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Abstract

S. Shaldon

Over 40 years ago, we published our initial studies on the dramatic results that were obtainable using dietary salt restriction to treat hypertension in anuric patients with end-stage renal disease receiving maintenance hemodialysis. I had been schooled in the benefits of salt restriction when I had worked with Sheila Sherlock treating patients with cirrhosis and ascites. I was already familiar with Walter Kempner’s original success with a rice diet in controlling hypertension in patients with chronic renal failure [Kempner 1944] and also the success that Belding Scribner [1960] had achieved in Seattle with his original patients. As our results were so dramatic, I have always preached the need for salt restriction in patients with chronic kidney disease. We were always impressed that the real benefit occurred several months after the patient had reached “dry body weight” [Comty et al. 1964]. This benefit was due to a hemodynamic phenomenon which has only recently been explained. The lag phenomenon (Figure 1), now recognized by several groups [Charra et al. 1998, Khosla and Johnson 2004, Shaldon 2002, 2005], was associated with a further reduction in blood pressure which was not associated with a further reduction in extracellular water. It was manifested by a reduction in peripheral resistance with a maintenance of cardiac output and an absence of postural hypotension after dialysis [Luik et al. 1988]. The possible explanation for this lag phenomenon may be linked to the reduction of non-osmotically active sodium which is potentially bound in the interstitial matrix lining the intimal surfaces of blood vessels containing proteoglycans and glycosaminoglycans [Ritz 2006, Titze et al. 2004]. This sodium store leaks out slowly and takes months to become normal if the patient is maintained on 5 g of salt intake per day [Heer et al. 2000]. Meanwhilst, it maybe associated with activation of the inflammatory cascade beginning with phosphorylation of hyperosmolarity glycerol HOG1 stress-associated protein or MAPK38 (mitogen-activated protein kinase). This sequence can lead to an inhibition of nitric oxide synthetase and an increase in asymmetric dimethylarginine (ADMA) and at the same time stimulates the formation of TGFb and the inflammatory cascade [Fujiwara et al. 2000, MacAllister et al. 1996, Sanders 2004, Shapiro and Dinarello 1995]. Reversal of these pathways occurs with a reduction of the excess sodium stored in non-osmotically active sites by means of a diet restricted in salt to 5 g per day or less. Attempts to achieve this “desalting” by lowering dialysate sodium concentration without a low dietary salt intake may lead to severe complications during dialysis. However, a reduction of the sodium content of the dialysate to below 137 mmol/l is recommended after the lag phenomenon has been observed as symptomatic dialysis hypotension rarely occurs.

S. Shaldon, MonacoCorrespondence to:
S. Shaldon, MD, FRCP
25 Le Michelangelo
7 Avenue de Papalins
Monaco 98000, Monaco
Email: stanley.shaldon@libello.com

Abstract

M. Rodríguez-Morán¹,², G. González-González³, M.V. Bermúdez-Barba³, C.E. Medina de la Garza³, H.E. Tamez-Pérez³, F.J. Martínez-Martínez³ and F. Guerrero-Romero¹,²

