Echocardiographic features in a patient with primary oxalosis.

Primary oxalosis is a rare congenital disorder of oxalate metabolism characterized by deposits of calcium oxalate in several organs, including the heart. We present the case of a 38-year-old man with primary oxalosis who had unique echocardiographic findings. Two-dimensional echocardiography revealed the sparkling high intensity echocardiographic pattern and concentric thickening of myocardial walls. Microscopic examinations showed the extensive deposits of calcium oxalate crystals in the myocardium. Therefore, we suggest that primary oxalosis should be given important consideration in the differential diagnosis of a hypertrophied myocardium with high intensity echocardiograms.

Dihydropyridine type calcium channel blocker-induced turbid dialysate in patients undergoing peritoneal dialysis.

We previously reported that manidipine, a new dihydropyridine type calcium channel blocker, produced chylous peritoneal dialysate being visually indistinguishable from infective peritonitis in 5 patients undergoing continuous ambulatory peritoneal dialysis (CAPD) [Yoshimoto et al. 1993]. To study whether such an adverse drug reaction would also be elicited by other commonly prescribed calcium channel blockers in CAPD patients, we have conducted postal inquiry to 15 collaborating hospitals and an institutional survey in International Medical Center of Japan as to the possible occurrence of calcium channel blocker-associated non-infective, turbid peritoneal dialysate in CAPD patients. Our diagnostic criteria for drug-induced turbidity of dialysate as a) it developed within 48 h after the administration of a newly introduced calcium channel blocker to the therapeutic regimen, b) absence of clinical symptoms of peritoneal inflammation (i.e., pyrexia, abdominal pain, nausea or vomiting), c) the fluid containing normal leukocyte counts and being negative for bacterial and fungal culture of the fluid, and d) it disappeared shortly after the withdrawal of the assumed causative agent. Results showed that 19 out of 251 CAPD patients given one of the calcium channel blockers developed non-infective turbid peritoneal dialysis that fulfilled all the above criteria. Four calcium channel blockers were suspected to be associated with the events: benidipine [2 out of 2 (100%) patients given the drug], manidipine [15 out of 36 (42%) patients], nisoldipine [1 out of 11 (9%) patients] and nifedipine [1 out of 159 (0.6%)] in descending order of frequency. None of the patients who received nicardipine, nilvadipine, nitrendipine, barnidipine and diltiazem (25, 7, 2, 1 and 8 patients, respectively) exhibited turbid dialysate. In conclusion, we consider that certain dihydropyridine type calcium channel blockers would cause turbid peritoneal dialysate being similar to that observed in patients developing infective peritonitis. To avoid unnecessary antibiotic therapy the possibility of this adverse reaction should be ruled out whenever a CAPD patient receiving a dihydropyridine type calcium channel blocker develops turbid dialysate.

Changes of plasma atrial and brain natriuretic peptide levels during hemodialysis.

OBJECTIVES: The purpose of this study was to evaluate the effect of hemodialysis on the plasma concentration of atrial and brain natriuretic peptides, and to determine the two-dimensional echocardiographic parameters affecting the changes of plasma atrial and brain natriuretic peptide levels in patients with chronic renal failure. BACKGROUND: Brain natriuretic peptide has been found in human cardiac tissue and increases in patients with congestive heart failure. However, the factors that stimulate the secretion of plasma brain natriuretic peptide have not yet been fully clarified. METHODS: In 15 patients with chronic renal failure, plasma atrial and brain natriuretic peptide levels and two-dimensional echocardiographic parameters were measured before and after each session of hemodialysis. RESULTS: Plasma atrial natriuretic peptide levels significantly decreased from 367 +/- 537 pg/mL to 138 +/- 167 pg/mL after hemodialysis (p < 0.01). However, plasma brain natriuretic peptide levels did not significantly change after hemodialysis. Left atrial dimension significantly decreased (41.1 +/- 6.6 vs. 36.3 +/- 6.2 mm, p < 0.01) and left ventricular end-diastolic dimension slightly decreased after hemodialysis (57.0 +/- 10.3 vs. 55.7 +/- 9.9 mm, p < 0.05). The decrease of left atrial dimension was greater than that of left ventricular end-diastolic dimension (4.9 +/- 1.6 vs. 1.3 +/- 0.6 mm, p < 0.05). Plasma brain natriuretic peptide levels significantly correlated with fractional shortening both before and after hemodialysis (r = 0.65, p < 0.05). CONCLUSION: Plasma atrial natriuretic peptide levels significantly decreased as the right and left atrial overloads decreased, and plasma brain natriuretic peptide levels did not significantly decrease after hemodialysis. Plasma brain natriuretic peptide levels were not significantly influenced by acute hemodynamic change, such as hemodialysis. However, plasma brain natriuretic peptide levels were significantly correlated with basic cardiac function.

