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.

Incidence, risk factors and clinical outcomes of acute kidney injury associated with scrub typhus: a retrospective study of 510 consecutive patients in South Korea (2001-2013).

OBJECTIVES: Renal involvement in scrub typhus ranges from simple urinary abnormalities to acute kidney injury (AKI) leading to death. This study evaluated the incidence, predictors and prognosis of AKI associated with scrub typhus according to the RIFLE (risk, injury, failure, loss, end-stage kidney disease) criteria. METHODS: We retrospectively evaluated the medical records of patients diagnosed with scrub typhus from January 2001 to November 2013 in Gyeongsang National University Hospital. RESULTS: During the study period, 510 patients were diagnosed with scrub typhus and the incidence of AKI was 35.9%. There were 132 (25.9%) patients at risk, 37 (7.3%) with injury and 14 (2.7%) with failure. In comparison with the non-AKI group, the AKI group was older (73.9 vs 63.4 years, p<0.001) and had more comorbidities such as hypertension, diabetes mellitus and chronic kidney disease (CKD). AKI frequently occurs in hypertensive patients taking angiotensin receptor blockers or ACE inhibitors (p=0.002), and in patients with diabetes with higher glycated haemoglobin levels (p=0.033). Haematuria and proteinuria were more frequent in the AKI group. There was no relationship between the severity of proteinuria and occurrence of AKI. Intensive care unit admission and death were more frequent in the AKI group. The renal function of most patients with AKI recovered without sequelae, except for 1 patient who had underlying CKD. Multivariate analysis showed that age, presence of CKD, serum albumin level and time to hospital presentation after symptom onset were independent predictors of AKI in patients with scrub typhus. CONCLUSIONS: Our current results suggest that the presence of underlying CKD, older age, lower serum albumin level and time to hospital presentation after symptom onset were important risk factors to determine occurrence of AKI. Whether earlier diagnosis and treatment in patients with the above risk factors reduce the incidence and severity of AKI deserves to be investigated.

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.

Hemolytic uremic syndrome associated with paraquat intoxication.

We report a case of a 66-year-old patient with paraquat intoxication resulting in the requirement for hemoperfusion, hemodialysis, and plasma exchange. His initial serum paraquat level was 0.24 µg/mL (0.0-0.1 µg/mL). Activated charcoal (50 g) was administered orally, and high-dose N-acetylcysteine (150 mg/kg) was administered intravenously. In addition, immediate 4 h hemoperfusion was also performed for three consecutive days after admission. Hemodialysis was started on the 4th day after admission because of uremia. On the 9th day after admission, laboratory findings demonstrated hemolytic uremic syndrome (HUS): microangiopathic hemolytic anemia (MAHA), thrombocytopenia, elevated reticulocyte count, and lactate dehydrogenase (LDH). Plasma exchange was performed three times consecutively. Anemia and thrombocytopenia were improved, and LDH was normalized after plasma exchange. Urine output increased to 2240 mL/day on the 18th day after admission, and hemodialysis was discontinued. He is currently being observed at our follow-up clinic without renal impairment or pulmonary dysfunction for 1.5 years since discharge. We should suspect paraquat-associated HUS when thrombocytopenia and anemia are maintained for a long time after paraquat intoxication.

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.

Iodine-induced thyrotoxic hypokalemic paralysis after ingestion of Salicornia herbace.

A 56-year-old Korean man visited to emergency room due to paroxysmal flaccid paralysis in his lower extremities. There was no family or personal history of periodic paralysis. His initial potassium levels were 1.8 mmol/L. The patient had been taking Salicornia herbacea for the treatment of diabetes and hypertension. Results of a thyroid function test were as follows: T3 = 130.40 ng/dL, TSH = 0.06 mIU/L, and free T4 = 1.73 ng/dL. A thyroid scan exhibited a decreased uptake (0.6%). His symptoms clearly improved and serum potassium levels increased to 4.4 mmol/L by intravenous infusion of only 40 mmol of potassium chloride. Eight months after the discontinuation of only Salicornia herbacea, the patient's thyroid function tests were normalized. Large amounts of iodine can induce hypokalemic thyrotoxic paralysis and it may be necessary to inquire about the ingestion of iatrogenic iodine compounds, such as Salicornia herbacea.

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.

Anuric acute renal failure associated with pericardial effusion without signs of cardiac tamponade.

This article describes the anuric acute renal failure (ARF) secondary to massive pericardial effusion without tamponade in an 84 year-old man. He was referred to our emergency room with progressive dyspnea and azotemia. An electrocardiogram showed sinus tachycardia. A two-dimensional echocardiogram confirmed the presence of severe pericardial effusion without prominent ventricular diastolic collapse and there were no changes in his vital signs. Laboratory findings showed that his blood urea nitrogen and serum creatinine levels were 91.8 and 3.77 mg/dL, respectively. Renal ultrasonography showed no signs of hydronephrosis. Urine output did not increase in spite of giving a saline and furosemide infusion but increased immediately after pericardiocentesis with drainage. His renal function was completely restored 3 days after the procedure. A pericardial biopsy demonstrated invasion of malignant cells. We should keep in mind that pericardial effusion is one of the causes of anuric ARF, although it is not accompanied by tamponade.

Obstructive uropathy by total uterine prolapse leading to end-stage renal disease.

A 74-year-old woman was admitted to our emergency room complaining of general weakness and anorexia that started 20 days earlier. She denied other underlying diseases that might have provoked chronic renal disease. Her serum creatinine was 12.35 mg/dL. A pelvic examination and computed tomography revealed severe bilateral hydroureteronephrosis with marked cortical thinning induced by total uterine prolapse. She was started on emergency hemodialysis due to her uremic symptoms and severe metabolic acidosis. Despite Foley catheter insertion and manual reduction of uterus for 1 month, renal function was not recovered. The department of gynecology was strongly opposed to performing a procedure to reverse the hydroureteronephrosis due to the irreversibility of her renal function. She is undergoing chronic maintenance hemodialysis. This is a case report of rare end-stage renal disease (ESRD) caused by obstructive uropathy due to pelvic organ prolapse (POP). We should consider POP as a cause of ESRD.