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Abstract

H. Nonoguchi, S. Kiyama, H. Inoue, Y. Nakayama, T. Inoue, Y. Kohda, K. Machida, A. Tajima, K. Kitamura, T. Miyoshi, H. Shimada, H. Shimada, M. Tajiri, Y. Honda, M. Tanaka and K. Tomita

¹Third Department of Internal Medicine, Kumamoto University School of Medicine, ²Department of Nephrology and Urology, Saiseikai Kumamoto Hospital, ³Shimada Hospital, ⁴Kumamoto Daiichi Clinic, ⁵Kengun Clinic, and ⁶Akebono Clinic, Kumamoto, Japan
Aims: Withdrawal of angiotensin-converting enzyme (ACE) inhibitors may affect the progression of chronic renal failure and an insertion/deletion (I/D) polymorphism of the ACE gene may influence it. Methods: We retrospectively collected patients with chronic glomerulonephritis and benign nephrosclerosis who discontinued ACE inhibitor use. The relationship between the decline of renal function after the withdrawal and the influencing factors such as ACE gene polymorphism, blood pressure and proteinuria were evaluated using multiple regression analysis. Results: Forty-two patients (initial serum creatinine 0.5 – 6.5 mg/dl) had been treated and discontinued ACE inhibitor use. Only patients with the II or DI genotypes of the ACE gene developed the deterioration of renal function, starting at 2 months after the withdrawal. Stepwise regression analysis revealed that the level of proteinuria after the withdrawal, presence of the insertion of ACE gene and serum creatinine level at the time of withdrawal mainly influenced the decline of renal function after the withdrawal (adjusted R2 = 0.48). Conclusion: Withdrawal of ACE inhibitor causes the deterioration of renal function in patients with the II or DI genotypes, high proteinuria after the withdrawal, and high serum creatinine level at the withdrawal, which probably causes the rebound increase in serum ACE activity.

Abstract

J.A. Schwimmer, G.S. Markowitz, A.M. Valeri, L.J. Imbriano, R. Alvis and V.D. D?Agati

¹Department of Medicine, ²Department of Pathology, Columbia University College of Physicians and Surgeons, New York, NY, ³Department of Medicine, SUNY at Stony Brook School of Medicine, Mineola, NY, and ⁴Department of Medicine, White Plains Hospital Cente
Background: Secondary focal segmental glomerulosclerosis (FSGS) is a pattern of glomerular injury mediated by hyperfiltration and other adaptive structural-functional responses. We describe 3 non-obese patients with elevated body mass index (BMI) owing to increased muscle mass who had renal biopsy findings favoring a form of secondary FSGS. Methods: Clinical and pathologic data were obtained on 3 patients with 1) renal biopsy findings of focal segmental and/or global glomerulosclerosis with glomerulomegaly; 2) BMI ³ 30; 3) body fat percentage < 20%; 4) “highly muscular” appearance, and 5) proteinuria ³ 1 g/d without nephrotic syndrome. 24-hour urine creatinine excretion was used to estimate lean body mass and percentage body fat. Results: The 3 patients were males (age 38 – 48 years) employed in jobs requiring strenuous physical activity. BMIs ranged from 30.4 – 32.1 kg/m2 with body fat percentages of 12.9 – 16.8%. Creatinine clearances at time of biopsy ranged from 113 – 208 ml/min. Renal biopsies showed focal segmental and/or global glomerulosclerosis affecting a minority of glomeruli with glomerular hypertrophy and minimal (mean 15%) foot process effacement. Treatments included angiotensin-converting enzyme inhibitor, angiotensin II receptor blocker, or weight loss. Over a mean follow-up time of 24.3 months, serum creatinine remained stable and proteinuria decreased in all patients. Conclusions: Non-obese patients with increased BMI due to elevated muscle mass are at risk of developing a secondary form of FSGS that resembles obesity-related glomerulopathy.