¹Medical Research Unit in Clinical Epidemiology of the Mexican Social Security Institute, ²Research Group on Diabetes and Chronic Illnesses, Durango, and ³Faculty of Medicine University of Nuevo Leon, Mexico
Aims: The purpose of this study was to identify the effect of pentoxifylline on the urinary protein excretion profile in type 2 diabetic patients. Methods: 40 type 2 nonhypertensive diabetic patients were randomly allocated to receive either pentoxifylline 400 mg t.i.d. or placebo daily for 16 weeks. Eligible subjects were those with urinary albumin excretion between 20 and 200 mg/min. Subjects receiving angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), calcium antagonists, and diuretics as well as those with reduced renal function, pregnancy, urinary tract infection, and smoking were not included. A 6-month pretreatment stabilization phase aimed to reduce and stabilize fasting serum glucose levels was carried out. Urinary proteins were identified by electrophoresis, and immunodetection was identified by Western blot. Electrophoretic analysis was performed using molecular weight markers of 150, 132, 77, and 66 kDa to identify high-weight proteins, and 54, 41, 36, 27, 21, 14.3, and 12 kDa to identify low-weight proteins. Results: At baseline, subjects in both groups who showed a glomerular tubular pattern did not differ in their urinary excretion profile. The urinary proteins identified were immunoglobulin G, ceruloplasmin, transferrin, and albumin (glomerular pattern) as well as a1-antitrypsin, a1-acid glycoprotein, collagenase inhibitor, a1-microglobulin, trypsin inhibitor, lysozyme, and b2-microglobulin (tubular pattern). Subjects who received pentoxifylline had reduced urinary excretion of high- and low-molecular weight proteins. Conclusions: Urinary protein excretion in type 2 diabetic subjects shows a mixed, glomerular and tubular, pattern. Pentoxifylline reduces the excretion of both high and low molecular-weight urinary proteins.Correspondence to:
M. Rodríguez-Morán, MD, MSc, PhD

Siqueiros 225 esq./Castañeda

34000 Durango, Dgo., Mexico
Email: rodriguez_moran@hotmail.com

Abstract

D. Lorber and D. Reddan

¹Division of Endocrinology, New York Hospital Queens, Flushing, NY, USA, ²Division of Nephrology, University College Galway, Unit ¹ Merlin Park Hospital, Galway, Ireland
Aims: Diabetes is the leading cause of chronic kidney disease (CKD) in the United States, and cardiac disease is the primary cause of death in patients with CKD and diabetes. The Prevalence of Anemia in Early Renal Insufficiency (PAERI) study evaluated the prevalence of anemia and associated comorbidities in a community-based sample of patients with CKD. The purpose of this post hoc analysis was to identify differences, if any, in the prevalence and severity of anemia (hemoglobin £ 12 g/dl (120 g/l)) and other clinical characteristics between CKD patients with diabetes and patients with CKD who did not have diabetes. Materials and methods: The PAERI study was a prospective, cross-sectional, multicenter survey. Eligible patients were ³ 18 years old with CKD, defined as serum creatinine 1.5 – 6.0 mg/dl (132.6 – 530.4 mmol/l) in females and 2.0 – 6.0 mg/dl (176.8 – 530.4 mmol/l) in males within 12 months before enrollment. Study duration for each patient was a single site visit. Results: Of the original 5,222 patients enrolled, 3,361 had diabetes and 1,861 did not. A family history of diabetes was present in 72.7% of diabetic patients vs. 27.2% of nondiabetic patients (p < 0.0001). Patients with diabetes had a significantly higher prevalence of anemia (52.7 vs. 39.4%, p < 0.0001) and cardiac disease (55.7 vs. 42.9%, p < 0.0001). The prevalence of hypertension was high in both groups (91.5 and 89.3%). Significantly more diabetic patients than nondiabetic patients received angiotensin-converting enzyme inhibitors (60.4 vs. 43.8%, p < 0.0001). Hyperlipidemia was more common in patients with diabetes (73.9 vs. 55.4%, p < 0.0001). Patients with diabetes were slightly younger and had a significantly higher mean body mass index and lower transferrin saturation compared with nondiabetic patients. In diabetic and nondiabetic patients, more than 97% had glomerular filtration rate < 60 ml/min/1.73 m2 and more than 70% had serum creatinine < 2.5 mg/dl (221.0 mmol/l). Conclusions: These findings underscore the extent and severity of concurrent illnesses in patients with both diabetes and CKD. In those patients, diabetes was associated with a greater prevalence of serious cardiac-related comorbidities than observed in nondiabetic patients.
Correspondence to:
D. Lorber, MD, FACP, CDE

