Volume 65, No. 4/2006(April)
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 Clinical Nephrology
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Editorial
Renal osteodystrophy: What’s in a name? Presentation of a clinically useful new model to interpret bone histologic findings
Abstract
H.H. Malluche and M.-C. Monier-Faugere
Division of Nephrology, Bone and Mineral Metabolism, University of Kentucky, Lexington, KY, USA
Renal osteodystrophy begins early in the course of chronic kidney disease and occurs almost without exception in all patients with Stage 5 disease (CKD-5). Bone biopsies and evaluation of mineralized bone sections after double tetracycline-labeling are currently considered the gold standard for diagnosis and classification of renal osteodystrophy. Nevertheless, bone biopsies are rarely employed. This is, at least in part, related to the paucity of nephrologists trained in performance of the procedure and the fact that reports of the histologic results are not easily translatable to clinical practice. Results are usually given qualitatively, using non-uniform classifications or by histomorphometric evaluations which are esoteric to most nephrologists. We suggest here that histomorphometric evaluation can be reserved for research and special situations. Also, the customarily used qualitative classification should be replaced by a clinically useful nomenclature, provided the interpretation is done by an individual with sufficient experience in bone pathology. We present a new interactive nomenclature for renal osteodystrophy that addresses abnormalities of turnover, abnormalities of bone balance, and abnormalities of mineralization. The new nomenclature, thus, includes disorders of high- and low-turnover with consideration of the interrelation with positive or negative bone balance with or without mineralization defect. In this schema, changes in bone status are described as deviations from a norm, and treatment is geared toward normalizing values rather than creating any absolute change in one direction or another. It is hoped that such a classification will be easily usable, clinically more relevant, and more amenable to individualized treatment guidance.Correspondence to:
H.H. Malluche, MD, FACP
Robert G. “Robin” Luke Chair in Nephrology, Professor and Chief
Division of Nephrology, Bone and Mineral Metabolism
Department of Medicine, University of Kentucky
Chandler Medical Center
800 Rose St., MN 564
Lexington, KY 40536-0298, USA
Email: hhmall@uky.edu
Originals
Clinical pathological correlates of renal biopsy in elderly patients
Abstract
G. Ferro, P. Dattolo, S. Nigrelli, S. Michelassi and F. Pizzarelli
Nephrology and Dialysis Unit, S.M. Annunziata Hospital, Florence, Italy
Background: Reports have shown that well-defined histological patterns do not always correspond to equally clear clinical pictures, particularly so in elderly patients. Methods: With the aim of assessing clinicopathological correlations in the population aged > 65 years with that of lower age, we retrospectively analyzed computerized records of renal needle biopsies consecutively performed in the decade 1991 – 2000 in our unit. Results: Among the 392 eligible subjects, there were 150 patients 65 years of age and more, 76 of whom were over 70. The average serum creatinine was 2.9 mg/dl, with values > 3.5 mg/dl in 25% of cases. The major indication to biopsy was nephrotic syndrome followed by chronic renal failure both in the young adult and the elderly population. The rapidly progressive form led more often to renal biopsy in the elderly patients, and the different prevalence was statistically significant (p < 0.05), as was the higher prevalence of urinary anomalies in the young-adult population. Regarding renal histology, the crescentic necrotizing forms were significantly more frequent in the elderly patients, while IgAN, minimal change disease and SLE predominate in young adults. The most relevant result is the greater prevalence of crescentic necrotizing glomerulonephritis in elderly patients, not only in the cases presenting clinically as rapidly progressive renal failure and acute renal failure, but also in those with the clinical picture of chronic renal failure. Conclusions: Re-evaluation of our case files verifies the importance of the bioptic approach in selected cases with stages 3 – 4 chronic kidney damage. This holds true especially for elderly patients.Correspondence to:
F. Pizzarelli, MD
Chief of Nephrology and Dialysis Unit
S.M. Annunziata Hospital
50011 Antella-Florence, Italy
