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Abstract

H. Akazawa, M. Nakajima, M. Nishiguchi, Y. Yamoto, Y. Sado, I. Naito and A. Yoshioka

¹Department of Pediatrics, Nara Medical University, Kashihara City, Nara, ²Shigei Medical Research Institute, Okayama City, Okayama, and ³Department of Human Morphology, Graduate School of Medicine and Dentistry, Okayama University, Okayama City, Okayama, Japan
Aim: Thin basement membrane disease (TBMD) is characterized histologically by diffuse thinning of glomerular basement membrane (GBM). Although recent genetic analysis has shown that TBMD might be included within type IV collagen disorders, conventional immunohistochemical studies demonstrated normal labeling of type IV collagen a chains in the GBM. We have, however, successfully used confocal laser scanning microscopy to demonstrate a significantly reduced signal of type IV collagen a5 chain (a5(IV)) along capillary walls in TBMD. In order to further understand the association of type IV collagen with TBMD, we used immunoelectron microscopy to examine renal biopsies from 6 children with TBMD and six control children with minimal change nephrotic syndrome. Methods: Ultrathin sections of LR gold resin were incubated with a rat monoclonal antibody against human a1(IV), a2(IV), a3(IV), a4(IV) a5(IV) or a6(IV) followed by colloidal gold conjugated goat anti-rat IgG. After taking electron micrographs, the labeling was quantitatively evaluated in the area occupied by the segments of basement membrane. The basement membrane was divided into three equal segments viz. subepithelial side, central portion and subendothelial side. Results: In control subjects, the number of gold particles for a1(IV) or a2(IV) was significantly greater in the subendothelial side and central portion than in the subepithelial side of the GBM, whilst a3(IV), a4(IV) or a5(IV) labeling was significantly more prominent in the central portion compared to the subepithelial and subendothelial side of the GBM. TBMD samples showed a similar distribution pattern except that the subepithelial side and central portion of the GBM had a significantly reduced amount of a5(IV) antigen compared to control subjects. Conclusion: This is the first report demonstrating a diminished labeling intensity of a5(IV) in the central portion and subepithelial side of the GBM in renal biopsy specimens from patients with TBMD. These findings suggest that an abnormality of a5(IV) might possibly be associated with the pathogenesis of TBMD.Correspondence to:
M. Nakajima, MD
Department of Pediatrics
Nara Medical University
840, Shijo-cho
Kashihara City, Nara, 634-8522, Japan
Email: jintarow@naramed-u.ac.jp

Abstract

C.-C. Szeto, P.Y.-K. Poon, F.M.-M. Lai, K.-M. Chow, C.Y.-K. Szeto and P.K.-T. Li

¹Department of Medicine and Therapeutics, and ²Department of Anatomical and Cellular Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, China
Background: The histology and function of the kidney deteriorates with age and progressive renal failure, but the mechanisms involved in renal ageing are not known. In vitro studies suggest that telomere shortening is important in replicative senescence, and is accelerated by stress factors that increase replication. We investigated whether IgA nephropathy, a prototype chronic kidney disease, is associated with localized intrarenal cellular ageing. Methods: We studied the mean length of terminal restriction fragments (TRF), a measure of average telomere size, in the DNA of peripheral blood mononuclear cells and urinary sediment of 15 patients with IgA nephropathy. Results: The mean TRF lengths in peripheral blood is 7043.8 ± 1 182.8 base pairs, and in urinary sediment is 6 749.7 ± 636.5 base pairs. The mean TRF lengths of urinary DNA significantly correlate with the serum creatinine ( r = –0.525, p = 0.044) and estimated glomerular filtration rate (GFR) (r = 0.651, p = 0.009). The mean TRF lengths of urinary DNA had an insignificant inverse correlation with patient age (r = –0.364, p = 0.2), and do not correlate with the degree of glomerulosclerosis (r = 0.004, p = 0.9) or tubulointerstitial scarring in renal biopsy (r = –0.032, p = 0.9). After 30 months of follow-up, the rate of decline of estimated GFR has an inverse correlation with the mean TRF lengths of urinary DNA (r = –0.699, p = 0.004). The TRF lengths of peripheral blood DNA do not correlate with any clinical or histological parameter or the rate of renal function decline. Conclusions: Although this is a pilot study, our observation indicates that the TRF lengths of genomic DNA extracted from urinary sediment is related to the degree of renal impairment. However, a long telomere length of genomic DNA in urinary sediment is associated with a more rapid decline of renal function. Our findings might be relevant to the pathogenesis of progressive renal failure.Correspondence to:
C.C. Szeto, MD
Department of Medicine and Therapeutics
Prince of Wales Hospital
Chinese University of Hong Kong
Shatin, N.T., Hong Kong, China
Email: ccszeto@cuhk.edu.hk

