Masako Uchida

Autopsy case of aluminum encephalopathy.

We report the case of a 59‐year‐old female aluminum encephalopathy patient who had chronic renal failure and took 3.0 g hydroxy‐aluminum gel per day for the control of serum phosphorus level during a 15‐year period. Nine months before her death she developed disorientation, memory disturbance, emotional incontinence, general convulsions and consciousness disturbance. Neuropathologically, the brain showed nerve cell atrophy and mild loss with stromal spongiosis, proliferation of astrocytes and microglia in the cerebral cortex, basal ganglia and thalamus. Some nerve cells were stained immunohistochemically by phosphorylated neurofilament, but apparent neurofibrillary tangles were not observed. Aluminum was detected in the nerve cells of the cerebral cortex by X‐ray microanalysis. Despite the long‐term intake of aluminum, there were no neuropathological findings of Alzheimers disease. The findings in our case suggested that aluminum alone might not develop Alzheimers disease.

Acute Progressive and Extensive Metastatic Calcifications in a Nephrotic Patient following Chronic Hemodialysis

We report on a 46-year-old female patient with a 5-year history of refractory nephrotic syndrome who rapidly developed extensive metastatic calcifications in lung, bone, blood vessels, skin, uterus and other soft tissues following maintenance hemodialysis. She was admitted for controlling anasarca. On admission, she suffered from severe nephrotic syndrome and chronic renal failure, showing 1.3 g/dl of serum albumin and 4.6 mg/dl of serum creatinine. She received bicarbonate dialysis combined with extracorporeal ultrafiltration to control anasarca. Following hemodialysis, she was treated with alfacalcidol and an increasing dose of calcium carbonate. Although anasarca was controlled, her nephrotic state remained unchanged. After 3 months of dialysis, roentgenograms of the body disclosed multiple metastatic calcifications. At this time, though the calcium-phosphorous product in serum was almost normal, the free calcium index was confirmed to have been high for 4 weeks. We considered that administration of calcium carbonate and alfacalcidol as well as an influx of free calcium from a dialysate resulted in increased serum ionized calcium which may be unable to be bound to serum protein because of lack of total protein, leading to ectopic deposition of calcium and phosphate. Our findings suggested that intensive care is needed to prevent metastatic calcification when uremic patients with severe nephrosis are treated with bicarbonate hemodialysis.

Effects of the Methylprednisolone Pulse Therapy on Renal Function

The effect of the methylprednisolone (MP) pulse therapy on renal function was examined in 15 patients with renal or collagen disease. Three nephrotic patients who had reduced renal function and active renal disease with progressive deterioration of renal function prior to the use of MP developed transient renal failure following an MP pulse therapy. The renal failure in each case was reversed by discontinuation of MP and/or by forced diuresis using albumin and furosemide. We examined the correlations between the individual changes in serum creatinine (Scr), body weight (BW) and urine volume (UV) before and after the pulse therapy and other laboratory data such as Scr, total serum protein and albumin. There were significant correlations between a change in Scr on the one hand and changes in BW and UV, Scr and serum albumin on the other. These findings mean that the effect of the MP pulse therapy on renal function depends on the clinical state of the patient and that renal deterioration after the pulse therapy may be more marked in patients who are more nephrotic and more impaired in renal function and suggest that increasing sodium and water retention during an MP therapy and the associated renal interstitial edema, proposed as one of the mechanisms of acute renal failure occurring in patients with minimal-change nephrotic syndrome, may be responsible for the MP-induced transient renal failure.

Rectal Stenosis Associated with Fungal Peritonitis: A Complication of Continuous Ambulatory Peritoneal Dialysis

Masako Uchida, Division of Nephrology, Department of Internal Medicine, Saga Medical School, Sanbonsugi, Nabeshimamachi, Saga 840-01 (Japan) Dear Sir, Fungal peritonitis is a rare but serious complication in patients on continuous ambulatory peritoneal dialysis (CAPD). We report on a patient on CAPD who developed severe rectal stenosis during the course of fungal peritonitis. Case Report A 56-year-old Japanese woman with a history of CAPD for 1.5 years was admitted to our hospital with the diagnosis of Staphylo-coccus aureus peritonitis on October 8 in 1988. After admission, she received cefazolin and tobramycin intraperitoneal and consequently abdominal pain rapidly disappeared. But she began to complain of abdominal pain again on the 13th hospital day. The bacteriological examination of the peritoneal fluid on the 18th hospital day revealed Candida parapsilosis as a causative agent. An X-ray film of the abdomen disclosed a curl-type Tenckhoff catheter placed in the pelvis. We started antifungal treatment with intravenous miconazole and oral fluorocytosine. Since peritonitis did not improve in spite of the treatment, we removed the Tenckhoff catheter on the 20th hospital day. Some fibrin clots were noted in a curl portion of the removed catheter. The peritonitis improved gradually, accompanied by the decrease of abdominal pain. On the 24th hospital day, she developed tarry stool without any symptoms such as hypotension, abdominal pain and aggravation of peritonitis. Emergent gastroduodenoscopic examination showed no significant abnormality. Melena disappeared gradually over several days. Hematocrit did not change during this episode. Barium enema examination performed on the 46th hospital day revealed severe stenosis about 5 cm in length in the upper third of the rectum (fig. 1). A colonoscopic examination showed clear stricture without mucosal changes such as atrophy, edema, hyperemia and fibrosis. A computed tomographic scan of the pelvis revealed no spaceoccupying lesion which surrounded the rectum. Examination of the small intestine showed no significant abnormality. Fig. 1. Barium enema examination reveals severe stenosis about 5 cm in length in the upper third of the rectum. Discussion