Abstract

M.J. Kemper, T. Meyer-Jark, M. Lilova and D.E. Müller-Wiefel

Pediatric Nephrology, University Children?s Hospital, Hamburg, Germany
Background: Growing evidence shows that steroid-sensitive nephrotic syndrome (SSNS) is the result of a primary T-cell disturbance and leads to secondary anatomical and functional, however, not to immunological glomerular changes. In addition, immunoglobulin abnormalities in SSNS indicate a role of B-cell involvement. Patients and methods: We therefore analyzed T- and B-cell activation markers in children with SSNS at different stages of the disease including different treatment regimens by measuring the soluble IL-2 receptor (sCD25) and the soluble low-affinity IgE receptor (sCD23), respectively. Seventy-five patients with SSNS (median age 8.0, range 2.5 – 18 years) were studied, 33 in relapse (RL) including 21 patients relapsing during alternate-day steroids (RL-SD). Forty-two patients were studied in remission (RM; 14 off treatment and 28 on alternate-day steroids (RM-AD)) and 22 age-matched children served as controls. Results: Serum concentrations of sCD25 were increased in RL (113.6 ± 19.5 mmol/l) compared to RM (79.8 ± 8 mmol/l, p < 0.02) and controls (74.8 ± 0.9 mmol/l, p < 0.02). Patients with RL-SD did not have elevated sCD25. In relapse, sCD25 was inversely correlated with age (R = –0.36, p < 0.04) and positively correlated with total IgG (R = 0.37, p < 0.04). Urinary excretion of sCD25 was also significantly elevated in RL of SSNS compared to RM and controls (71.2 ± 11.9 mmol/g creatinine vs. 39.1 ± 4.8 and 32.0 ± 4.2 mmol/g, p < 0.05). Serum levels of sCD 23 were significantly elevated in RL (6.22 ± 0.65 mg/l) compared to RM (3.1 ± 0.83 mg/l, p < 0.02) and to controls (3.4 ± 0.93 mg/l). The highest values, however, were found in RL-SD (7.8 ± 1.7 mg/l) vs. untreated RL (p < 0.007) and RM-AD (p < 0.002). In untreated RL there was a significant correlation of sCD23 and total IgE (R = 0.67, p < 0.02) and in RL-SD with total IgG (R = 0.45, p < 0.05). sCD23 and sCD25 were not correlated with each other. Conclusion: These data document parallel abnormalities of both CD23-mediated B as well as CD25-mediated T-cell activation and suggest that SSNS is not solely a disorder of T-cell dysfunction.

Abstract

A.-M. Teppo, T. Törnroth, E. Honkanen and C. Grönhagen-Riska

Department of Medicine, Division of Nephrology, Helsinki University Hospital, Helsinki, Finland
Aim: Since the elevated concentration of serum C-reactive protein (CRP) is a sensitive indicator of underlying inflammation, we investigated the association between serum CRP during the initial 6 post-transplantation months and histopathological changes in the 6-month protocol biopsies in 79 patients. We stained the biopsies for CRP and C3 to elucidate a possible role of CRP in renal injuries. Results: Forty patients showed no or minimal (Grade 0 – 1) tubular atrophy or interstitial fibrosis and 39 patients mild to moderate (Grade ³ 2) chronic histopathological changes. The latter group had had higher concentration of CRP during the first 6 post-transplant months. Because the histopathological changes predict poor long-term prognosis, we followed – from 6th month onwards – 40 patients who had no or minimal histopathologic changes, and analyzed the association between CRP elevation and development of chronic allograft dysfunction. During this follow-up period (mean 51, range 14 – 72 months), 23 of 40 patients retained normal CRP level (Group A, mean CRP 1.12 mg/l), and 17 patients had elevated CRP concentrations (Group B, mean CRP 4.16 mg/l); 24-hour creatinine clearance improved or remained the same in all Group A patients, whereas it decreased in 7 of 17 (41%) of Group B patients (p < 0.001). In Group B patients, the annual change of creatinine clearance correlated inversely with the mean CRP concentration (r = –0.682, p < 0.01). Conclusion: Our results show that histological changes in 6-month biopsies were more prominent in patients with more transplantation-associated complications, infections and frequently higher CRP levels during the initial 6 post-transplant months than in those with lower CRP levels. During post-biopsy follow-up, we found low-grade systemic inflammation – measured as elevated CRP – to associate with impairment of graft function in patients with no or minimal histological findings in 6-month biopsies, and permanently low CRP to rule out chronic allograft dysfunction.

