental pulmonary artery, thrombi in right atrium and ventricle, and hyperhomocysteinemia. Accordingly, HSS associated with hyperhomocysteinemia was diagnosed, and the clinical and radiological improvement was achieved after treatment with prednisolone, warfarin, and folic acid.