Abstract

T. Vas¹, Z. Wagner¹, V. Jenei³, Z. Varga³, T. Kovács¹, I. Wittmann¹, R. Schinzel², G. Balla³, J. Balla³, A. Heidland⁴ and J. Nagy¹

¹Second Department of Internal Medicine and Nephrological Center, Faculty of Medicine, University of Pécs, Pécs, Hungary, ²Physiological Chemistry I, University of Würzburg, Würzburg, Germany, ³First Department of Medicine and Neonatology, Division of Nephrology, Health and Medical Science Centre, University of Debrecen, Debrecen, Hungary, and ⁴Department of Internal Medicine, University of Würzburg, Würzburg, Germany
Aim: Approximately 20 – 50% of IgA nephropathy patients develop end-stage renal disease. We have previously found enhanced oxidative stress and decreased antioxidant capacity in red blood cells of IgA nephropathy patients. In this study we assess oxidative stress, non-enzymatic glycation, oxidative resistance of low-density lipoprotein and its a-tocopherol content in these patients. Patients and methods: Non-enzymatic glycation and oxidative stress were assessed in 88 IgA nephropathy patients by measuring advanced glycation end products, Ne-carboxymethyl-lysine, thiobarbituric acid reactive substances, oxidative resistance of low-density lipoprotein and its a-tocopherol content. Results: Advanced glycation end products (2659 ± 958 a.u.) and Ne-carboxymethyl-lysine (563 ± 215 ng/ml) were significantly higher in IgA nephropathy patients with decreased renal function compared to those with normal renal function (p < 0.002) or controls (p < 0.001). Thiobarbituric acid-reactive substances in plasma and associated with low-density lipoprotein were significantly elevated and oxidative resistance of low-density lipoprotein was significantly reduced in all groups of IgA nephropathy patients. There was no significant difference in circulating fluorescent advanced glycation end products, Ne-carboxymethyl-lysine, thiobarbituric acidreactive substances levels, oxidative resistance of low-density lipoprotein and its atocopherol content between patients with normal vs. impaired glucose metabolism. Low a-tocopherol content of low-density lipoprotein was accompanied with decreased oxidative resistance, depletion in polyunsaturated fatty acids, elevated saturated fatty acids and thiobarbituric acid-reactive substances within low-density lipoprotein suggesting enhanced lipid peroxidation. Conclusions: Decreased oxidative resistance of low-density lipoprotein and enhanced oxidative stress are common features in IgA nephropathy, while increased non-enzymatic glycation occurs as renal function declines.Correspondence to:
Prof. Dr. J. Nagy
2nd Department of Internal Medicine and Nephrological Center
University of Pécs
Pacsirta str. 1.
7624, Pécs, Hungary
Email: judit.nagy@aok.pte.hu