Abstract

B. Zhang, S. Eto, P. Fan, C. Bian, E. Shimoji, T. Saito and K. Saku

Departments of ¹Cardiology and ²Nephrology, Fukuoka University School of Medicine, Fukuoka University, Fukuoka, Japan
Patients with diabetic nephropathy have an increased risk of coronary heart disease (CHD). Paraoxonase (Pon1) is a high-density lipoprotein- (HDL) associated enzyme that protects low-density lipoprotein from oxidation and also protects against atherosclerosis. We investigated the relationship of serum Pon1 activity, Pon1 Q192R polymorphism and HDL-C level to type 2 diabetes mellitus (DM) in patients on maintenance hemodialysis (HD). DM patients (n = 56, F/M = 17/39, aged 64.5 ± 7.5 years) and non-DM patients (n = 89, F/M = 28/61, aged 62.7 ± 8.3 years) under HD were included in this study. Salt-stimulated serum Pon1 activities were measured using paraoxon as a substrate. Pon1 Q192R polymorphism was detected by the mutagenically separated polymerase chain reaction. DM patients on HD had significantly lower HDL-C levels and serum Pon1 activities than non-DM patients on HD (657 ± 277 vs. 763 ± 257 IU/l, p < 0.01). The distribution of Pon1 Q192R genotypes in all subjects did not differ from that predicted from the Hardy-Weinberg equilibrium. Serum Pon1 activities in both DM and non-DM patients on HD were regulated by Pon1 Q192R polymorphism: RR > QR > QQ. However, the reduced Pon1 activities in DM patients on HD were related to DM independent of the Pon1 genotype: reduced Pon1 activity was related to DM in RR carriers. Serum Pon1 activities were positively correlated with HDL-C levels. The association between HDL-C and DM in hemodialyzed patients was independent of Pon1 activity as assessed by an analysis of variance. But the relation between Pon1 activity and DM was modified by HDL-C levels: significantly when HDL-C was below 50 mg/dl, but not significantly when HDL-C was above 50 mg/dl. The results of a logistic regression analysis show that reduced serum Pon1 activities and low HDL-C levels were additively associated with DM. In conclusion, Pon1 status and HDL levels are independently associated with DM in patients on hemodialysis and may contribute to the increased risk of CHD in diabetic nephropathy.

Abstract

K.M. Chow, C.C. Szeto and P.K.-T. Li

Department of Medicine and Therapeutics, Division of Nephrology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong SAR, China
Background: Pulse pressure, a surrogate for arterial stiffness, has been shown to have substantial impact on predicting patient mortality. Excess cardiac risk in the end-stage renal disease population could be mediated by elevated arterial stiffness, which might in turn result from secondary hyperparathyroidism and abnormal calcium metabolism. Methods: A cross-sectional study was carried out to examine a possible relationship between pulse pressure and secondary hyperparathyroidism among 126 prevalent patients undergoing continuous ambulatory peritoneal dialysis. Results: The mean values for calcium and intact parathyroid hormone level were 2.48 mmol/l and 50.5 pmol/l, respectively. No correlation was found between pulse pressure and the plasma PTH levels (r = –0.15, p = 0.11) or calcium-phosphorus product (r = –0.08, p = 0.38). In a multivariate regression analysis, on the other hand, elevated pulse pressure was directly associated with age (2.1 mmHg per 10-year increase) and the presence of diabetes mellitus (6.9 mmHg) (both p < 0.001). Pulse pressure was also inversely associated with hemoglobin level. Conclusion: The magnitude of arterial pulse pressure in a peritoneal dialysis population was not significantly affected by parathyroid disease and alterations in mineral metabolism with end-stage renal disease. In agreement with similar observations in hemodialysis populations, it is postulated that abnormalities in conduit vessel stiffness (as measured by pulse pressure) are substantially caused by atherosclerosis, in which intimal calcification (as distinct from medial calcification in the context of hyperparathyroidism) plays a more important role.

