Soo Jeong Choi

Changes in body fat mass in patients after starting peritoneal dialysis.

♦ Background: Peritoneal dialysis (PD) is characterized by gain in fat mass. Visceral fat mass is associated with metabolic syndrome and atherosclerosis rather than subcutaneous fat mass. In addition, the change in visceral fat mass is a more reliable predictor of survival in PD patients. In this study, we prospectively examined serial changes in fat composition and nutritional status and analyzed factors associated with gain in fat mass in patients undergoing PD. ♦ Methods: Body composition was assessed by bioelectric impedance analysis (BIA) and computed tomogram (CT). Nutrition status was assessed by Subjective Global Assessment (SGA), protein equivalent of nitrogen appearance (nPNA), serum albumin, C-reactive protein (CRP), and lipid profile. All measurements except BIA were performed on the seventh day and at 6 and 12 months after the start of PD. ♦ Results: 60 patients (30 men; mean age 55.0 ± 12.5 years) were enrolled. Increase in body weight continued during the 12 months but visceral and subcutaneous fat mass increased during the first 6 months and decreased during the second 6 months. While hematocrit and serum albumin decreased during the first 6 months, they did not change during the second 6 months. Serum creatinine, total cholesterol, and triglyceride increased similarly to the weight pattern. While nPNA decreased during the 12 months, Kt/V, SGA, and CRP did not change. Patients that had more visceral fat mass at the start of PD had less gain of visceral fat mass during the first 6 months (r = –0.821, p = 0.002). Patients that had more subcutaneous fat mass at the start of PD had less gain of subcutaneous fat mass (r = –0.709, p = 0.015). The change in weight was not associated with the change in visceral or subcutaneous fat during the first 6 months. ♦ Conclusion: Patients starting PD experience weight gain, including visceral and subcutaneous fat, during the first 6 months of PD. Patients with high baseline fat mass had less increase in fat mass than those with low baseline fat mass, regardless of visceral or subcutaneous fat mass.

Ischemic monomelic neuropathy: a rare complication after vascular access formation

To the Editor, Patients with end-stage renal disease require an arteriovenous fistula (AVF). Although an AVF has numerous advantages, it can result in neurological or ischemic problems with hemodynamic disturbance. In 1983, Wilbourn et al. [1] described ischemic monomelic neuropathy (IMN), defined as a type of multiple axonal-loss mononeuropathy distally in a limb, resulting from an impaired blood supply after graft insertion. IMN is a very rare complication, but requires an early diagnosis and treatment. We report a case of IMN after an AVF operation and the results of a literature review. A 44-year-old woman visited a vascular surgeon for hemodialysis access. She had been diagnosed with type 2 diabetes 15 years previously. She had a 3-year history of hypertension and chronic kidney disease and was a hepatitis B virus carrier. Laboratory studies showed a white blood cell count of 5,600/mL, hemoglobin of 9.1 g/dL, blood urea nitrogen (BUN) of 49.3 mg/dL, and serum creatinine of 7.6 mg/dL. The patient had outpatient surgery with a brachiocephalic graft on the left elbow. The patient was admitted 7 days af ter the operation for weight gain, dyspnea, and general weakness. At that time, the hemoglobin was 8.2 g/dL, BUN 93.3 mg/dL, and serum creatinine 17.6 mg/dL. Metabolic acidosis was noted and a chest X-ray showed mild pulmonary congestion. The patient underwent emergency hemodialysis via a jugular vein catheter. After her uremia improved, she complained of swelling and numbness of the left hand and reduced grip strength. On examination, the fistula was patent and her radial pulse was palpable. The movement of the thumb was weak and she could not move her other fingers. She had no sensation in any modality. Nerve conduction studies performed 3 weeks postoperatively showed a decreased nerve conduction velocity and amplitude for the motor and sensory parts of the left hand (Table 1). Both lower legs had markedly decreased motor and sensory function, compatible with a diabetic patient. We diagnosed IMN of the left hand and peripheral polyneuropathy of both legs. Table 1 Nerve conduction study of upper extremities: initially Although she required fistula ligation, we and the surgeon decided to observe her because 1 month had already passed since the first operation and an extra ligation would require another operation for access. Her diabetic polyneuropathy was treated with pregabalin. After 2 months, she could grip a pencil. A follow-up nerve conduction test revealed improvement in the ulnar nerve, although defects remained in the median nerve (Table 2). She did not want to undergo more surgery. So we continued to observe her as an outpatient. Table 2 Nerve conduction study of upper extremities: after 2 months IMN is a sensory/motor impairment without tissue necrosis, but with a transient reduction in blood flow. IMN is a form of steal phenomenon as the access surgery steals blood flow from distal nerve tissue [2], causing multiple axonal-loss mononeuropathy distally in the limb. IMN is often under-recognized and misdiagnosed, but its known incidence is 0.5% to 3.0% [3]. If a patient on hemodialysis complains of hand pain, physicians need to consider many diseases, including soft tissue swelling, wound hematoma, carpal tunnel syndrome, vascular steal syndrome, and IMN [4]. The most important factor in diagnosing IMN is that of the clinical manifestations. Acute pain, weakness, and muscle paralysis immediately after an operation are common symptoms. Since these symptoms are nonspecific, after AVF formation, the motor or sensory function of the operated hand should be checked and nerve conduction studies should be done. Low amplitudes and reduced or even undetectable motor or sensory nerve conduction velocities are compatible with IMN. Axonal loss of the median, radial, and ulnar nerves can also be observed [3]. Electromyograms show denervation, including fibrillation potentials and motor unit loss. Since past neuropathy can be assumed to lower the ischemic injury threshold, diabetes, atherosclerotic disease, and women have an increased risk of IMN [2,4,5]. Nevertheless, IMN has been reported for a patient with no risk factors. In addition, a brachiocephalic fistula is commonly associated with this complication because the brachial artery is the only blood supply to the distal arm. The most important treatment for IMN is immediate closure of the access; this increases the probability of recovery [3,4]. Early closure of the fistula leads to partial or full restoration of the sensory and motor function [5]. Some clinicians reported treatment using a banding operation [3]. Redfern and Zimmerman [5] reported an improvement in two patients under observation, like our case. However, it is not clear whether those patients had IMN [5]. Anticonvulsants, antidepressants, and narcotics have been used for pain control [2]. Better education and awareness on the part of the surgeon and nephrologist should lead to an early diagnosis and the proper management of IMN [4]. Therefore, we report this case of IMN after an AVF operation with a literature review.

