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A subset of patients on long-term hemodialysis have sustained hypotension, defined as a predialysis systolic pressure of < 100 mmHg. To determine the role of nitric oxide (NO), an important vasodilator, in this condition, the authors measured the plasma levels of nitrite (NO2-) and nitrate (NO3-), the known NO metabolites taken as an index of NO production, in 10 hypotensive patients on long-term hemodialysis. None of them had diabetes, cirrhosis of the liver, congestive heart failure, or infection. Fifteen age and gender-matched normotensive patients on hemodialysis were selected as control subjects. Measurements of plasma levels of nitrite and nitrate based on the Greiss reaction were made. There was no significant difference in hematocrit, serum intact parathyroid hormone, total calcium, inorganic phosphorus, albumin, heart rate, cardiac index, or interdialysis weight gain between these two groups. Plasma nitrite and nitrate levels did not correlate with either predialysis serum creatinine or blood urea nitrogen. The mean arterial pressure (MAP) was significantly lower and plasma nitrite and nitrate levels were significantly higher in chronic hypotensive patients than in normotensive patients (MAP: 68.30 +/- 3.24 mmHg vs 95.20 +/- 2.44 mmHg, p < 0.001; plasma nitrite and nitrate: 72.49 +/- 14.41 mumol/L vs 36.42 +/- 5.45 mumol/L, p < 0.05). In addition, MAP from hypotensive and normotensive patients on hemodialysis was inversely correlated with plasma levels of nitrite and nitrate (r = -0.54, p < 0.01). It was concluded that enhanced NO production in this subset of patients on hemodialysis may contribute to their chronic hypotension.

Patients on long-term dialysis may develop secondary hyperparathyroidism (SHPT) with increased serum concentrations of bone resorption markers such as the cross-linked N-telopeptide of type I collagen (NTX) and type-5b tartrate-resistant acid phosphatase (TRAP). When SHPT proves refractory to treatment, parathyroidectomy (PTX) may be needed. Renal patients on maintenance HD who received PTX for refractory SHPT (n=23) or who did not develop refractory SHPT (control subjects;n=25) were followed prospectively for 4 weeks. Serum intact parathyroid hormone (iPTH), NTX, TRAP, and bone alkaline phosphatase (BAP) concentrations were measured serially and correlation analyses were performed. iPTH values decreased rapidly and dramatically. BAP values increased progressively with peak increases observed at 2 weeks after surgery. NTX and TRAP values decreased concurrently and progressively through 4 weeks following PTX. A significant correlation between TRAP and NTX values was observed before PTX but not at 4 weeks after PTX. Additionally, the fractional changes in serum TRAP were larger than those in serum NTX at all times examined after PTX. Serum iPTH, TRAP, and NTX values declined rapidly following PTX for SHPT. Serum TRAP values declined to greater degrees than serum NTX values throughout the 4-week period following PTX.

1. Secondary hyperparathyroidism in chronic renal failure may contribute to abnormalities of lipid metabolism and glucose tolerance. Amelioration of secondary hyperparathyroidism has been reported to mitigate the hyperlipidaemia and improve glucose tolerance experimentally. 2. The effect of the partial suppression of hyperparathyroidism by intravenous calcitriol on lipid levels and glucose tolerance was studied in 15 haemodialysis patients with secondary hyperparathyroidism. All received intravenous calcitriol 1 μg at the end of haemodialysis thrice weekly for eight weeks. Oral glucose tolerance test and plasma lipid profiles including triglyceride, total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), apoprotein A-I and apoprotein B were determined simultaneously before and after eight weeks of therapy. 3. Before calcitriol treatment, uraemic patients with secondary hyperparathyroidism displayed a significant higher triglyceride and a significant lower HDL-C and apoprotein A-I as well as marked glucose intolerance with an increment of the area below the glucose curve when compared with healthy control subjects. 4. After eight weeks of calcitriol treatment, there was a significant decrement in serum intact parathyroid hormone (476.45 ± 48.33 versus 191 37 ± 30.17 ng/l, P < 0.001) and plasma triglyceride (2.24 ± 0.34 versus 1.80 ± 0.29 mmol/l, P < 0.05) as well as a significant increment of plasma apoprotein A-I (38.13 ± 2.14 versus 44.19 ± 2.18 μmol/l, P < 0.05), whereas there was no significant change in serum total cholesterol, LDL-C, HDL-C, and apoprotein B. These patients also became more glucose tolerant with a significant decrease of the area below the glucose curve and a significant rise in the area under the insulin curve after glucose load. Furthermore, the insulinogenic index increased significantly. 5. It was concluded that in addition to 1,25-dihydroxyvitamin D3 deficiency, secondary hyperparathyroidism may participate in the abnormal lipid metabolism, glucose tolerance and insulin secretion seen in dialysis patients and these abnormalities could be, at least in part, improved by intravenous calcitriol treatment.