Acute Renal Failure and Nephrotic Syndrome in a Patient with T-Cell Lymphoma

Takanobu Sakemi MD, Division of Nephrology, Department of Internal Medicine, Saga Medical School, Nabeshima, Saga (Japan) Dear Sir, Hodgkin’s disease is representative of the neoplasms which cause nephrotic syndrome [ 1 ]. Non-Hodgkin’s lymphoma (NHL) is also reported to induce nephrotic syndrome, but rarely to result in acute renal failure (ARF) [2]. Herein we report on a case of T-cell type NHL presenting with pleural effusion, pro-teinuria and acute renal failure, probably associated with vascular permeability factors which may be released by abnormal T cells. A 59-year-old man was admitted because of fever, weight loss and systemic lymphade-nopathy. On admission, laboratory tests revealed negative urinary protein, hematocrit 38.7%, serum albumin 3.5 g/dl and normal levels of serum creatinine. Immunohistological examination of biopsy specimens from the lymph nodes revealed T cell NHL of the diffuse, large-cell type. After admission, he developed systemic eruption, followed by a gradual decrease in urine output, resulting in the development of edema and bilateral pleural effusion (fig. 1). Serum creatinine acutely rose from 0.90 to 6.60mg/dl accompanied by 7 kg of weight gain and a rise in blood pressure from 84/50 to 150/80 mm Hg. At this time urinalysis showed a 3+ test for protein and serum albumin decreased to 2.6 g/dl. The fractional excretion of urinary sodium (FENa) was 0.08%. Ultrasonographic study and a computed tomographic scan revealed neither compression of the renal artery or ureter by lymphadenopathy nor enlargement of the kidneys. Chemotherapy resulted in diuresis and recovery of renal function. Urinary protein, however, rapidly increased, amounting to 2.5-3.2 g/day and he became Chemotherapy X Fig. 1. Clinical course. WBC = Leukocyte count; S-Cr = serum creatinine; UP = urinary protein; BW = body weight; UV = urine volume; HD = hemodialysis; RBx = renal biopsy; P.Effusion = pleural effusion; FENa = fractional excretion of urinary sodium. Renal biopsy performed at this time showed no infiltration of atypical lymphoma cells. The enhanced vascular permeability factors released by abnormal T cells are suggested to cause nephrotic syndrome [3,4]. Symptoms observed in our case such as eruption, nephrotic with serum albumin levels of 2.5-2.9 g/dl. When the leukocyte count recovered from the nadir, the second episode of acute renal failure occurred with findings similar to the first one, though to a lesser extent, and resolved after chemotherapy.

A case of acute renal failure due to rhabdomyolysis associated with diabetic ketoacidosis.

膵島炎による糖尿病性ケトアシドーシスからrhabdomyolysisによる腎性腎不全を呈した興味ある1例を報告する.症例は糖尿病の既往のない67歳の男性. 1990年11月下旬より嘔吐・下痢症状のあと, 異常行動が出現し意識不明となる. 収縮期血圧50mmHg, BUN 78mg/dl, Cr 6.2mg/dl, 血糖値1,650mg/dl, および血清アミラーゼ, CPKの高値を示した. 近医で高血糖と急性腎不全の治療を受け, 一時腎機能の改善が見られたが再び悪化し当科に入院, 抗ラ氏島抗体が陽性のため, 急性発症のIDDMと診断した. 腎機能は血液透析を施行後, 正常になったがIDDMは残存した. また, 入院時血清ミオグロビンの高値を認めた. 本例は膵島炎による著明な糖尿病性ケトアシドーシスとそれに伴う低血圧による腎前性腎不全を生じ, さらに, rhabdomyolysisによる腎性腎不全が生じたものと考えられた.