Use of multidetector computed tomography for evaluating coronary artery disease in patients undergoing dialysis

Aim:  Cardiovascular disease is the most common cause of death in patients undergoing dialysis. The accuracy of multidetector computed tomography (MDCT) for detecting coronary disease has not been determined, and little information is available regarding the performance of MDCT in patients undergoing dialysis.

Ferritin as a predictor of decline in residual renal function in peritoneal dialysis patients

Background/Aims Aims: Inflammation is an important factor in renal injury. Ferritin, an inflammatory marker, is considered an independent predictor of rapid renal progression in patients with chronic kidney disease. However, the relationship between ferritin and residual renal function (RRF) in patients undergoing peritoneal dialysis (PD) remains unclear. Methods We reviewed the medical records of patients who started PD between June 2001 and March 2012 at Soonchunhyang University Bucheon Hospital, Korea. A total of 123 patients were enrolled in the study. At 1 month after the initiation of PD, RRF was determined by a 24-hour urine collection and measured every 6 months thereafter. Clinical and biochemical data at the time of the initial 24-hour urine collection were considered as baseline. Results The RRF reduction rate was significantly greater in patients with high ferritin (ferritin ≥ 250 ng/mL) compared with those with low ferritin (ferritin < 250 ng/mL; -1.71 ± 1.36 mL/min/yr/1.73 m2 vs. -0.84 ± 1.63 mL/min/yr/1.73 m2, respectively; p = 0.007). Pearson correlation analysis revealed a significant negative correlation between the baseline serum ferritin level and the RRF reduction rate (r = -0.219, p = 0.015). Using multiple linear regression analysis and adjusting for other risk factors, baseline serum ferritin was an independent factor for the RRF reduction rate (β = -0.002, p = 0.002). Conclusions In this study we showed that a higher ferritin level was significantly associated with a more rapid RRF decline in patients undergoing PD.