Secondary hyperparathyroidism (SHPT) is a common complication in chronic renal disease. Osteoprotegerin (OPG), an extracellular cytokine receptor secreted by osteoblasts, can promote bone formation by inhibiting the function of osteoclasts. Hemodialysis (HD) patients have elevated serum OPG levels. OPG secretion can be suppressed with high parathyroid hormone (PTH) levels. HD patients with refractory SHPT can benefit from parathyroidectomy (PTX) treatment, but the changes of serum OPG, bone turnover markers and bone mineral density (BMD) following PTX in HD patients remain unclear. In this study, patients on maintenance HD who received PTX for refractory SHPT (n = 28) were prospectively followed for 1 year. Serum intact PTH (iPTH), alkaline phosphatase (Alk-P), and OPG were measured serially; BMD was measured pre-PTX and at 1 year after PTX. After PTX, serum iPTH levels reduced profoundly. Serum Alk-P levels increased rapidly, peaking at 2 weeks post-PTX, while serum OPG levels gradually increased at 2 weeks after PTX and peaked at 2 months. BMD improved in both femoral neck (FN; cancellous and cortical bone) and lumbar spine (LS; cancellous bone). Higher baseline iPTH levels were associated with greater FN and LS BMD improvements at one year after PTX. The increment of serum OPG was correlated with the increase in LS BMD, implying that inhibition of osteoclastic bone resorption may improve BMD within the first year after PTX. These findings suggest that PTX removes the suppressive effects of high PTH on OPG secretion, resulting in the increased serum OPG levels that may contribute to BMD improvement.

Osteomalacia can be a late but unrecognized complication following jejunoileal bypass. We describe a 53-year-old man who underwent jejunoileal bypass for morbid obesity twenty years earlier who suffered from progressive diffuse bony pain refractory to nonsteroidal anti-inflammatory drugs. He was initially diagnosed with a malignancy with bone metastasis. However, pertinent laboratory data were notable for hypocalcemia (7.5 mg/dL, albumin 4.1 mg/dL) with low urinary calcium excretion (14 mg/day), hypophosphatemia (2.0 mg/dL) with low urinary phosphate excretion (53 mg/day), hypomagnesemia (1.5 mg/dL) with low urine magnesium excretion (23 mg/day), low 1, 25 (OH)2 vitamin D3, and elevated serum alkaline phosphatase and intact parathyroid hormone (iPTH). These laboratory findings pointed to a defect in calcium, phosphate, and magnesium handling in the gastrointestinal tract. Bone biopsy of the iliac crest clearly demonstrated typical changes of osteomalacia with excessive osteoid accumulation and reduced mineralization. His clinical symptoms were refractory to oral 1, 25 (OH)2 vitamin D3 and calcium supplementation but significantly improved with the addition of intermittent intravenous active 1, 25 (OH)2 vitamin D3, calcium, phosphate, and magnesium supplementation. Osteomalacia is an easily misdiagnosed late complication of jejunoileal bypass. Early recognition can avoid circuitous diagnosis and inappropriate management.

A 68-year-old woman was admitted because of severe lower back pain for 2 months. She had diabetes nephropathy in uremic state and began regular hemodialysis for 2 years. Her blood pressure was 130/70 mmHg, body temperature 37°C, pulse rate 70 beats/min and respiratory rate 18 breaths/min. On examination, tenderness of L-spine without any neurological deficient was noted. Laboratory data showed white blood cell counts 13 100/μl with a left shift, and C-reactive protein …

Fanconi syndrome and chronic kidney disease associated with paroxysmal nocturnal hemoglobinuria is rarely reported. We describe a 51-year-old woman with glomerular filtration rate decrease and hypokalemia, glucosuria, and proteinuria during a 4-year period. Paroxysmal nocturnal hemoglobinuria was diagnosed 17 years earlier, and she has received multiple blood transfusions because of hemolytic episodes during the last 5 years. Deteriorating kidney function and persistent Fanconi syndrome were accompanied by a progressive increase in serum ferritin levels. Laboratory studies showed proximal renal tubular acidosis, hypophosphotemic hyperphosphaturia, normoglycemic glucosuria, and aminoaciduria. Serologic testing, tumor markers, Bence-Jones protein, and heavy-metal screening results were negative. Abdominal magnetic resonance imaging showed characteristic features of iron deposition in the bilateral renal cortices. Kidney biopsy showed chronic interstitial nephritis with prominent hemosiderin deposition in the proximal tubules. With potassium citrate, calcitriol, and deferoxamine therapy, Fanconi syndrome persisted, but kidney function was stable. Renal hemosiderosis secondary to both chronic repetitive hemolytic episodes and transfusion-related iron overload in patients with paroxysmal nocturnal hemoglobinuria can lead to Fanconi syndrome and chronic kidney disease.

