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Abstract

U.C. Brewster and M.A. Perazella

Section of Nephrology, Yale University School of Medicine, New Haven, CTt, USA
Proton pump inhibitors (PPIs) are widely prescribed to treat a number of gastrointestinal disorders due to excessive acid production. While effective and safe, adverse renal effects have been described. Most concerning is the ever increasing number of cases of acute interstitial nephritis (AIN) associated with PPI therapy. It appears to be a class effect as all PPIs have been documented to cause AIN. Several adverse drug event registries now note PPIs as the most common cause of drug-induced AIN. While most patients recover kidney function, many are left with some level of chronic kidney disease. Hyponatremia is an extremely rare complication and is thought to result from inappropriate ADH secretion. Interactions with calcineurin inhibitors may occur with certain PPIs when used in susceptible patients, particularly those with polymorphisms in the cytochrome P450-2C19 enzyme gene. This paper will critically review the effect of PPIs on the kidney.Correspondence to:
M.A. Perazella, MD, FACP Associate Professor of Medicine, Director, Nephrology Fellowship Program, Section of Nephrology Yale University School of Medicine FMP 107, 330 Cedar Street New Haven, CT 06520-8029, USA
Email: mark.perazella@yale.edu

Abstract

M. Maruyama, H. Sugiyama, K. Sada, M. Kobayashi, Y. Maeshima, Y. Yamasaki and H. Makino

¹Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, ²Department of Medicine, Hiroshima City Hospital, Hiroshima, Japan
Aims and method: Idiopathic membranous nephropathy (IMN) is the most common cause of nephrotic syndrome in adults worldwide. Many patients with IMN are elderly, but little is known about the relationship regarding the morphological stage determined by electron microscopy (EM), the amount of proteinuria, and the expression of glomerular podocyte markers such as desmin and nephrin in nephrotic glomeruli in IMN. We studied 59 patients with histopathologically proven IMN. We compared the clinical features, EM stage classification, and the immunohistochemical features of glomerular expression of podocyte markers, including desmin and nephrin, between older (age >= 60 years) and younger (age < 60 years) patients. We also investigated these parameters in patients with minimal-change nephrotic syndrome (MCNS), minor glomerular abnormalities (MGA), and normal kidneys as age-matched controls. Results: Prevalence of nephrotic syndrome was significantly higher in the older (52.9%) than the younger group (20.0%) of IMN. The level of proteinuria was higher in early stages (Stages I + II) than in late stages (Stages III + IV) in IMN. The glomerular expression of desmin in podocytes was significantly higher in IMN as compared to MCNS, MGA, or age-matched controls. Desmin expression was significantly increased in earlier EM stages (Stages I + II) and in higher proteinuric group (daily proteinuria >= 1 g) of older patients with IMN. Reciprocally, the reduced expression of nephrin was associated with the early EM stages (Stages I + II) of patients with IMN. Conclusions: We conclude that the expression of desmin in podocytes is upregulated in patients with IMN as compared to other glomerular diseases including MCNS or MGA, or to controls. In elderly patients with IMN, desmin expression was associated with early EM stages and heavy proteinuria, which may reflect phenotypic alteration of the podocyte.Correspondence to:
Dr. H. Sugiyama Department of Medicine and Clinical Science, Dentistry, and Pharmaceutical Sciences Okayama University Graduate School of Medicine, 2-5-1 Shikata-cho Okayama 700-8558, Japan
Email: hitoshis@md.okayama-u.ac.jp

