Isolated idiopathic transient hyperphosphatasemia in an adult patient after renal transplantation: a case report.

Transient hyperphosphatasemia (TH) is characterized by the isolated elevation of serum alkaline phosphatase (ALP) in children. There is no evidence of liver or bone disease and the ALP levels return to normal within 4 months. Few adult cases have been reported. Here, we report the case of TH in a 54-year-old woman, who for 4 years after receiving a renal transplant, was regularly followed up at a renal outpatient clinic. Her underlying disease was chronic glomerulonephritis, for which she was taking immunosuppressive drugs (cyclosporine and mycophenolate mofetil). Routine laboratory analyses revealed that her ALP level had risen to 909 IU/l, which is a seven-fold increase relative to the upper normal limit (35 - 130 IU/l). The levels of intact parathyroid hormone; the tumor markers CEA, α-FP, CA 19-9, and CA 125; and other serum parameters were normal. The patient lacked symptoms, relevant clinical signs, and evidence of acute infection or acute chronic gastrointestinal disease. Lymph node enlargement and malignancy were not detected on a physical examination and ultrasonographic analysis of the abdomen, respectively. A bone scan showed no evidence of bone pathology. ALP isoenzyme analysis by electrophoresis showed patterns similar to those seen in TH of infancy and childhood. The ALP levels of the patient returned spontaneously to 126 IU/l 5 months after diagnosis. While isolated hyperphosphatasemia in renal transplantation patients may be a benign condition, we recommend that such cases be differentially diagnosed from other diseases that can trigger hyperphosphatasemia, including malignancy, infection, bone and liver diseases.

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.

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.

Fatal interstitial pneumonitis in a patient with relapsed diffuse large B cell lymphoma following yttrium-90 ibritumomab tiuxetan.

There is no previous report of fatal interstitial pneumonitis related to the administration of yttirum-90 ibritumomab tiuxetan. We report first case of fatal interstitial pneumonitis in a 35-year-old female patient with relapsed diffuse large B cell lymphoma following yttrium-90 ibritumomab tiuxetan. A pathological evaluation through a surgical lung biopsy demonstrated a "interstitial pneumonitis" pattern. Although high-dose methylprednisolone was administered, she died due to acute respiratory distress syndrome, secondary to radioimmunotherapy-induced interstitial pneumonitis. In this report, we discuss the etiology, diagnosis, and management of radioimmunotherapy-induced interstitial pneumonitis.

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

BACKGROUND: Transcatheter 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). METHODS: A 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. RESULTS: RCIN 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). CONCLUSIONS: RCIN 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.

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 staff's knowledge. After stopping the metformin, the patient's neurologic signs and symptoms disappeared and the Magnetic resonance imaging findings after 20 days were markedly improved.

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.