Sir, Chryseobacterium meningosepticum (C. meningosepticum), an unusual opportunistic pathogen resistant to multiple antimicrobial agents, was rarely reported to be a cause of bacteraemia in haemodialysis patients. A 77-year-old female with end-stage renal disease was admitted with fever, chills and tenderness on the insertion site of the femoral double-lumen catheter 2 weeks after the start of haemodialysis. Her body temperature was 38.4°C. Erythema and swelling were present around the exit site of the double-lumen catheter. Laboratory evaluation revealed a haemoglobin of 7.6 g/dL and a C-reactive protein of 7.3 mg/dL. A provisional diagnosis of catheter-related bacteraemia was made. The double-lumen vein catheter was removed along with empiric antimicrobial agents with intravenous vancomycin (2 g/week) plus oral rifampin (450 mg/day). Blood cultures grew C. meningosepticum that was resistant to gentamicin, amikacin and all cephalosporins, but only susceptible to ciprofloxacin and vancomycin. Cultures of the exit site and the tip of catheter also grew C. meningosepticum. Despite 1-week antibiotic therapy, blood cultures still grew the same pathogen. At this time, an echocardiogram was normal. The addition of oral ciprofloxacin (250 mg q12 h) to vancomycin for another 2 weeks achieved uneventful recovery without subsequent growth of this organism. Cultures for tap water and dialysate were also negative for this pathogen. Chryseobacterium spp. are of low virulence but give rise to severe infections in neonate and immunocompromised hosts. C. meningosepticum was the most common species of human pathogens. In neonates, C. meningosepticum meningitis is the most common infection, whereas pneumonia and sepsis were the most common infections in adults with impaired immunity [1]. Patients with uraemia are at a risk for C. meningosepticum infection due to their compromised T- and B-cell immunity. To date, there were only few reports regarding C. meningosepticum infections in uraemic patients on dialysis (Table ​(Table1)1) [2–5]. Among 42 episodes in 41 dialysis patients, a majority (37/42, 88%) of episodes were related to peritoneal dialysis (PD) catheter peritonitis and a minority (5/42, 12%) of episodes had bacteraemia in patients on haemodialysis. Initial antibiotics to eradicate C. meningosepticum infections were usually inappropriate, leading to the necessity of removal of the catheter in most patients. Four (4/41, 10%) patients died from C. meningosepticum infection. In C. meningosepticum bacteraemia, the exact port of entry was unknown in three episodes. C. meningosepticum was isolated from sink water in only one episode. Although C. meningosepticum was not identified in tap, tank and dialysis water, in our patient it was also isolated from the exit site and the tip of the double-lumen catheter, suggesting that the port of entry be the disruption of skin integrity by internal placement of the catheter. Our case is the first report of C. meningosepticum bacteraemia associated with catheter-related infection in a haemodialysis patient. Table 1 Demographic data of the reported patients on dialysis with Chryseobacterium meningosepticum infection Although vancomycin has been previously recommended as the drug of choice for C. meningosepticum infection, recent reports and our case revealed that C. meningosepticum infection failed to respond to vancomycin administration alone [6]. Vancomycin should not be used alone to treat C. meningosepticum infections, especially associated with bacteraemia [6], as shown in the patient. In conclusion, C. meningosepticum should be considered as a causative pathogen of gram-negative bacilli catheter-related bacteremia in haemodialysis patients. Early recognition of this pathogen with appropriate antimicrobial agent administration will avoid the loss of the catheter and even mortality. Conflict of interest statement. None declared.

Recruits frequently develop hypocalcemia in exertional heat stroke (ExHS) with rhabdomyolysis and acute renal failure (ARF) from intensive training. It usually indicated severe skeletal muscle damage. However, the relative risk of ARF in ExHS patients complicated with hypocalcemia was unknown. The present study was undertaken to evaluate the value of peak serum creatine phosphokinase (CPK) level in predicting ARF in ExHS patients with hypocalcemia. Sixty-eight army recruits with ExHS were hospitalized at the Tri-Service General Hospital, Taiwan: 17 with ARF and hypocalcemia (group A); 7 with ARF but without hypocalcemia (group B); 20 without ARF but with hypocalcemia (group C); and 24 without ARF or hypocalcemia (group D). In the 24 patients with ARF (groups A and B) the serum phosphate and peak CPK levels were significantly higher than in patients without ARF (groups C and D; p0.001), serum calcium levels were also significantly lower in the former (p0.001). In the 37 patients with hypocalcemia (groups A and C), the peak serum CPK levels were significantly higher than in those without hypocalcemia (groups B and D; p0.001). There was a higher proportion of hypocalcemic patients with peak serum CPK levels greater than 10,000 U/l among ARF compared with patients without ARF (chi 2 = 12.48, p0.001). In 24 patients with ARF, there was a negative correlation between serum Ca and peak CPK levels (t = 3.37, r = -0.58, p0.01). However, a positive correlation was found between serum creatinine and peak serum CPK levels in 37 patients with hypocalcemia (t = 2.47, r = 0.39, p0.02).(ABSTRACT TRUNCATED AT 250 WORDS)