Abstract

C. Ogata, K. Kamide, Y. Suzuki, O. Sasaki, Y. Kubota, H. Sato, S. Takiuchi, T. Horio, T. Inenaga and Y. Kawano

¹Department of Medicine, Division of Hypertension and Nephrology, and ²Departments of Clinical Physiology, National Cardiovascular Center, Osaka, Japan
Aims: It has been shown that both angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin II type 1 receptor blockers (ARB) have renoprotective effects via mechanisms that are independent of blood pressure reduction. The aim of this study was to evaluate the intrarenal hemodynamic change with ARB by renal Doppler ultrasonography (RDU) and to assess the mechanism of ARB in patients with hypertension. Methods: Thirty hypertensive patients with renal insufficiency caused by glomerular diseases, diabetes and hypertensive nephrosclerosis were included in this study. RDU was performed before and one week after taking ARB. Resistance index (RI) (peak systolic velocity – end diastolic velocity/peak systolic velocity) in the intrarenal segmental artery were calculated, and the amounts of urinary protein or albumin were determined. Results: We defined patients whose microalbuminuria or proteinuria was reduced by greater than 30% by ARB as responders (n = 22) and defined other patients as non-responders (n = 8). There were no significant differences between the responder and non-responder groups in baseline characteristics. RI was significantly improved by ARB in the responder group, but not in the non-responder group. The reduction of RI after ARB treatment was most prominent in patients with hypertensive nephrosclerosis. Conclusions: Improvement in intrarenal hemodynamics might play an important role in the mechanisms of the renoprotective effect of ARB in patients with hypertension.Correspondence to:
K. Kamide, MD
Division of Hypertension and Nephrology
Department of Medicine
National Cardiovascular Center
5-7-1 Fujishirodai
Suita city, Osaka 565-8565, Japan
Email: kamide@hsp.ncvc.go.jp

Abstract

M. Nakayama¹, H. Nakano²,³, N. Tsuboi³, T. Kurosawa⁴, Y. Tsuruta⁵, Y. Iwasaki⁶, K. Yokoyama³, T. Hosoya³ and M. Fukagawa⁷

¹Research Division of Dialysis and Chronic Kidney Disease, Tohoku University Graduate School of Medicine, Sendai, ²Dialysis Center, Kashima Hospital, Iwaki, ³Department of Kidney and Hypertension, The Jikei University School of Medicine, Tokyo, ⁴Dialysis Division, Sumiyoshi Clinic Hospital, Mito, ⁵Dialysis Division, Meiyo Clinic, Toyohashi, Aichi, ⁶Nursing and Health Science, Oita University of Nursing and Health Sciences, Oita, ⁷Division of Nephrology and Dialysis Center, Kobe University School of Medicine, Kobe, Japan
Objective: It is revealed that LVH is one of risk factors for the development of cardiac complications in long-term HD patients. Therefore, maneuvers to reduce hypertrophy of cardium are very important for improving life prognosis. Angiotensin II receptor blockade (ARB) could reduce LVH in general populations without renal failure. However, no conclusive data has been available regarding the clinical consequences of ARB administration on the regression of LVH in HD patients. Furthermore, it has not clearly determined if ACE gene polymorphism has a possible influential effect on it. This study is conducted to clarify these issues. Subjects and method: 32 hypertensive patients on regular HD (male/female: 21/11, mean age: 60.5 years, mean duration of HD: 52.8 months) were studied. Patients were classified into two groups according to the different type of ACE gene polymorphism: cases with D allele (DD/ID; D group: n = 13) and those without (II; non-D group: n = 19). All patients were administered ARB (losartan 50 – 100 mg/day) and echocardiography (UCG) was performed at 6-month-interval regularly until the end of observation (24 months). Results: Before the commencement of ARB, no differences were found between the two groups, neither in mean blood pressure (MBP: D group/non-D group: 120 ± 13 vs. 115 ± 14 mmHg) nor in left ventricular mass index (LVMI: D/non-D: 172 ± 41 vs. 165 ± 41 g/m2). During the 24-month follow-up, there were significant and similar reductions in MBP in both groups. In respect to LVMI, a significant reduction of LVMI was found in the D group after six months (p < 0.01 vs. basal) with a final reduction rate (FRR) –26 ± 13%, whereas in the non-D group it was found at 24 months (p < 0.01 vs. basal) with FRR –11 ± 16% (p < 0.01 vs. D group). There were significant differences between the two groups at all points (p < 0.05 at 6, 18 and 24 months, p < 0.005 at 12 months, respectively). Conclusion: It is indicated that ARB could insert a regression effect on LVH predominantly in patients with D allele ACE polymorphism, due partly to factor (s) independent of its anti-hypertensive effect.Correspondence to:
M. Nakayama, MD
Research Division of Dialysis and Chronic Kidney Disease
Tohoku University Graduate School of Medicine
Seiryo machi 1-1 Aoba-ku
Sendai, 980-8574, Japan
Email: mnakayama@mail.tains.tohoku.ac.jp