Email: fpizzarelli@yahoo.com
Originals
Acute and concomitant deterioration of hyponatremia and renal dysfunction associated with heart and liver failure
Abstract
E.J. Hoorn, J. Lindemans and R. Zietse
1Department of Internal Medicine, 2Department of Clinical Chemistry, Erasmus Medical Center, Rotterdam, The Netherlands
Background: Although hyponatremia with concomitant renal dysfunction has been described anecdotally, little is known about how these two conditions are related, which type of renal dysfunction usually occurs, and which patients are at risk. Methods: From 3,029 measured serum sodium (SNa) concentrations in 3 months, patients with at least one SNa £ 125 mmol/l were selected, and divided in patients with at least 1 SCreat ³ 125 mmol/l (study group, n = 20), and patients whose SCreat remained normal (control group, n = 50). Results: During the first 5 days of hospitalization, SCreat almost doubled in the study group from 125 ± 40 mmol/l to 207 ± 72 mmol/l, while SNa decreased concurrently from 130 ± 2 mmol/l to 122 ± 3 mmol/l. The peak SCreat and SNa values coincided, and the average courses were highly correlated (r = 0.88, p < 0.001). The study group more often had heart failure (10/20 vs. 1/50, p < 0.001) and liver failure (7/20 vs. 4/50, p = 0.009), and received more often loop diuretics (13/20 vs. 12/50, p = 0.002), spironolactone (11/20 vs. 7/50, p = 0.001), and/or angiotensin-converting enzyme inhibitors (5/20 vs. 2/50, p = 0.02). Four patients were admitted to the intensive care (10 in control group, p = 1.0), and 5 patients died (10 in control group, p = 0.7). Conclusions: Renal dysfunction is common in severe hyponatremia and usually develops in an acute-on-chronic fashion with concomitant deterioration of both conditions. This concourse is associated with heart failure, liver failure, and/or a renal drug regimen. Given the recent results of clinical trials, this patient group may be especially suitable for treatment with vasopressin antagonists.Correspondence to:
E.J. Hoorn, MD
Erasmus Medical Center
Dialysis Unit, Room Bd 391
Dr. Molewaterplein 40
3015 GD Rotterdam, The Netherlands
Email: ejhoorn@gmail.com
Originals
The prevalence and risk factors of microalbuminuria in normoglycemic, normotensive adults
Abstract
H.S. Choi, K.C. Sung and K.-B. Lee
1Division of Nephrology and 2Division of Cardiology, Sungkyunkwan University, School of Medicine, Kangbuk Samsung Hospital, Seoul, Korea
Aims: Microalbuminuria is a risk factor for renal and cardiovascular disease. Recent studies have established this important relationship in patients with diabetes or hypertension, yet few studies have shown this relationship in healthy subjects. The purpose of this study is to examine the prevalence and the risk factors of microalbuminuria in normoglycemic, normotensive adults. Subjects and methods: We examined the prevalence of microalbuminuria in the adults who voluntarily took part in a health examination program. As a cross-sectional study, we examined the risk factors of microalbuminuria in 4,883 normoglycemic, normotensive healthy adults. Results: The prevalence of microalbuminuria was 2.8% in the normoglycemic, normotensive group (n = 4,883), 10.1% in the hypertensive group (n = 1,250), 16.0% in the diabetes group (n = 455) and 5.4% in the total subjects (n = 6,588). The systolic blood pressure, high sensitive C-reactive protein (hsCRP) and insulin resistance were independently related with microalbuminuria on the logistic regression analysis. The odds ratio of microalbuminuria were 1.04 (1.02 – 1.05, 95% CI), 1.29 (1.10 – 1.51, 95% CI), and 1.83 (1.15 – 2.92, 95% CI), respectively. Conclusions: These finding suggest that the systolic blood pressure, hsCRP and insulin resistance are the independent risk factors for microalbuminuria in normoglycemic, normotensive adults.Correspondence to:
K.-B. Lee, MD
Division of Nephrology
Kangbuk Samsung Hospital
Pyung dong, Jongro-Ku, Seoul, 110-746, Korea
Email: leekyubeck@yahoo.co.kr
Originals
Functional characterization of SLC7A9 polymorphisms assumed to influence the cystinuria phenotype
Abstract
E. Brauers, C. Schmidt, K. Zerres and T. Eggermann
1Institute of Human Genetics, University Hospital, RWTH Aachen, 2Children’s Hospital, University Hospital Munich, Germany