Abstract

G. Wolf, N. Müller, A. Mandecka and U.A. Müller

Clinic for Internal Medicine III, University Clinic, Friedrich Schiller University Jena, Germany
Aims: It takes years for microvascular complications in diabetes mellitus such as diabetic retinopathy (RP) and nephropathy (NP) to develop. Since retinal and renal vessels are exposed to the diabetic milieu, it is often assumed that progression of diabetic RP and NP occurs at the same time. However, smaller studies have demonstrated that this may not always be the case. The present study was undertaken to correlate diabetic retinopathy with parameters of renal function in a large ambulatory collective of patients with Types 1 and 2 diabetes. Methods: The study design was cross-sectional. Ambulatory patients from a large university out-patient clinic were studied (323 patients with Type 1, 906 patients with Type 2 diabetes). RP status was obtained through retinal photography by an experienced ophthalmologist and was grouped into no RP, RP Stages 1 – 3, or blind. Retinal pathology was correlated with clinical parameters of renal function (proteinuria, estimated glomerular filtration rate according to the MDRD formula, presence of urinary sediment abnormalities, hypertension). Results: No patient showed urinary sediment abnormalities (e.g. presence of hematuria or acanthocytes) or increased urinary excretion of immunoglobulin light chains suggesting the absence of other nondiabetic renal diseases. The majority of Type 1 diabetes patients with macroalbuminuria (>= 200 mg/l) had some signs of RP independent of the presence of hypertension. There was a correlation between RP and microalbuminuria (r = 0.164, p < 0.01). In contrast, up to 47.5% of the hypertensive patients with Type 2 diabetes and overt proteinuria had no signs of RP. There was also discordance of microalbuminuria and RP in patients with Type 2 diabetes. Stratification according to K/DOQI States 2 – 5 (MDRD formula) showed that the majority of patients with Type 1 diabetes in States 3 – 5 had signs of RP, albeit the absolute number of patients in these K/DOQI stages was very small. In contrast, up to 40% of dialysis-dependent Type 2 diabetics (K/DOQI State 5) showed no evidence of RP. Conclusions: This study revealed that many patients with Type 2 diabetes and renal abnormalities (proteinuria and/or renal insufficiency) showed, in contrast to Type 1 diabetics, no signs of RP. Our study was, however, limited by the lack of renal biopsies. Although urinary sediment analysis was normal in these patients, other causes for renal insufficiency (e.g. vascular nephropathy), especially in Type 2 diabetics, cannot be excluded. Nevertheless, we believe that absence of RP in patients with Type 2 diabetes does not imply that renal abnormalities including diabetic nephropathy, are also absent. It is recommended that these patients undergo renal biopsy.
Correspondence to:
Prof. G. Wolf

University of Jena

Department of Medicine

Erlanger Allee 101

07740 Jena, Germany
Email: Gunter.Wolf@med.uni-jena.de

Abstract

L. Craver, M. Paz Marco, F. Sarro, M.L. Martin, M. Borras, J.M. Valdivielso and E. Fernández

¹Hospital Universitari Arnau de Vilanova, Lleida, ²University of Lleida, Lleida, Spain
Background: Pulse pressure (PP) increase has been associated with hypertension, ageing and chronic kidney disease. Although hyperparathyroidism and phosphate imbalance have been suspect in PP increase in hemodialysis patients, the link between these parameters and pulse pressure, in renal disease before dialysis, has not been established. Methods and patients: 1966 chronic kidney disease (CKD) patients. Statistics: ANOVA, Student’s t-and Chi-square, rank correlations (Spearman) and multivariate analysis, with PP as the dependent variable, while adjusting for other covariables. Results: There was an increase of pulse pressure parallel to renal function deterioration, and a significant influence of age, diabetes, hypertension, phosphate and PTH on pulse pressure in the whole population, as well as in patients with glomerular filtration rate < 60 ml/min. The impact of phosphate was particularly high after the age of 50. Conclusion: PP increase present in renal disease patients might be primarily due to the underlying mineral metabolism disturbances.Correspondence to:
M. Paz Marco, MD