Director, Division of Endocrinology

New York Hospital Queens

59-45 161st Street

Flushing, NY 11365, USA
Email: lorberdan@aol.com

Abstract

W.C. Lin, Y. Yang, Y.K. Wen and C.C. Chang

¹Department of Internal Medicine, Division of Nephrology, Changhua Christian Hospital, Changhua, ²Institute of Environmental Health, China Medical University College of Public Health, Taichung, Taiwan
Objective and methods: There is a growing interest in the safety and efficacy of percutaneous kidney biopsy for outpatients in Taiwan. We conducted a retrospective study for patients receiving the biopsy in 2002 and 2003. Complication and mortality associated with the biopsy were compared between 147 inpatients and 183 outpatients who had been judged to need no hospitalization. All biopsies were performed using the ultrasound guidance and an automated spring-loaded biopsy device. Results: There were no death and no significant difference in complication rates between the two groups. No delayed gross hematuria, delayed pain, fever or biopsy site bleeding developed in outpatients, who were followed-up by telephone contacts for 1 – 5 days after they had been discharged. Both outpatients and inpatients with hematoma were younger than those without (p < 0.05). Template bleeding time was longer for inpatients with hematuria compared with inpatients without (12.0 vs. 5.8 minutes in average, p = 0.036), but not for outpatients (4.5 vs. 6.0 minutes in average, p = 0.282). There were moderate differences in platelet count between outpatients with hematuria and those without (p = 0.057), and in serum creatinine between inpatients with hematuria and those without (p = 0.069). Conclusion: The outpatient renal biopsy appears to be equally as safe and efficient as the inpatient biopsy. However, we suggest checking template bleeding time and platelet count before biopsy for patients with clinical bleeding tendency, such as patients with a serum creatinine level over 4 mg/dl (approaching CKD stages IV, V) due to a higher risk of prolonged bleeding time. Outpatient biopsy with a 6-hour inpatient observation can be considered as a medically adequate procedure.Correspondence to:
Y. Yang, MD, Director

Division of Nephrology

Department of Internal Medicine

Changhua Christian Hospital

135 Nansiao Street

Changhua 500, Taiwan
Email: 2219@cch.org.tw

Abstract

J.-M. Chang, M.-C. Kuo, H.-M. Chen, C.-H. Lee, Y.-H. Lai, H.-C. Chen and S.-J. Hwang

¹Department of Internal Medicine, Division of Nephrology, Kaohsiung Medical University Chung-Ho Memorial Hospital, ²Department of Internal Medicine, Faculty of Medicine, College of Medicine, ³Department of Surgery, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
Objective: Parathyroid cells synthesize and release endothelin-1 (ET-1). ET-1 displays an in vitro inhibitory effect on basal parathyroid hormone (PTH) secretion and also counteracts PTH hypersecretion stimulated by low calcium. Such effects are further demonstrated in vivo, independent of the changes in calcitonin. We propose that ET-1 may regulate the pathogenesis of uremic hyperparathyroidism. However, this was not directly demonstrated in human parathyroid glands. Design: Hyperplastic parathyroid glands are obtained from the surgical operation for uremic hyperparathyroidism. Cells are isolated by enzyme digestion and treated with ET-1, and are assessed for PTH mRNA expression. PTH in the plasma and the medium is measured by a newly developed method to detect the whole PTH (1-84). Patients: Uremic patients with severe secondary hyperparathyroidism and ultrasonography-proved hypertrophy of parathyroid glands received elective surgical approaches under general anesthesia. The resected glands were immediately taken to the laboratory for fresh isolation. Measurements: Following ET-1 treatment, PTH mRNA expression is evaluated by RT-PCR method. ET-1 is detected with radioimmunoassay kit and PTH is measured by a new commercially available Duo PTH kit. Results: ET-1 exhibited a dose-dependent inhibitory effect (from 10–12 – 10–7 M) on PTH mRNA expression of parathyroid cells, either in the basal or in the low-calcium-stimulated states. Release of PTH into the medium is also gradually inhibited by the increase in ET-1 concentrations. Conclusions: Our results demonstrate that ET-1 attenuates PTH mRNA expression in freshly isolated human parathyroid cells, and PTH release is also decreased. This result is consistent with our previously reported in vitro and in vivo experiments. Correspondence to:
S.-J. Hwang, MD