Elevated serum pepsinogens in chronic renal failure patients.

Human pepsinogens, the precursors of pepsin, originating from the stomach mucosa, are classified into two biochemically distinct groups, namely pepsinogen I (PG I) and pepsinogen II (PG II). We studied the serum levels of PG I and II in 51 normal volunteers, 23 chronic glomerulonephritis patients, 21 continuous ambulatory peritoneal dialysis (CAPD) patients and 40 hemodialysis patients. Serum pepsinogen levels were measured with a competitive binding double antibody radioimmunoassay. In the group of chronic glomerulonephritis patients, a positive correlation between the serum creatinine and the pepsinogen levels were found. The serum pepsinogen levels were remarkably elevated in CAPD and hemodialysis patients. The median levels of post-hemodialysis PG I (265.4 +/- 165.2 ng/ml) and PG II (41.7 +/- 38.0 ng/ml) were significantly higher than prehemodialysis values (PG I 207.4 +/- 127.5 ng/ml, PG II 29.0 +/- 16.6 ng/ml). Pepsinogen release by isolated gastric glands of guinea pigs was suppressed by guanidinosuccinic acid and was facilitated by calcium. The data suggest that both removal of guanidinosuccinic acid and infusion of calcium during hemodialysis contribute to the raised serum levels of these pepsinogens after hemodialysis.

Treatment of dialysis-induced hypotension with L-threo-3,4-dihydroxyphenylserine.

L-threo-3,4-dihydroxyphenylserine (L-DOPS), a precursor of noradrenaline (norepinephrine), which is converted into noradrenaline when orally administered, was given orally to haemodialysed patients exhibiting dialysis-induced hypotension. In five patients given 300 mg L-DOPS plasma concentrations reached a peak of 1.43 +/- 0.59 micrograms/ml 6 h after administration and decreased slowly to disappear after 36 h. Plasma noradrenaline concentrations showed a significant increase (P < 0.05), reaching a peak of 1.28 +/- 0.64 ng/ml after 24 h and declined to 0.75 +/- 0.47 ng/ml by 48 h. Administration of L-DOPS to six patients during dialysis for 6 consecutive weeks showed no accumulation in the blood. Oral administration of 200-400 mg L-DOPS to 34 patients 1 h before dialysis prevented dialysis-induced hypotension and decreased the number of concurrent treatments required for hypotension. The signs and symptoms of hypotension were improved in 73.5% of the patients and persisted after dialysis in 64.7%. The preventive effect of L-DOPS was significantly more prominent in patients with predialysis systolic blood pressure less than 100 mmHg and in patients with non-diabetic nephropathy. L-DOPS appeared to be an effective and well-tolerated treatment for the prevention of dialysis-induced hypotension.

Niceritrol reduces plasma lipoprotein(a) levels in patients undergoing maintenance hemodialysis.

