Byung Kee Bang

Calcium-Free Hemodialysis for the Management of Hypercalcemia

The drug therapies for hypercalcemia of malignancy have been known to be associated with either limited efficacy or cumulative toxicity in patients with advanced renal failure. To establish the guidelines for the use of dialysis and to determine its optimal prescription for hypercalcemia, calcium-free hemodialysis was performed in 6 hypercalcemic patients with renal failure not responding enough to forced saline diuresis. Calcium-free dialysate contained sodium 135, potassium 2.5, chloride 108, magnesium 0.75, bicarbonate 30 mmol/l. Mean hemodialysis time was 160 +/- 27 min and mean Kt/V urea was 0.75 +/- 0.2. Plasma calcium concentrations fell from a mean value of 2.92 +/- 0.21 mmol/l (range 2.55-3.25) to 2.58 +/- 0.16 mmol/l at 1 h of hemodialysis and to 2.16 +/- 0.33 mmol/l (range 1.63-2.53) following 2-3 h of hemodialysis. The ionized calcium (n = 4) decreased from 1.44 +/- 0.14 mmol/l to 0.99 +/- 0.2 mmol/l. No patient showed any hypocalcemic symptoms and signs during hemodialysis. The rate of decrease in plasma calcium did not appear to produce adverse effects in any of the patients. There was a significant positive correlation between the decrease in plasma calcium concentration and the Kt/V urea (y = 1.4x - 0.29, r = 0.92, p < 0.01). We conclude that calcium-free hemodialysis is indicated when the presence of severe renal failure prevents the administration of large volumes of intravenous fluids to hypercalcemic patients. The amount of dialysis (Kt/V urea) can be used to predict the decrease in plasma calcium concentration during calcium-free hemodialysis.

Immunotactoid glomerulopathy associated with idiopathic hypereosinophilic syndrome.

A case of immunotactoid glomerulopathy in an 18-year-old man with an idiopathic hypereosinophilic syndrome is presented. The patient showed cervical lymphadenopathy, asymptomatic proteinuria of nephrotic range, and hematuria without any defined immunologic disease. Marked and prolonged hypereosinophilia was found in peripheral blood (eosinophil count; 6,248/mm3) and bone marrow (eosinophil series; 32%). Diffuse and/or nodular eosinophilic infiltration was identified in multiple organs such as kidney, stomach, liver, lymph node, and skin. Renal biopsy revealed endocapillary proliferative features of typical immunotactoid glomerulopathy with IgG and C3 deposition and microtubular structures of variable size, 20–80 nm in diameter, mainly in the subendothelium. This study suggests that immunotactoid glomerulopathy may be a secondary immunologic manifestation of the tissue damage by eosinophils in the idiopathic hypereosinophilic syndrome.

Treatment of Severe Acute Hypernatremia and Renal Failure by Hemodialysis

Chul Woo Yang, MD, Department of Internal Medicine, Catholic University, Medical College, Kangnam St. Mary’s Hospital, 505, Ban Po Dong, Seo Cho Ku, Seoul 137-040 (Korea) 210 250 cessive days. Hemodialysis prescription was as follows: dialysate sodium 138 mEq/l, blood flow rate 100-150 ml/min, no ultrafil-tration and 2 h dialysis time. After initial dialysis, he responded to questions appropriately, and sodium decreased from 193 to 168 mEq/l; after second hemodialysis sodium decreased from 168 to 158 mEq/l, and after third hemodialysis sodium decreased from 158 to 148 mEq/l (fig. 1). During heDear Sir, Concerning the treatment of acute hypernatremia, Pazimno and Pazimno [ 1 ] recently reported successful treatment of acute hypernatremia with hypotonic hemodialysis (dialysate sodium 110 mEq/1). The authors reported that acute hypernatremia can be corrected by a diluted dialysate fluid on opposite sides of a semipermeable membrane without neurologic sequelae, and opted for acute hypotonic hemodialysis to avoid serious problems that could occur with acute hypernatremia. We here report a case of hypernatremia accompanied by renal failure, which was successfully corrected with hypotonic hemodialysis. A 21-year-old man was transferred to our hospital due to a drowsy mental state and anuria. He was serving in the armed forces and trained in hot weather. Nausea, vomiting and oliguria had developed 2 days earlier and his mental state became drowsy and disoriented. At admission, he was stuporous and blood pressure was 140/90 mm Hg. Laboratory findings were as follows: sodium 193 mEq/1, potassium 5.9 mEq/1, chloride 148 mEq/1, uric acid 22.7 mg/dl, creatinine 13.5 mg/dl, blood urea nitrogen 203.5 mg/dl, CPK 2,309 U/l, serum myoglobin 2,850 ng/ ml. Calculated osmolality was 465.2 mosm/ kg. Arterial blood gas analysis showed pH 7.22, p02 94.1 mm Hg, HC03 9.1 mEq/l. Under the provisional diagnosis of acute renal failure due to rhabdomyolysis, emergency hemodialysis was commenced for 5 suc-

