Dong Jun Park

N-acetylcysteine attenuates glycerol-induced acute kidney injury by regulating MAPKs and Bcl-2 family proteins.

BACKGROUNDnRhabdomyolysis-induced acute kidney injury (AKI) accounts for about 10 to 40% of all cases of AKI. It is known that N-acetylcysteine (NAC) is effective in various experimental renal injury models; however, little information is available about the rat model of glycerol-induced rhabdomyolysis. In this study, we hypothesize that NAC plays a renoprotective role via the anti-apoptotic pathway.nnnMETHODSnMale Sprague-Dawley rats were divided into four groups: (i) saline control group, (ii) NAC-treated group (N-acetylcysteine) (150 mg/kg), (iii) glycerol-treated group (50%, 8 ml/kg, IM) and (iv) NAC plus glycerol-treated group. Rats were sacrificed at 24 h after glycerol injection, and the blood and renal tissues were harvested.nnnRESULTSnGlycerol administration caused severe renal dysfunction, which included marked renal oxidative stress, significantly increased blood urea nitrogen (BUN) and serum creatinine levels. Histopathological findings, such as cast formation and tubular necrosis, confirmed renal impairment. We noted a marked activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK), but not p-38, in the glycerol-treated group. We also observed high expression of Bax and Bad but only weak expression of Bcl-2 and Bcl-xL in the glycerol-treated group. However, NAC pretreatment significantly improved renal function and decreased the activation of ERK, JNK, Bax and Bad, whereas it increased Bcl-2 and Bcl-xL.nnnCONCLUSIONnThese results demonstrate that NAC protects against renal dysfunction, morphological damage and biochemical changes via the anti-apoptotic pathway in the glycerol-induced rhabdomyolysis model in rats.

Metformin‐induced encephalopathy without lactic acidosis in a patient with contraindication for metformin

A 51‐year‐old Korean man with end‐stage renal disease and who was on intermittent hemodialysis was admitted with progressive dysarthria, gait disturbance, and myoclonus. The liver function tests and the electrolyte and arterial gas analyses were normal. The Magnetic resonance imaging scan showed a diffuse symmetric high signal intensity in the basal ganglia on the T2‐weighted image. After a thorough history taking, we knew that he had been treated with metformin for 3 months at other hospital without our hospitals staffs knowledge. After stopping the metformin, the patients neurologic signs and symptoms disappeared and the Magnetic resonance imaging findings after 20 days were markedly improved.

Incidence and risk factors for radiocontrast-induced nephropathy in patients with hepatocellular carcinoma undergoing transcatheter arterial chemoembolization

BackgroundTranscatheter arterial chemoembolization (TACE) is an effective treatment for unresectable hepatocellular carcinoma (HCC); however, large volumes of radiocontrast agents are used for TACE and may induce renal dysfunction. Most patients with HCC have coexisting liver cirrhosis (LC) at the time of diagnosis. Advanced cirrhosis is characterized by peripheral vasodilatation associated with decreased renal perfusion due to the activation of vasoconstrictor systems. We retrospectively investigated patients with HCC who had undergone TACE to determine the incidence and risk factors for radiocontrast-induced nephropathy (RCIN).MethodsA total of 101 patients with HCC who underwent a combined 221 TACE treatment sessions were included. Follow-up serum creatinine levels within 96 h after TACE were confirmed in these patients. RCIN was defined as an increase of at least 25% in baseline serum creatinine levels between 48 and 96 h after TACE.ResultsRCIN developed in 20 (9%) of the 221 treatment sessions after TACE. A univariate analysis showed that the Child–Pugh score (6.0 ± 1.3 vs. 6.7 ± 1.9, P = 0.005), ascites (14.4 vs. 40%, P = 0.008), contrast medium volume (257.3 ± 66.8 vs. 275.0 ± 44.0 ml, P = 0.009), total bilirubin (1.3 ± 1.7 vs. 3.4 ± 8.0 mg/dl, P < 0.001), basal serum creatinine levels (0.9 ± 0.3 vs. 1.0 ± 0.5 mg/dl, P < 0.001) and glomerular filtration rate using the modification of diet in renal disease formula (90.5 ± 21.8 vs. 88.4 ± 29.6 ml/min, P = 0.015) were significantly associated with the development of RCIN. A multivariate analysis revealed that the Child–Pugh score was associated with RCIN [odds ratio (OR) 1.5; P = 0.015]. Overall, in-hospital mortality after TACE was 4.07% (with RCIN, 30%; without RCIN, 1.5%; P < 0.001). The multivariate analysis also showed that the Child–Pugh score and the occurrence of RCIN were associated with in-hospital mortality after TACE (OR 2.8; P = 0.001; OR 26.7, P = 0.002, respectively).ConclusionsRCIN after TACE was closely associated with the severity of LC. Effective preventive measures remain to be determined in patients with HCC and advanced LC who are undergoing TACE.

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

BackgroundTerlipressin, 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.MethodsThis 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.ResultsTerlipressin was prescribed for bleeding control (99) and management of hepatorenal syndrome (28). Serum sodium level decreased from 134.0u2009±u20096.5xa0mmol/L to 130.4u2009±u20096.2xa0mmol/L during or after terlipressin treatment (Pu2009<u20090.001) in all patients. In 45 patients (35.4%), the serum sodium concentration decreased byu2009>u20095xa0mmol/L, in 29 patients (22.8%); by 5–10xa0mmol/L; and in 16 patients (12.6%), byu2009>u200910xa0mmol/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.ConclusionAn 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.

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.

Renal involvement of mantle cell lymphoma 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 3u2009years to 4u2009years. 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 3u2009years 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 1.5u2009years later; after refusing chemotherapy, the patient was lost on follow‐up in the final 10u2009months. On presentation at the emergency room, the patients serum blood urea nitrogen was 109.5u2009mg/dL, and creatinine was 11.1u2009mg/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 12u2009months until his death. This patient represents the first case report of the renal involvement of MCL leading to end stage renal disease.

Two Cases of Postoperative Thrombotic Thrombocytopenic Purpura

usually fatal in untreated individuals with over 80% mortality. Both HSV-1 and HSV-2 have been detected as causes of this disease; the seroprevalence of HSV-2 has been detected as being higher in individuals undergoing dialysis therapy (7). Antiviral agent choices for HSV infection include acyclovir, valacyclovir, and famciclovir; high-dose parenteral acyclovir is recommended in the case of HSV-1 hepatitis. In our opinion, hemodialysis patients, when exposed to a herpes virus, may develop viremia instead of latency. In the case of acute hepatitis in these populations, even rare pathogens should be kept in mind.

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 patients blood pressure was 150/90u2003mmHg, and he had no symptoms or signs of uremia, except for the visual disturbance. Blood tests showed an elevated serum creatinine of 6.0u2003mg/dL and serum BUN of 53.6u2003mg/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 patients visual acuity and visual field improved following hemodialysis and corticosteroid treatment. The swelling of the patients 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.

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.