Lp(a) is an LDL-like lipoprotein carrying the apoprotein(a) glycoprotein and has recently been recognized to be an independent risk factor for coronary heart disease. We studied plasma Lp(a) levels in 40 patients undergoing maintenance hemodialysis (24 male, 16 female; aged 16-83 years). Fasting plasma Lp(a) levels were measured by an enzyme-linked immunosorbent assay. The median value of plasma Lp(a) concentrations in hemodialysis patients was significantly higher than that of the normal volunteers (26.0 +/- 2.7 vs. 10.8 +/- 3.7 mg/dL, p < .05). Lp(a) levels did not correlate with age, duration of hemodialysis, total cholesterol, triglyceride, HDL cholesterol, or LDL cholesterol. The 11 patients whose plasma Lp(a) concentrations exceeded 20 mg/dL received niceritrol, a prodrug of nicotinic acid, at a dosage of 500 mg t.i.d. for 4 weeks. The plasma Lp(a) levels were significantly lower after 4 weeks of treatment (38.3 +/- 4.2 vs. 31.5 +/- 3.2 mg/dL, p < .01).

[Argyrosis of the urinary tract after silver nitrate instillation: report of a case].

A 69-year-old woman was referred to our hospital for evaluation of pyuria and renal dysfunction. Twenty days earlier, the patient had undergone silver nitrate retrograde instillations for essential renal bleeding. Routine laboratory findings showed renal dysfunction with a serum creatinine concentration of 7.2 mg/dl and blood urea nitrogen concentration of 68 mg/dl. The urine contained numerous red cells and white cells. The plain X-ray film of the abdomen revealed right renal calcification. Computed tomographic scan confirmed the calcifications in the right renal collecting systems and parenchyma. The most likely diagnosis was argyrosis of the upper urinary tract. The patient underwent a right nephrectomy. Histopathological examination of the specimen showed that the renal pelvis was filled with blood clots. Laboratory evaluation including serum creatinine concentration and urinalysis revealed normal parameters postoperatively. We conclude that this patient developed argyrosis of the urinary tract, and review previously published papers concerning complications of silver nitrate instillation.

Evaluation of hemodialysis efficiency by an edema fluid model.

The concentrations of urea, creatinine, and uric acid were measured in edema fluid and plasma during hemodialysis and 18 h after hemodialysis. The concentrations of these solutes in plasma were 15-17% lower than in the edema fluid after hemodialysis. Eighteen hours after hemodialysis, however, the concentrations in plasma were almost the same as those in edema fluid. These data suggest that the removal of these solutes from the extracellular space is delayed during hemodialysis. The plasma concentrations obtained at 18 h after hemodialysis are better indicators of hemodialysis efficiency.

Plasma interleukin-6 levels in continuous ambulatory peritoneal dialysis and hemodialysis patients.

Plasma levels of interleukin-6 (IL-6), a cytokine known to be involved in lymphocyte activation and in inflammation, were studied in 10 normal volunteers, 21 continuous ambulatory peritoneal dialysis (CAPD) patients and 41 hemodialysis patients. Plasma IL-6 levels in hemodialysis patients were significantly higher than those in normal volunteers and CAPD patients (p less than 0.05). The means of plasma IL-6 concentrations before and after hemodialysis did not change significantly. While IL-6 in peritoneal dialysate was detectable in only 3 of the 21 CAPD patients without peritonitis, it was extremely high in 2 patients with bacterial peritonitis. IL-6 levels decreased as peritonitis subsided.

Pharmacokinetics of denopamine in hemodialysis patients.

The pharmacokinetics of denopamine on a hemodialysis day and on an interdialysis day was evaluated in 11 hemodialysis patients. Tmax was the only pharmacokinetical parameter that differed significantly between healthy volunteers and hemodialysis patients. It is suggested that denopamine can be administered to hemodialysis both on hemodialysis days and on interdialysis days without dosage adjustments.

[Renal pelvic tumor in chronic renal failure: report of a case].