Abstract

J.H. Crabtree and N.A. Garcia

¹Department of Surgery and ²Division of Infectious Disease, Department of Medicine, Southern California Permanente Medical Group, Kaiser Permanente Bellflower Medical Center, Bellflower, California, USA
Background: Regarded as normal flora of the human skin and mucus membranes, non-diphtheria corynebacteria are frequently dismissed as contaminants or harmless colonizers. Recently, the pathogenic potential of C. striatum has been realized in immunocompromised patients with indwelling medical devices and previous antibiotic exposure. Objective: We report here the diagnosis, treatment and clinical outcome of a peritoneal dialysis patient with a C. striatum infection of the catheter exit site. The aim is to present important features to assist in identifying clinically significant infections and provide guidelines for treatment. Results: An immunocompromised patient with previous antimicrobial exposure developed an acute dialysis catheter exit site infection. C. striatum was isolated in pure growth. After initial treatment failure with oral antibiotics and intensified wound care, a satisfactory outcome was ultimately achieved without relapse or loss of the catheter with a 1-month course of vancomycin, 1 g intravenously, administered at 5-day intervals. Conclusions: The virulent capacity of Corynebacterium species should not be underestimated, particularly in high-risk patients. The presence of clinical signs of infection with isolation of the organism in pure culture and the presence of Gram-positive rods on direct Gram stain, especially in association with a leukocyte reaction, supports a cause and effect relationship. Because corynebacteria may be multiresistant, susceptibility testing should be performed on clinically significant isolates. Initial antibiotic selection is influenced by the severity of the infection, however, current experience favors vancomycin in significant infections.

Abstract

Y. Kaneko, Y. Kamijo, N. Kobayashi, M. Higuchi, T. Ehara, K. Hora, H. Shigematsu and K. Kiyosawa

¹Second Department of Internal Medicine, ²Department of Pathology, and ³Division of Blood Purification, Shinshu University School of Medicine, Matsumoto, Japan
It is known that nephrotic syndrome rarely accompanies myeloperoxidase-specific antineutrophil cytoplasmic antibody- (MPO-ANCA) related glomerulonephritis. We present a case of younger onset MPO-ANCA-related glomerulonephritis accompanied with nephrotic syndrome in a female patient. It was diagnosed through the renal biopsy and the detection of a high titer of MPO-ANCA and steroid therapy (intravenous steroid pulse therapy and oral administration), anticoagulant therapy and antiplatelet therapy were initiated. Since her nephrotic syndrome persisted in spite of the decrease of MPO-ANCA, we conducted a second renal biopsy. We found active necrotizing crescentic glomerulonephritis with a small deposition of immunoglobulin and fibrinogen on the glomeruli. To suppress her disease activity, we administered second steroid-pulse therapy and MPO-ANCA titer disappeared. However, as her nephrotic syndrome, which was accompanied by severe hyperlipidemia, persisted, we tried to treat her using low-density lipoprotein (LDL) apheresis. It was effective temporarily, but she finally fell into end-stage renal failure. We discuss here the possibility of double nephropathy by considering her clinical and renal pathologic features.