Serum Levels of Lipoprotein (a) after Renal Transplantation: Short-Term Follow-Up

Chul Woo Yang, MD, Dept. of Internal Medicine, Kang Nam St. Mary’s Hospital, Catholic University Medical College, No. 505 Banpo-Dong Seocho-Ku, 137-040 Seoul (Korea) Fig. 1. Serum levels of Lp(a) in controls, before and after RT. *p = 0.00004, **p = 0.01, compared to controls. – = Median. 20References Loscaltzo J: Lipoprotein (a), a unique risk factor for atherothrombotic disease. Atherosclerosis 1992;10:672-679. Kandoussi AK, Cachera C, Doninique P, Dra-con M, Fruchart JC, Tacquet A: Plasma level of lipoprotein Lp(a) is high in predialysis or hemo-dialysis, but not in CAPD. Kidney Int 1992 ;42: 424^125. Dear Sir, Lipoprotein (a) [Lp(a)] is an independent risk factor of atherosclerotic vascular disease [1]. Although it has been known that Lp(a) levels in chronic renal failure undergoing hemodialysis were elevated compared to normal controls [2], the precise mechanism is unclear. Therefore, this study was undertaken to see whether improved uremic condition or renal function after renal transplantation (RT) will decrease serum Lp(a) levels in renal transplant recipients. The study group consisted of chronically hemodialyzed patients, 16 males and 14 females, aged between 24 and 45 years (mean 34). Healthy controls were blood bank donors, 13 males and 17 females aged between 26 and 42 years (mean 39). All renal transplant recipients took cyclosporine and prediniso-lone as sheduled and showed no episodes of acute rejection during the follow-up period. Serum samples were collected form the patients before and after RT (1 week, 4 weeks and 6 months) and were stored at -70 °C until the study was performed. Lp(a) levels were measured using an ELISA assay. For this purpose, we used a commercially available assay (Immuno GmbH Co.). This test kit is based on a well coated with monospecific, polyclonal antiapolipoprotein (a) antibody, and conjugates consisted of second monospecific antiapolipoprotein (a) antibodies and peroxidase. All samples were read with

Nephrocalcinosis Associated with Primary Aldosteronism

Chul Woo Yang. MD, Department of internal Medieine, Kang Nam St. Mary’s Hospital, Catholic University Medical College, No. 505 Banpo-Dong Seoeho-Ku, 137-040 (South Korea) Dear Sir, It has been known that prolonged hypo-kalemia is associated with renal interstitial fibrosis, renal cyst formation and impairment of renal function [Tj; however, nephrocalcinosis associated with primary aldosteronism is rarely reported [2]. A 45-year-old woman was admitted to our hospital because of intermittent muscle cramps, polyuria and polydip-sia which developed 7 years earlier. At admission, blood pressure was 200/110 mm Hg. Biochemical findings indicated sodium 146 mEq/1, potassium 2.2 mEq/1, chloride 109 mEq/1, BUN 8.6 mg/dl, creatinine 0.8 mg/dl, total protein 7.8 g/dl, albumin 4.4 g/dl, AST 19 IU/1, ALT 13 IU/1, alkaline phosphatase 113 IU/1, calcium 8.9 mg/dl, phosphorus 2.5 mg/dl, magnesium 2.2 mg/dl. Twenty-four hour urine collections indicated sodium 135 mEq, potassium 50 mEq, calcium 102 mg, phosphorus 168 mg, magnesium 4.2 mg. Arterial blood gas analysis showed pH 7.42. pO: 89.5 mm Hg. HCO, 29.5 mm Hg, PCCK 44.7 mm Hg, and urine gas analysis showed pH 6.87, P02 119.4 mm Hg. PC02 36.6 mm Hg. HCO, 9.2 mm Hg. The hormone study revealed PTH 0.24 ng/ml (normal: -0.88 g/ml). 25-(OH) vitamin D 11.6 ng/ml (normal: 9-42 ng/ml), ACTH 3.0 pg/ml (normal: -37 pg/ml), 24-hour urine cortisol 57.8 μg/day (normal: 10-80 μg/day), metane-phrine 1.0 mg/day (normalup to 1.2 mg/ day), VMA 4.1 mg/day (normal: below 5 mg/ day). Plasma renin activity and aldosterone concentration before and after adrenalec-tomy are shown on table 1. Intravenous pyelography findings were unremarkable. The computed tomography of the abdomen showed bilateral medullary calcification and adrenal mass (2× 1 cm) consistent with adrenal tumor (fig. 1. 2). Adrenalec-tomy was performed on the 9th hospital day, and clinical symptoms, blood pressure and hypokalemia improved shortly after operation. This case shows that prolonged hypokalemia in primary aldosteronism can be one of the causes of nephrocalcinosis. The causes of nephrocalcinosis are primary hyperparathy-

Early Graft Dysfunction Due to Renal Vein Compression

We here report on an unusual case of early renal transplant dysfunction due to renal vein compression. Graft function was initially good but oliguria and massive hematuria developed on the 3rd day after transplantation. Duplex sonography showed turbulent blood flow of the renal vein, and renal venography confirmed renal vein compression. Exploratory laparotomy was performed and diuresis was initiated just after nephropexy. In conclusion, renal vein compression is a rare complication but should be included in the possible causes of early renal transplant dysfunction since this can be simply diagnosed by duplex sonography and is easily remedied by nephropexy.