Cystinuria is a hereditary disorder of cystine and dibasic amino acid transport across the luminal membrane of renal tubules and intestine, resulting in recurrent nephrolithiasis. While mutations in the SLC3A1 gene cause type I cystinuria, patients with non-type I cystinuria mostly carry mutations in the SLC7A9 gene. However, there is evidence that further genetic factors cause and influence the cystinuria phenotype. We recently demonstrated that specific polymorphisms in Exons 3, 4, 5 and 6 of the SLC7A9 gene show a significant different allelic distribution between cystinuria patients and controls. To determine the role of the variants in these exons we transfected COS7 cells with expression constructs containing different haplotypes. Sequencing of cDNAs derived from the resulting SLC7A9 mRNAs did not reveal any differences in expression between the minigenes of the specific haplotypes. Our findings suggest that the variants in SLC7A9 do not influence splicing behavior. Thus, the reasons for the different allelic distribution between cystinuria patients and controls remain unclear. It is conceivable that this distribution is caused by the association of certain alleles with so far undetected mutations in the gene.Correspondence to:
Dr. T. Eggermann
Institute of Human Genetics
University Hospital
Pauwelsstraße 30
53074 Aachen, Germany
Email: teggermann@ukaachen.de
Originals
The isoflavone genistein inhibits LPS-stimulated TNFa, but not IL-6 expression in monocytes from hemodialysis patients and healthy subjects
Abstract
R. Asmis, J. Stevens, J.G. Begley, B. Grimes, G. Van Zant and P. Fanti
1Division of Nephrology, University of Texas Health Science Center at San Antonio, Texas, 2Department of Medicine, University of Kentucky, Lexington, USA
Background: Whole blood and peripheral blood mononuclear cells from hemodialysis (HD) patients show increased production and secretion of inflammatory cytokines. We determined the contribution of blood monocytes to the production of inflammatory cytokines in whole blood from HD patients. Methods: Whole blood and isolated mononuclear cells from HD patients and healthy control subjects were preincubated with the isoflavone genistein and stimulated with LPS. TNFa, IL-6 and IL-10 formation in the whole blood was measured with ELISA and intracellular cytokine formation in CD14positive monocytes was determined by flow cytometry. Results: Unstimulated blood levels of TNFa, IL-6 and IL-10 were significantly elevated in HD patients compared to controls, but intracellular monocyte content of these cytokines was identical between groups. LPS induced a robust TNFa response in both whole blood and monocytes, and TNFa formation was 2.3-fold higher in blood from HD patients compared to controls. A similar trend was observed in monocytes. Conversely, LPS stimulation increased IL-6 levels > 1,000-fold in whole blood, albeit without a noticeable difference between groups. Only minor increases in monocyte IL-6 content were observed. The isoflavone genistein did not inhibit IL-6 formation and did not alter basal TNFa levels, but genistein selectively blocked LPS-induced TNFa formation in whole blood and monocytes from both groups. Conclusion: Intracellular levels of TNFa, IL-6 and IL-10 in monocytes are indistinguishable between HD patients and healthy controls. However, monocytes from HD patients are selectively primed for enhanced TNFa secretion in response to LPS. The selective inhibition of monocyte TNFa production by genistein may explain the anti-inflammatory action of this phytochemical observed in vivo.Correspondence to:
R. Asmis, PhD
Division of Nephrology
University of Texas Health Science Center at San Antonio
7703 Floyd Curl Drive
San Antonio, TX 78229, USA
Email: asmis@uthscsa.edu
Case reports
Good response of membranous lupus nephritis to tacrolimus
Abstract
M. Maruyama, Y. Yamasaki, K. Sada, A. Sarai, K. Ujike, Y. Maeshima, Y. Nakamura, H. Sugiyama and H. Makino
1Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine and Dentistry, 2Department of Medicine, Hiroshima City Hospital, Hiroshima, Japan
A 22-year-old woman hospitalized for polyarthralgia was diagnosed with systemic lupus erythematosus (SLE). She was treated with prednisolone, and her clinical manifestations improved. However, she was re-admitted for renal biopsy because of persistent hypocomplementemia and development of proteinuria. The biopsy revealed segmental spike formation of basement membrane and subepithelial immune complex deposition, and membranous lupus nephritis (class V) was diagnosed. When tacrolimus was added to prednisolone, the serum complement titer quickly improved and proteinuria disappeared after about 11 months. Nevertheless, when tacrolimus was replaced examination showed cyclosporine due to gastrointestinal symptoms, she complained about arthralgia. Examination showed drop in the serum complement titer and recurrence of proteinuria. Renal biopsy at the time of recurrence showed increased subepithelial immune complex deposition in the capillary loops as compared to the first biopsy, a high degree of thickening of the basement membrane, and segmental circumferential interposition in some of the glomeruli. Membranous lupus nephritis (classes V + III) was diagnosed. By changing to tacrolimus and higher doses of steroids, the serum complement titer improved and proteinuria disappeared. This case indicates that tacrolimus can be an effective therapeutic agent for membranous lupus nephritis.Correspondence to:
Y. Yamasaki, MD
Department of Medicine
Hiroshima City Hospital
7-33, Motomachi, Naka-ku, Hiroshima, 730-8518, Japan
Email: yyamasak@city-hosp.naka.hiroshima.jp
Case reports
The “nutcracker phenomenon” with orthostatic proteinuria: case reports
Abstract
M. Ekim1, Z.B. Özçakar1, S. Fitoz2, T. Soygür3, S. Yüksel1, B. Acar1, F. Yalçinkaya1 and N. Arikan3
1Department of Pediatric Nephrology, 2Department of Radiodiagnostic and 3Department of Pediatric Urology, Ankara University Medical School, Ankara, Turkey
The nutcracker phenomenon refers to compression of the left renal vein between the aorta and the superior mesenteric artery. Clinical features are hematuria, abdominal pain, left flank pain, pelvic or scrotal discomfort due to varicocele or ovarian vein syndrome. In this report, 2 patients with orthostatic proteinuria, in whom nutcracker phenomenon was detected as a cause, are presented. One of them had posterior nutcracker with also asymptomatic varicocele that was detected during ultrasonographic examination. Nutcracker phenomenon is a rare but important clinical condition that should be considered in the differential diagnosis of patients with proteinuria and hematuria.Correspondence to:
Z.B. Özçakar, MD
Yeni Ankara sok. 27/1 Cebeci, Ankara, Turkey
Email: zbozcakar@yahoo.com
Case reports
Crescentic glomerulonephritis associated with rifampicin in a patient co-infected with tuberculosis and human immunodeficiency virus
Abstract
Y.K. Wen and M.L. Chen
1Division of Nephrology, Department of Medicine, 2Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan
A 73-year-old man presented with acute renal failure after 3-month standard antituberculosis therapy with rifampicin for pulmonary tuberculosis. Previously undiagnosed human immunodeficiency virus (HIV) infection was found at the same time. A kidney biopsy showed crescentic glomerulonephritis and tubulointerstitial nephritis. Furthermore, endothelial tubuloreticular inclusions were seen on electron microscopy. Rifampicin was stopped because it was considered as the most possible cause responsible for the rapidly progressive glomerulonephritis (RPGN). Immunosuppressive therapy was not carried out because of the risk of aggravation of underlying infectious diseases including tuberculosis and HIV. Fortunately, renal function recovered 1 month after discontinuation of rifampicin. This case presented a clinical challenge in the differential diagnosis of the cause for RPGN in such a complex condition and the therapeutic dilemma regarding the use of immunosuppressive drugs.Correspondence to:
Dr. Y.K. Wen
Division of Nephrology
Department of Medicine
Changhua Christian Hospital
135 Nansiao St., Changhua, 500, Taiwan
Email: 9965@cch.org.tw
Case reports
A case of refractory uremic pleuropericarditis - successful corticosteroid treatment
Abstract
M. Iyoda, Y. Ajiro, K. Sato, A. Kuroki, T. Shibata, K. Kitazawa and T. Sugisaki
Department of Nephrology, Showa University School of Medicine, Tokyo, Japan
We report the case of a patient with uremic pleuropericarditis who showed a marked improvement following corticosteroid therapy. A 66-year-old man who had been on hemodialysis therapy for 13 years was admitted to our hospital presenting with increases in bilateral pleural effusions and pericardial effusion. Repeated thoracentesis showed hemorrhagic and exudative findings. Pleural and pericardial fluid cytologic examination, bacterial culture and acid-fast staining showed negative findings. Despite the administration of antibiotics and antituberculosis drugs, low-grade fever continued and C-reactive protein level remained high. A pleural biopsy revealed fibrinous pleuritis without infectious disease or malignancy. He was diagnosed as having uremic pleuropericarditis on the basis of the clinicopathological features, but had been unresponsive to conventional treatments including repeated thoracentesis and the continuance of hemodiafiltration using nafamostat mesylate. Ultimately, both pleural and pericardial effusions were controlled after the treatment with prednisolone at an initial dose of 50 mg per day. In conclusion, corticosteroid therapy seems to be useful for treating patients with conventional therapy-resistant uremic pleuropericarditis.Correspondence to:
M. Iyoda, MD, PhD
Department of Nephrology
Showa University School of Medicine
1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan
Email: iyoda@med.showa-u.ac.jp
Case reports
Successful maintenance of continuous ambulatory peritoneal dialysis in a patient after fungal peritonitis and dialysate leakage
Abstract
M. Koch, R. Trapp and M. Goepel
1Center of Nephrology, Mettmann, 2Department of Urology and Pediatric Urology, Klinikum Niederberg, Academic Hospital, Germany
Fungal peritonitis (FP) and dialysate leakage have often been reported in association with continuous ambulatory peritoneal dialysis (CAPD), which has to be discontinued in many cases due to these complications. This report describes the first case of dialysate leakage into the urinary bladder of a 70-year-old male patient, after the area of the left ureteral ostium had been very deeply resected. The leakage probably led to severe fungal peritonitis developing 1 day after the ostium resection. The ostium resection was performed in November 2003 after detection of a carcinoma in situ (Cis) in this area and after previous bilateral nephroureterectomies due to multifocal urothelial carcinoma in the kidneys, ureters and bladder. In spite of prior fungal peritonitis and dialysate leakage, CAPD could be successfully initiated 41 days after biochemical manifestation of peritonitis and could be maintained in the patient because of the following reasons: early and effective treatment of FP with fluconazole and voriconazole, spontaneous occlusion of the slitted ostium area, allowance of enough healing time after 2 major abdominal surgeries, during which the patient was placed on extracorporal hemodialysis (which had been started 1 day after nephroureterectomy and ended after the antimycotic treatment) and thorough monitoring of the patient after starting CAPD. In January 2004, the patient could be placed on a cycler peritoneal dialysis and was fully rehabilitated 1 year later.Correspondence to:
Dr. M. Koch
Gartenstraße 8
40822 Mettmann, Germany
Email: Koch@dialyse-mettmann.de
Case reports
Tuberculous spondylitis in patients with end-stage renal disease undergoing chronic hemodialysis therapy
Abstract
D.J. Verettas, A.N. Ververidis, C. Boyiatzis, S. Panagoutsos, V. Galanis, P. Passadakis, K. Kazakos and V. Vargemezis
1Department of Orthopedics and Trauma, and 2Department of Nephrology, Democritus University of Thrace, University General Hospital of Alexandroupolis, Alexandroupolis, Greece
Tuberculosis of the spine is not rare in immunocompromised patients and particularly in those with end-stage renal disease (ESRD). Furthermore, the possible vascular compromise of the spinal cord in patients with diabetic nephropathy may result in symptoms of neurological involvement that could lead to deterioration and paralysis. We report a series of 4 patients with ESRD undergoing dialysis that developed tuberculous spondylitis of the thoracic spine. Diabetic nephropathy was the primary cause for chronic kidney disease in 2 patients; 3 of these patients were treated conservatively with anti-tuberculous medication and orthotic splints and were cured. The fourth patient with diabetes mellitus and clinically evident signs and symptoms of severe vascular insufficiency has additionally developed incomplete paraplegia. A complete sensory recovery and partial recovery of the hip flexors and abductors within 3 months occurred, following decompression of the spine and drainage of the abscess, in combination with long-term anti-tuberculous treatment and spinal orthosis.Correspondence to:
Dr. S.A. Panagoutsos
6, I Kaviri Street
68100 Alexandroupolis, Greece
Email: panag1@vivodinet.gr,spanagou@med.duth.gr
Letters to the Editor
Bilateral renal enlargement: an unusual presentation of bacterial pyelonephritis
Abstract
P.A. Noseworthy, S.L. Chicano, R.T. McCluskey and H. Bazari
Letters to the Editor
Prominent hypophosphatemia due to proximal tubulopathy mimicking Fanconi's syndrome in a patient with obstructive jaundice
Abstract
G. Kalambokis, H.J. Milionis, M. Economou, E.V. Tsianos and M.S. Elisaf
Letters to the Editor
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