Abstract

D. Yuen, R.M.A. Richardson and C.T. Chan

Division of Nephrology, Toronto General Hospital – University Health Network, University of Toronto, Toronto, Ontario, Canada
Background: Hyperphosphatemia is an independent risk factor for mortality in hemodialysis (HD) patients. The relative importance of HD frequency and duration for phosphate removal is not clear. Short daily hemodialysis (SDHD) is a form of HD which offers increased treatment frequency. SDHD studies have not been shown to normalize serum phosphate. Methods: Twenty-one patients were converted from conventional thrice weekly HD (CHD, 4 h/session) to SDHD (2 – 3.75 h/session, 5 – 6 sessions per week). The primary endpoint was the change in predialysis serum phosphate levels after conversion from CHD to SDHD. Changes in serum calcium levels, phosphate binder and vitamin D analogue usage, and serum parathyroid hormone (PTH) levels were measured as secondary endpoints. Results: Mean duration of SDHD was 17.7 ± 1.9 months. Mean treatment time was 2.63 ± 0.10 h, and mean frequency was 5.3 ± 0.1 sessions per week. Predialysis serum phosphate decreased from 1.99 ± 0.12 mM at three months pre conversion to 1.27 ± 0.10 mM at six months post conversion to SDHD (p = 0.002). Serum phosphate remained stable between six and 12 months post conversion (1.27 ± 0.10 mM to 1.38 ± 0.14 mM, p = 0.8). When patients were grouped according to SDHD sessional frequency (five sessions/week versus six sessions/ week) and compared, no significant differences were found in predialysis serum phosphate levels at six or 12 months post conversion. There were no changes in serum calcium. Overall phosphate binder usage did not change pre and post conversion to SDHD. Serum PTH tended to decrease after one year of SDHD (44.2 ± 13.4 pM to 21.4 ± 5.9 pM, p = 0.07). Conclusion: Conversion to SDHD significantly decreased serum phosphate. There may be a minimum hemodialysis duration below which increases in frequency are not able to compensate to achieve normal phosphate levels. Future studies are necessary to better characterize the relationship between HD duration and frequency with respect to phosphate removal. Correspondence to:
C.T. Chan, MD
8 N – Room 842
Toronto General Hospital
University Health Network
200 Elizabeth Street
Toronto, ON, M5G 2C4, Canada
Email: christopher.chan@uhn.on.ca

Abstract

D.W. Dempster, J.L. Rosenstock, J.A. Schwimmer, G. Panagopoulos, M.V. DeVita and M.F. Michelis