Division of of Nephrology

Kaohsiung Medical University

100 Shih-Chuan 1st Rd, Kaohsiung 807, Taiwan
Email: sjhwang@kmu.edu.tw

Abstract

S. Cottone, A. Palermo, F. Vaccaro, A. Vadala, B. Buscemi and G. Cerasola

Dipartimento di Medicina Interna, Malattie Cardiovascolari e Nefro-Urologiche, Divisione di Medicina Interna, Nefrologia ed Ipertensione, Cattedra di Medicina Interna, Universitá di Palermo, Italy
Introduction: Several studies have shown that chronic renal failure (CRF) is characterized by “accelerated atherosclerosis”. More recent studies emphasize that inflammation and oxidative stress play a central role in atherosclerosis, and it is well-established that C-reactive protein (CRP) is a cardiovascular risk marker in the general population, in end-stage renal disease (ESRD) patients and in allograft recipients. Methods: We measured the serum concentration of high sensitivity CRP, TNFa, 8-iso-prostaglandin F2a (8-iso-PGF2a, an in vivo oxidative stress marker) in 15 CRF patients and in 15 transplant recipients. Exclusion criteria were age < 30 and > 65 years, smoking, diabetes mellitus and history of cardiovascular diseases. Immunosuppressive therapy was not withdrawn, and antihypertensive treatment was the same for both groups. Systolic (SBP) and diastolic blood pressure (DBP), serum creatinine (sCr) and estimated glomerular filtration rate (GFR) were also evaluated. 15 healthy subjects were enrolled as controls. Results: The transplanted group showed significantly higher values than controls of CRP (p < 0.05), TNFa (p < 0.05), 8-iso-PGF2a (p < 0.05). The CRF group as well exhibited, in comparison with controls significantly higher concentrations of CRP (p < 0.05), TNFa (p < 0.05), and 8-iso-PGF2a (p < 0.05). SBP, DBP and sCr were not different between transplanted and CRF patients. CRP was higher in transplant recipients than in CRF patients (p < 0.05). No difference in TNFa levels between the 2 groups was found. 8-iso-PGF2a was significantly higher in CRF than in the transplanted group (p < 0.05). In this latter, 8-iso-PGF2a showed a positive correlation with TNFa (p < 0.001), sCr (p < 0.001), SBP (p < 0.05) and DBP (p < 0.05). In the same group both 8-isoPGF2a and TNFa were negatively correlated with GFR (r = –0.873 and –0.912, respectively, p < 0.001 for both). Conclusion: Our data have shown the coexistence of an increased oxidative stress and an inflammatory state in long-term renal graft recipients. Correspondence to:
S. Cottone, MD

Via del Vespro 129

90127 Palermo, Italy
Email: sancott@tin.it

Abstract

M.J. Koziolek, S. Gauczinski, E. Kahler, C.P. Bramlage, A.K. Scheel, G.A. Mueller and F. Strutz