Fabry disease previously diagnosed as Henoch- Schonlein purpura

To the Editor, Henoch-Schonlein purpura (HSP) is a generalized vasculitis characterized by manifestations of the skin, joints, gastrointestinal tract, and renal involvement. Although HSP can occur at any age and is usually a self-limited disease in children, it is less common and has a poor prognosis in adults. Renal involvement affects approximately one-third of HSP patients, and varies from intermittent hematuria and proteinuria, to severe nephrotic-nephritic syndrome with kidney histology being identical to that of immunoglobin A (IgA) nephropathy. Fabry disease is an X-linked glycosphingolipid disorder caused by deficient activity of the enzyme α-galactosidase A (a-GLA), which results in the systemic accumulation of globotriaosylceramide (Gb3) in all tissues of the body, including the skin, cornea, heart, and kidneys. The coexistence of Fabry disease and IgA nephropathy has been previously described [1-5]. Here, we report a case of Fabry disease previously diagnosed as HSP. A 45-year-old male was admitted to the clinic with abdominal pain and hematochezia. A gastroscopy and colonoscopy revealed an active duodenal ulcer and colitis, respectively. The patient’s medical history revealed a pontine hemorrhage and hypertension. He had also been consulting a dermatologist for 3 years for petechiae and keloids on his legs and upper arms. The patient was a carrier of hepatitis B for the past 5 years, and had been undergoing treatment with entecavir (0.25 mg) for the past 4 months. The patient had a family history of hepatitis B, and quit smoking and consuming alcohol after his pontine hemorrhagic event. He had hematuria (10 to 29 red blood cells/high power field) and proteinuria (1,582 mg/day), and his serum creatinine level was 1.8 mg/dL. Immunofluorescence microscopy of a renal biopsy (Fig. 1) revealed mesangial IgA deposition, and electron microscopy revealed laminated structures mimicking zebra bodies that had not been recognized at the initial observation. The patient was diagnosed with HSP and prescribed prednisolone (30 mg/day) and eprosartan (600 mg/day). After 2 months, the patient’s serum creatinine and urinary protein levels were 1.9 mg/dL and 1,262.2 mg/day, respectively, and his prednisolone dose was tapered to 10 mg every other day. Figure 1. (A) Light microscopy shows mesangial expansion (×200). (B) Immunofluorescence stain shows the immunoglobulin A deposition in mesangium

Serum uric acid and mortality risk among maintenance hemodialysis patients

the general population has changed since the 1950s [1]. Hyperuricemia was originally considered to be a consequence of renal insufficiency and associated with a variety of cardiovascular diseases, and several studies suggested that hyperuricemia can cause hypertension, renal insufficiency and metabolic syndrome. However, the role of serum uric acid remains unclear in the maintenance hemodialysis (MHD) patient population. In the MHD population, traditional cardiovascular risk factors, such as body mass index (BMI), serum cholesterol, and blood pressure were paradoxically associated with better outcomes [2]. This evidence for “reverse epidemiology”, is partly explained by the presence of ‘malnutrition-inflammation complex syndrome’ among the MHD patients. Uremic malnutrition, which is now referred to as “protein-energy wasting” (PEW), leads to low BMI and hypocholesterolemia and is common in dialysis patients. PEW is caused by inadequate nutrient intake, nutrient loss during dialysis, hyper-catabolism associated with dialysis, metabolic acidosis, and endocrine disorders of uremia. PEW has wide overlap with inflammation and other etiologic factors which can be used as assessment tools; this association between PEW and inflammation is believed to be the main cause of cardiovascular disease. Recently, the role of uric acid has also been re-evaluated in the context of other traditional and non-traditional risk factors in the MHD population. Several studies have found that serum uric acid concentrations were closely correlated with nutritional parameters, including dietary protein intake as measured by normalized protein catabolic rate (nPCR), BMI, albumin and phosphorus and that low serum uric acid concentrations were associated with higher mortality, especially among patients with lower protein intake as reflected by nPCR [3]. Furthermore, nPCR underestimates protein intake among patients with substantial residual renal function if renal urea clearance is not taken into account; therefore, serum uric acid may be an alternative laboratory marker of nutrition intake, compared to nPCR, when patients have substantial residual renal function. The relationship between low serum uric acid and ‘malnutrition-inflammation complex syndrome’ may be responsible for this newly discovered ‘reverse epidemiology’ phenomenon. In this issue of Kidney Research and Clinical Practice, Kim et al [4] examined the relationship between serum uric acid concentrations with all-cause mortality using a retrospective analysis of the data from 7,333 MHD patients documented in the End-Stage Renal Disease Serum uric acid and mortality risk among maintenance hemodialysis patients Inkyong Hur, Soo Jeong Choi, Kamyar Kalantar-Zadeh Harold Simmons Center of Kidney Disease Research and Epidemiology, Division of Nephrology and Hypertension, University of California Irvine School of Medicine, Orange and Irvine, CA, USA Division of Nephrology, Semyeong Christianity Hospital, Pohang, Korea Division of Nephrology, Soonchunhyang University College of Medicine, Bucheon, Korea Long Beach VA Healthcare System, Long Beach, CA, USA Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA Department of Epidemiology, UCLA Fielding School of Public Health, Los Angeles, CA, USA Editorial