Department of Medicine, Division of Nephrology, Lenox Hill Hospital, New York, NY, USA
Background: Patients on hemodialysis are at high risk for cardiovascular disease (CVD). Aspirin is an established therapy for primary and secondary prevention of CVD that may be underutilized in hemodialysis patients. To better understand the use of aspirin in hemodialysis patients, we examined the experience of an urban hemodialysis center. Guidelines for use as well as associated risks and benefits are reviewed. Methods: Medical records for patients receiving hemodialysis treatment at our center (New York City, USA) in May 2004 were reviewed for aspirin use, presence of CVD, and potential contraindications to aspirin therapy. CVD was defined as a history of coronary artery disease, ischemic stroke, transient ischemic attack, or peripheral vascular disease. Potential contraindications to aspirin therapy included history of clinically significant bleeding or increased risk of bleeding, aspirin allergy and routine treatment with other anticoagulants. Results: 176 patients were eligible for the study and 172 (98%) were included. Although 74 patients had a history of CVD, only 38 (51%) of these were treated with aspirin. Among patients with a history of CVD who were not treated with aspirin, 19 (53%) had no identifiable contraindications to aspirin therapy for secondary prevention of CVD. Ninetyeight patients had no history of CVD, and 18 (18%) of these were treated with aspirin. Of patients without a history of CVD who were not treated with aspirin, 57 (71%) had no identifiable contraindications to aspirin therapy for primary prevention of CVD. Conclusions: Aspirin is underutilized in hemodialysis patients for the primary and secondary prevention of CVD. Given the high risk of CVD in hemodialysis patients, therapy with aspirin may be of significant benefit and prospective studies of aspirin therapy are needed.Correspondence to:
J.L. Rosenstock, MD 130 East 77th Street New York, NY 10021, USA
Email: JRosenstock@lenoxhill.net

Abstract

M. de Lourdes Ribeiro de Souza da Cunha, A.C. Montelli, A.M. Fioravante, J.E. Neves Batalha, J.C. Teixeira Caramori and P. Barretti

¹Department of Microbiology and Immunology, Bioscience Institute, ²Department of Internal Medicine of Botucatu Medical School, and ³Department of Biostatistics of Bioscience Institute, UNESP, Botucatu, SP, Brazil
Background and aims: Staphylococcus epidermidis and other coagulase-negative staphylococci (CoNS) are the most common agents of continuous ambulatory peritoneal dialysis (CAPD) peritonitis. Episodes caused by Staphylococcus aureus evolve with a high method failure rate while CoNS peritonitis is generally benign. The purpose of this study was to compare episodes of peritonitis caused by CoNS species and S. aureus to evaluate the microbiological and host factors that affect outcome. Material and methods: Microbiological and clinical data were retrospectively studied from 86 new episodes of peritonitis caused by staphylococci species between January 1996 and December 2000 in a university dialysis center. The influence of microbiological and host factors (age, sex, diabetes, use of vancomycin, exchange system and treatment time on CAPD) was analyzed by logistic regression model. The clinical outcome was classified into two results (resolution and non-resolution). Results: The odds of peritonitis resolution were not influenced by host factors. Oxacillin susceptibility was present in 30 of 35 S. aureus lineages and 22 of 51 CoNS (p = 0.001). There were 32 of 52 (61.5%) episodes caused by oxacillin-susceptible and 20 of 34 (58.8%) by oxacillin-resistant lineages resolved (p = 0.9713). Of the 35 cases caused by S. aureus, 17 (48.6%) resolved and among 51 CoNS episodes 40 (78.4%) resolved. Resolution odds were 7.1 times higher for S. epidermidis than S. aureus (p = 0.0278), while other CoNS had 7.6 times higher odds resolution than S. epidermidis cases (p = 0.052). Episodes caused by S. haemolyticus had similar resolution odds to S. epidermidis (p = 0.859). Conclusions: S. aureus etiology is an independent factor associated with peritonitis non-resolution in CAPD, while S. epidermidis and S. haemolyticus have a lower resolution rate than other CoNS. Possibly the aggressive nature of these agents, particularly S. aureus, can be explained by their recognized pathogenic factors, more than antibiotic resistance.Correspondence to:
P. Barretti, MD
Departamento de Clínica Médica
Faculdade de Medicina de Botucatu
UNESP, Rubião Júnior
Botucatu, SP, Brasil, Caixa Postal 584 CEP 18618-000
Email: pbarretti@uol.com.br