¹Department of Nephrology and Rheumatology, ²Department of Medical Statistics, Georg August University Göttingen, Germany
Background: Intradialytic hypotension (IDH) is one of the most severe complications during hemodialysis. Its appearance is caused in part by rapid fluid removal with concomitant failure in blood pressure regulation but also by other dialytic-dependent and independent factors. Patients and methods: We investigated total (TBW), extracellular (ECW) and intracellular water (ICW) in chronic intermittent hemodialysis dialysis hypotension-prone (CRF-HP, n = 11) and nonhypotension-prone (CRF-NHP, n = 10) patients with end-stage renal disease before, every 30 minutes during, as well as after dialysis and within onset of intradialytic hypotension by multifrequent bioimpedance analysis (BIA). Additionally, intradialytic time course of BIA in patients with acute renal failure (ARF) and septic shock (n = 10) was observed. Results: IDH occurred in 72.1% of CRF-HP and in 80% of ARF patients. In CRF-HP and CRF-NHP, ECW significantly decreased by –12.44 ± 4.22% in CRF-HP and –9.0 ± 6.2% in CRF-NHP comparing pre- and post-dialysis values (each p < 0.01). Conversely, ICW increased by +11.5 ± 11.3% in CRF-HP and +18.4 ± 25.2% in CRF-NHP (each p < 0.05). In patients with ARF no significant changes could be detected. Calculated ECW/ICW and ECW/TBW ratio significantly decreased in CRF patients with a higher rate in CRF-HP patients (p < 0.05). Neither ECW/ICW nor ECW/TBW ratio correlated with mean arterial pressure. The onset of intradialytic hypotension (n = 35) did not differ intraindividually compared to normotensive periods (n = 411). Fluid removal in CRF patients seems to be mainly from the extracellular space. The reduced decreases in ECW/ICW and ECW/TBW ratios in CRF-HP compared to CRF-NHP may indicate an insufficient refilling from intra- to extracellular compartment in CRF-HP. Conclusion: In conclusion, multifrequent BIA is not capable to predict hypotension in the individual patient during a particular dialysis session. Correspondence to:
M. Koziolek, MD
Abteilung für Nephrologie und Rheumatologie
Georg-August-Universität Göttingen
Robert-Koch-Straße 40
37075 Göttingen, Germany
37075 Göttingen, Germany

37075 G�ttingen, Germany
Email: mkoziolek@med.uni-goettingen.de

Abstract

A. Casquero, A. Ramos, A. Barat, F. Mampaso, C. Caramelo, J. Egido and A. Ortiz

¹Internal Medicine, ²Division of Nephrology and Hypertension, ³Pathology, Jiménez Díaz Foundation, Autonomous University of Madrid, Reina Sofía Institute of Nephrological Investigations, and ⁴Ramon y Cajal Hospital, Alcala University, Madrid, Spain
Recurrent acute postinfectious glomerulonephritis is infrequent in childhood and exceptional in adults. The factors that determine recurrence are poorly understood. Selective IgA deficiency is characterized by an increased incidence of gastrointestinal and respiratory infections. The case of a 33-year-old man with a history of repetitive sinopulmonary infections and diagnosed with selective IgA deficiency is described. He suffered 2 episodes of postinfectious glomerulonephritis within a 15-year period. Selective IgA deficiency may have predisposed to the development of recurrent postinfectious glomerulonephritis.Correspondence to:
A. Ortiz, MD, PhD
Associate Chief of the Nephrology Division
Dialysis Unit, Jiménez Díaz Foundation
Avda Reyes Católicos 2
28040 Madrid, Spain
Email: aortiz@fjd.es

Abstract

M. Cobo, D. Hernández, C. Rodriguez and L. Pérez-Tamajón

Department of Nephrology, Hospital Universitario de Canarias, Tenerife, The Canary Islands, Spain
We present the case of a 57-year-old man with nephrotic syndrome secondary to idiopathic membranous glomerulonephritis unsuccessfully treated with angiotensin-converting enzyme inhibitor (ACEI), angiotensin II receptor antagonist (ARA), prednisone and chlorambucil. After treatment with rituximab, we observed a progressive decrease of proteinuria and normalization of serum albumin. 18 months after treatment, he remained in remission. No adverse reactions to rituximab were noted throughout follow-up.Correspondence to:
M. Cobo Caso, MD
Department of Nephrology
University Hospital of the Canary Islands
Ofra s/n 38320-La Laguna
Tenerife, The Canary Islands, Spain
Email: macobo@comtf.es