A 44-year-old female was admitted because of gross hematuria six years after beginning hemodialysis for chronic renal failure. There was a past history of hematuria one year before admission. Retrograde pyelography, computed tomographic scan and angiography had been performed, and a probable malignant tumor of left renal pelvis had been found in 1986. We recommended surgery at the time, but she refused treatment and was followed up. On June 22, 1987, the patient had a second attack of gross hematuria resulting in bladder tamponade, and hematuria from the left ureteric orifice was confirmed at cystoscopy. Ultrasound showed left obstructive nephropathy. Left nephrectomy was performed because of the presumptive diagnosis of malignant tumor. The histological diagnosis was transitional cell carcinoma of the left renal pelvis. Two courses of M-VAC (methotiexate, vinblastine, adriamycin and cisplatin) chemotherapy were accordingly given postoperatively. The incidence of renal pelvic tumor and its chemotherapy in patients with chronic renal failure are discussed.

Effects of latamoxef on in vitro and ex vivo thromboxane A2 generation in human platelets.

Although beta-lactam antibiotics cause similar platelet abnormalities in vitro and in vivo, it is still unclear whether the mechanism(s) leading to the defects in both conditions are the same. The present work compared in vitro and ex vivo effects of latamoxef (LMOX) on aggregation and thromboxane (TX)A2 generation, determined as TXB2 generation. In the in vitro systems, LMOX interfered with both responses induced with all agonists tested (ADP, collagen and thrombin). Furthermore, although LMOX did not suppress arachidonic acid (AA)-induced TXB2 generation, it significantly suppressed the aggregation. In ex vivo systems performed with four healthy subjects, LMOX administration clearly suppressed the ADP-induced responses, but not the responses induced with the other agonists or AA. These differences observed in vitro and ex vivo are discussed from the viewpoint of different action mechanisms of LMOX under the two conditions.

Plasma concentration and peritoneal clearance of oxalate in patients on continuous ambulatory peritoneal dialysis (CAPD).

Accumulation of oxalate, resulting in high plasma levels, is a common finding in end-stage renal disease. We investigated plasma concentration and peritoneal clearance of oxalate in 14 patients on continuous ambulatory peritoneal dialysis. The plasma oxalate levels in these patients (30.2 +/- 11.2 mumol/l) were as high as those in hemodialysis patients before dialysis (31.9 +/- 11.1 mumol/l). There was a significant correlation between plasma oxalate and urea nitrogen appearance (UNA). Dietary protein seems to be an important oxalate source in these patients, because the UNA reflects protein intake in stable patients. The mean peritoneal oxalate clearance was 6.64 +/- 1.56 l/day, close to the creatinine clearance. These results suggest that the plasma oxalate levels in CAPD patients may be sufficiently high to induce calcium oxalate deposition, and that methods of increasing oxalate removal and reducing oxalate burden are necessary for CAPD patients.

Hypoxemia and hemodialysis-induced symptomatic hypotension.

We studied a possible involvement of hypoxemia in the pathophysiology of hemodialysis (HD)-induced symptomatic hypotension (SH). SH frequently recurred in 16 of 33 patients undergoing routine HD. These 16 patients showed a significantly (p less than 0.001) lower arterial oxygen tension (PaO2) prior to the start of HD than the remaining 17 patients without SH. This was the case when 10 patients with SH who had no additive risk factors for SH such as older age, excessive fluid loss and autonomic neuropathy were compared with a corresponding 11 patients without SH (p less than 0.001). Sequential monitoring of PaO2 throughout HD using the intravascular O2 electrode revealed that SH was never associated with particular changes in PaO2. The pattern of the decrease in, and the minimum value for, PaO2 during HD was not significantly different between the patients with and without SH. Furthermore, O2 administration during HD failed to prevent the occurrence of SH. These data suggest that pre-existing, but not HD-induced, hypoxemia is profoundly related to the pathophysiology of SH.