Abstract

U. Schönermarck¹, C.A. Schirren², N. Mistry-Burchardi¹, M. Weiss³, P. Eichhorn⁴ and W. Samtleben¹

¹Nephrology Department, Medical Clinic I, ²Medical Clinic II, ³Institute of Pathology, ⁴Department of Clinical Chemistry, University Hospital München-Großhadern, LMU München, Germany
We present the case of a 75-year-old female with weight loss, anemia, systemic signs of inflammation, mild renal insufficiency, microscopic hematuria, mixed glomerular and tubular proteinuria, and high titers of PR3-ANCA. Renal biopsy demonstrated interstitial nephritis with some sclerosed but otherwise normal glomeruli. Extensive work-up showed no signs of granulomatous inflammation or other vasculitic organ involvement. We presumed this to be a rare renal manifestation of ANCA-associated disease with the presence of sclerosed glomeruli suggesting a previous history of glomerular involvement. In view of the absence of active vasculitic or granulomatous disease, treatment was limited to low-dose corticosteroids with good response.Correspondence to:
U. Schönermarck, MD
Nephrology Department
Medical Clinic I
University Hospital München-Großhadern
81366 München, Germany
Email: Ulf.Schoenermarck@med.uni-muenchen.de

Abstract

K. Harada¹, Y. Akai¹, M. Iwano¹, K. Nakatani¹, T. Nishino¹, T. Fujimoto², H. Shiiki¹ and Y. Saito¹

¹First Department of Internal Medicine, and ²Department of General Medicine and Clinical Investigation, Nara Medical University, Kashihara, Nara, Japan
We report a case of hypokalemic nephropathy associated with primary Sjögren’s syndrome (SS). The patient presented with profound and persistent hypokalemia secondary to distal renal tubular acidosis (RTA). A renal biopsy exhibited tubular degeneration, marked interstitial fibrosis and intense macrophage infiltration. Hypokalemia has been reported to induce macrophage infiltration in experimental animal models but not in humans. This is the first report of intense tubulointerstitial macrophage infiltration in a patient with hypokalemic nephropathy associated with SS.Correspondence to:
M. Iwano, MD
First Department of nternal Medicine
Nara Medical University
840 Shijo, Kashihara, Nara 634-8522, Japan
Email: miwano@naramed-u.ac.jp

Abstract

S. Kursat, T. Alici and H.B. Colak

¹Nephrology Department and ²Internal Medicine Department, Celal Bayar University, Manisa, Turkey
Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle contents into the systemic circulation. We hereby report a patient proved to be a case of unrecognized hypothyroidism presenting with rhabdomyolytic acute renal failure precipitated by the combined use of statin and fenofibrate. A 63-year-old woman was referred to our department because of fatigue, diffuse muscle pain and oliguria. On the basis of pathogenesis, clinical and laboratory examination the diagnoses of acute renal failure secondary to the statin-fibrate-derivative combination induced rhabdomyolysis and auto-immune thyroiditis induced hypothyroidism were made. Although saline, furosemide and sodium bicarbonate infusions enabled diuresis and have led to a rapid recovery of renal function and normalization of blood pressure in five days (creatinine level decreased from 4.5 mg/dl to 1.2 mg/dl), only thyroid replacement therapy (0,1 mg thyroxine) that begun after the exclusion of adrenal insufficiency resulted in complete resolution of rhabdomyolysis. This prompted the diagnosis of background, clinically silent rhabdomyolysis aggrevated by the statin-fibrate-derivative combination. To our knowledge this case illustrates the first example of rhabdomyolytic acute renal failure induced by a statin-fibrate-derivative combination with underlying hypothyroidism which was responsible for the basal clinically unobservable rhabdomyolysis.
Correspondence to:
S. Kursat, MD Nephrology Department Celal Bayar University Manisa, Turkey
Email: seyhunkursat@ttnet.net.tr

Abstract

M. Tanaka, K. Itoh, K. Matsushita, K. Matsushita and M. Fukagawa

Abstract

I. Garcia-Pacheco, A. Khan and K.K. Venkat

Abstract

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Volume 64, No. 5/2005(November)