Abstract

Y.K. Wen and M.L. Chen

¹Division of Nephrology, Department of Medicine, ²Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan
Hemolytic-uremic syndrome (HUS) is a rare complication occurring in solid-organ and bone marrow transplant recipients treated with calcineurin inhibitors cyclosporine or tacrolimus. We report here about a 30-year-old female cadaveric renal transplant recipient receiving cyclosporine who developed HUS in the early post-transplant period. Renal allograft biopsy specimens showed the characteristic features of thrombotic microangiopathy and acute cyclosporine nephrotoxicity. Cyclosporine was discontinued and the patient was switched to tacrolimus in conjunction with plasma exchange. Unfortunately, plasma exchange was interrupted by bleeding complication resulting from placement of double-lumen catheter. Intravenous immunoglobulin (IVIG) was then administrated as an alternative therapy. Hematological resolution occurred promptly and renal function recovered uneventfully. Our presenting case suggests the beneficial effect of IVIG on cyclosporine-associated HUS.Correspondence to:
Dr. Y.K. Wen Division of Nephrology Department of Medicine Changhua Christian Hospital 135 Nansiao St. Changhua, 500, Taiwan
Email: 45440@cch.org.tw

Abstract

I. Pela, S. Gasperini, E. Pasquini and M.A. Donati

¹Pediatric Nephrology Unit, ²Metabolic Diseases Unit, Department of Pediatrics, Pediatric University of Florence, Firenze, Italy
The patients affected by vitamin B12-unresponsive methylmalonic acidemia (MMA) on the long run develop chronic renal disease with interstitial nephropathy and progressive renal insufficiency. The mechanism of nephrotoxicity in vitamin B12-unresponsive MMA is not yet known. Chronic hyporeninemic hypoaldosteronism has been found in many cases of methylmalonic acidemia, hyperkalemia and renal tubular acidosis type 4. We report 2 patients affected by B12-unresponsive methylmalonic acidemia diagnosed at the age of 23 months and 5 years, respectively, with normal glomerular filtration and function. They showed hyporeninemic hypoaldosteronism and significant hyperkalemia requiring sodium potassium exchange resin (Kayexalate) therapy after an episode of metabolic decompensation leading to diagnosis of MMA. In both children, hyporeninemic hypoaldosteronism and hyperkalemia disappeared after 6 months of good metabolic control.Correspondence to:
I. Pela, PhD Associate Professor Pediatric Nephrology Department of Pediatrics University of Florence Via Luca Giordano 13 50132 Firenze, Italy
Email: vana.pela@unifi.it

Abstract

C.A. Benavides, Z. Csapo, K. Timmins, L. Holley, S.M. Katz, C.T. Van Buren and B.D. Kahan

¹Division of Immunology and Organ Transplantation, University of Texas Medical School at Houston, ²Division of Nephrology, St. Luke’s Episcopal Hospital, Fannin, ³Division of Pathology, St. Luke’s Episcopal Hospital, Houston, TX, USA
We report the extremely rare recurrence of intimal fibroplasia, a rare form of fibromuscular dysplasia, in a kidney recipient at 6 months after transplantation from a living-related donor. The patient was successfully treated and maintains good kidney function, however, the case raises the question of whether kidneys with fibromuscular dysplasia should be included in the expanded criteria for kidney transplantation.Correspondence to:
Carlos Benavides
University of Texas Medical School at Houston
6431 Fannin, MSB 6.240
Houston, TX 77030, USA
Email: benavides.carlos@javeriana.edu.co

Abstract

M. Rho and J. Renda

Abstract

T. Fujita, A. Satomura and K. Matsumoto

Abstract

G. Efstratiadis, G. Tsiaousis, M. Leontsini, L. Gionanlis, A. Papagianni and D. Memmos

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Volume 66, No. 1/2006(July)