BK Polyomavirus Interstitial Nephritis in a Renal Allograft Recipient

Human polyomavirus (PV) interstitial nephritis has recently been recognized as a cause of severe renal allograft dysfunction. It occurs in immunosuppressed patients after reactivation of the latent virus PV type BK (BK virus) in the renal epithelium. BK disease is defined as a morphologically manifest renal infection with cytopathic signs accompanied by varying degrees of interstitial inflammatory cell infiltrates and functional impairment. It is also identified by the presence of cells containing viral inclusion bodies (decoy cells) in the urine. The authors report a case of BK PV interstitial nephritis in a 36-year-old renal allograft recipient. Under light microscopy the chief diagnostic indicator was detection of intranuclear viral inclusions, which were found exclusively in tubular epithelial cells. Cells with viral changes were often enlarged with nuclear atypia and chromatin basophilia. Widespread interstitial plasma cell infiltrates associated with tubulitis were present. Intranuclear paracrystalline arrays of virus particles 35-38 nm in diameter were present as characteristic ultrastructural indicators. Urine samples revealed decoy cells with ground-glass-type intranuclear inclusions positive for BK virus by electron microcopy.

Prevention of posttransplant peptic ulcer by misoprostol.

Misoprostol is effective in protecting the gastric mucosa against various injuries (cytoprotection), but its role in preventing peptic ulcer disease (PUD) is controversial. Therefore, this study was designed to evaluate the effect of misoprostol on preventing posttransplant PUD. 87 patients undergoing kidney transplantation (KT) were randomly separated into three groups according to the antiulcer regimen. Group 1 (n = 28) received antacid and ranitidine; group 2 (n = 34) received antacid, ranitidine, and bismuth (De Nol), and group 3 (n = 25) received antacid, ranitidine, and misprostol (prostaglandin E1). Antiulcer drugs started 1 week before KT and were continued after surgery. A pretransplant gastrofibroscopy was performed 1 month before KT, and a follow-up gastroscopy was performed 2-3 weeks after KT. The incidence of peptic ulcer in groups 1 and 2 was 50.0% (14/28) and 35.3% (12/34), respectively (p > 0.05 groups 1 vs. 2). In group 3, 12.0% (3/25) of the patients showed PUD (p < 0.05 when compared with group 1 or 2). The known risk factors of posttransplant PUD were not significantly different in three groups, but the KT recipients of groups 1 and 2 had 7.8 times the risk of PUD when compared with group 3. In conclusion, the antiulcer regimen including misoprostol is more effective than ranitidine or bismuth in preventing posttransplant PUD, and the antiulcer effect of misoprostol seems to be related to the cytoprotective effect of the drug.

TRANSIENT ISCHEMIC JEJUNITIS IN A RENAL TRANSPLANT RECIPIENT

Chul Woo Yang, MD, Department of internal Medicine, Kang Nam St. Mary’s Hospital, Catholic University Medical College, 505 Banpo-Dong, Seocho-Ku, 137-040 (Korea) Dear Sir, Gastrointestinal complication after renal transplantation is frequent and often shows fatal clinical course [1]. The etiology is multi-factorial and the usual clinical manifestations are peptic ulcer, intestinal perforation and obstruction, acute pancreatitis, infection-associated colitis and diverticulitis [1-4]. We recently experienced a 35-year-old male patient who developed bloody stool after repeated solumedrol pulse therapy (fig.l). He showed gradual increase in serum creatinine after renal transplantation. We performed renal biopsy, and findings were consistent with acute rejection. The patient was treated with two courses of solumedrol pulse therapy (one course: 500 mg per day for 3 successive days, and then 250 mg per day for 3 successive days). Five days after two courses of pulse therapy, he complained about abdominal pain, and physical examination revealed abdominal pain and rebound tenderness on the whole abdomen. The simple abdomen showed thumb printing appearance in small intestine and abdomen CT revealed marked thickening of the jejunal wall (fig.2). Stool study for parasite and infection was negative, and blood coagulation tests were normal. At first, we planned explolaparotomy to rule out mesenteric vein thrombosis because of high mortality by medical treatment, but clinical symptoms gradually improved after low dose of solumedrol therapy (30^10 mg/ day, single injection). From follow-up abdomen CT, we confirmed the improvement of edema of intestinal wall, and he was discharged on the 56th hospital day with normal renal function.