Abstract

J. Suzuki, S. Suzuki, R. Nozawa, Y. Kawasaki and H. Suzuki

Department of Pediatrics, Fukushima Medical University, School of Medicine, Fukushima, Japan
A 10-year-old female patient was found positive for urine protein and occult blood on Japanese school urinary screening. Examination of the blood was normal except low values of the complement system with CH50 13.5 U/ml, C3 45 mg/dl and C4 3 mg/dl. Renal biopsy demonstrated a focal membranoproliferative glomerulonephritis (MPGN). As for the activity of each component of the complement in the early stage of the disease, the C4 activity was markedly declined and the activity of classical pathway component was also decreased, but the activity of alternative pathway component was normal. On the HLA examination, the patient demonstrated a C4 double null haplotype (C4A2, Q0, BQ0 phenotype). A null C4 gene at both the C4A and C4B loci was found in her mother, aunt and grandfather on the mother’s side and C4B null allele in her father and her grandmother on the mother’s side. The development of the disease is found in 1 case and not in the other, although both have the genetic defect and the mechanism by which the complement is activated remains unknown. Thus, there appear to be many subjects to be studied as to the relationship between the defect of C4 gene and immune competence.

Abstract

A. Komatsuda, H. Wakui, H. Ohtani, N. Maki, T. Nimura, H. Takatsu, A. Yamaguchi, H. Imai and K. Sawada

¹Third Department of Internal Medicine, Akita University School of Medicine, and ²Department of Internal Medicine, Senboku General Hospital, Akita, Japan
A 53-year-old man developed chronic renal failure during a protracted course of sarcoidosis. A renal biopsy showed Congo red-positive homogenous deposits in the subendothelial space of glomerular capillary walls and arterial walls. On electron microscopy, amyloid fibrils were observed in the deposits. Immunohistochemistry showed positive staining for amyloid A (AA) protein. Treatment with prednisolone resulted in poor response, followed by progressive deterioration of renal function requiring hemodialysis. To our knowledge, there are 5 cases with histologically proven renal amyloidosis accompanied by sarcoidosis. Prognosis in these patients is extremely poor. AA-type amyloidosis should be considered as a rare renal complication in the setting of long-standing sarcoidosis.

Abstract

A. Ersoy¹, M. Güllülü¹, M. Usta¹, T. Özçelik², E. Ylmaz³, E.K. Uzaslan⁴, H. Vuruskan⁵, M. Yavuz¹, B. Oktay⁵, K. Dilek¹ and M. Yurtkuran¹

Divisions of ¹Nephrology, ²Hematology, ³Infection and Microbiology,
⁴Chest Diseases and Tuberculous, and ⁵Urology, Uludag School of Medicine, Bursa, Turkey
Visceral leishmaniasis (VL) is an acute or subacute disease that is almost invariably fatal if untreated. It is a rare disease in renal transplant recipients and frequently reported together with other infectious agents. A 39-year-old renal transplant patient was admitted to hospital for elective coronary surgery. In the post-operative period, he developed spiking fever and non-productive cough and his general condition deteriorated. While he was taking medication for non-specific pneumonia, a cavitary lesion occurred in his lung, and he had the diagnosis of pulmonary tuberculosis and antituberculous treatment was started. Despite treatment, his fever continued. As the patient developed pancytopenia and splenomegaly, a bone marrow aspiration was done. Evaluation of bone marrow aspirate indicated Leishmania parasites. He was successfully treated with a more intensive liposomal amphotericin (L-AmB). Complete cure was achieved during follow-up period of 10 months without clinical relapse. In the existence of fever and long-standing pancytopenia, VL should be suspected although the patient had another proved infection and did not live or visit an endemic area. L-AmB usage can be safely preferred for treatment of selected renal transplant recipients with VL as first-line therapy.

Abstract

S.W. Reinhold, M. Fischereder, G.A.J. Riegger and B.K.Krämer

Abstract

O. Baysal, H. Taskapan, C. Taskapan, E. Kaya, I. Sahin, H. Kirimlioglu and N. Karakas

Abstract

K.M. Chow and C.C. Szeto

Abstract

D. Goldsmith

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Volume 60, No. 4/2003(October)