Servicio de Nefrologia

Hospital Universitari Arnau de Vilanova

25198, Lleida, Spain
Email: mmarco@arnau.scs.es

Abstract

C. Matsunaga, S. Izumi, T. Furukubo, M. Satoh, T. Yamakawa, T. Uchida, D. Kadowaki and S. Hirata

¹Department of Pharmacy Services, ²Department of Medicine, Shirasagi Hospital, Osaka, ³School of Pharmaceutical Sciences, Mukogawa Women’s University, Nishinomiya, ⁴Division of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Kumamoto University, Kumamato, Japan
Aims: Histamine H2 receptor antagonists (HRA) or proton pump inhibitors (PPI) are frequently administered to patients on hemodialysis, because their intestinal mucosa is fragile. Although three studies have indicated that concomitant HRA administration causes a decrease in the binding of phosphate by calcium carbonate, the HRA doses tested in these studies were 2 – 4 times higher than the recommended dose for hemodialysis patients. In addition, it remains unclear whether PPI therapy affects serum phosphate levels in hemodialysis patients taking calcium carbonate. Accordingly, the aim of this study was to evaluate the influence of lansoprazole and the recommended dose of famotidine on serum phosphate and calcium levels in hemodialysis patients. Methods: The study included 115 hemodialysis patients who were taking calcium carbonate and who were also treated with either famotidine (10 mg/ day) or lansoprazole (30 mg/day). Changes of the mean serum phosphate and calcium levels over 2 months before and after the start of famotidine or lansoprazole therapy were compared. The same parameters were also compared when famotidine was switched to lansoprazole. Results: The mean serum phosphate level increased significantly after administration of either famotidine or lansoprazole (by 6.6 ± 21.9% or 13.0 ± 26.3%, p = 0.032 and p = 0.029, respectively). The mean serum calcium level was unchanged after administration of famotidine, but showed a significant decrease after administration of lansoprazole (by 3.44 ± 7.73%, p = 0.013). Therefore, the calcium × phosphorus product was significantly increased by administration of famotidine, but not by administration of lansoprazole (6.68 ± 23.37% and 8.73 ± 27.41%, p = 0.046 and p = 0.251, respectively). When famotidine was switched to lansoprazole, the serum phosophate level did not change, but serum calcium decreased significantly by 3.8 ± 13.0% (p = 0.0006). Conclusion: Not only administration of 20 mg/ day of famotidine as previously reported, but also 10 mg/day of this drug (the recommended dose for hemodialysis patients) caused a significant increase of serum phosphate in patients taking calcium carbonate. PPIs have been reported to show no effect on the serum phosphate level, but 30 mg/day of lansoprazole also caused a significant increase of serum phosphate in patients taking calcium carbonate.Correspondence to:
S. Hirata, PhD

Division of Clinical Pharmacology

Faculty of Pharmaceutical Sciences

Kumamoto University

5-1, Oe-Honmachi

Kumamoto 862-0973, Japan
Email: hirata@kumamoto-u.ac.jp

Abstract

Y.K. Wen and M.L. Chen

¹Division of Nephrology, Department of Medicine, ²Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan
We report an unusual case of nephrotic syndrome due to membranous glomerulonephritis that responded to high-dose trimethoprim-sulfamethoxazole (TMP-SMX) treatment. A 52-year-old man presented with nephrotic syndrome and was diagnosed to have idiopathic membranous glomerulonephritis. At the time of diagnosis, his serum creatinine level was 1.2 mg/dl and daily urine protein excretion was 7.45 g. The patient was initially treated with angiotensin-converting enzyme inhibitor and diuretics. After a 6-month period, the patient remained symptomatic. Therefore, immunosuppressive therapy with a 6-month course of alternating corticosteroids with cyclophosphamide was commenced. Unfortunately, as a sequel of the immunocompromised state, the patient acquired severe pneumonia due to Pneumocystis jiroveci infection when he was on the fourth month of immunosuppressive therapy. At this time, he still had nephrotic range proteinuria and hypoalbuminemia. Because of the risk of aggravating infection, immunosuppressive agents were discontinued. A 14-day course of intravenous high-dose TMP-SMX therapy was given for the treatment of Pneumocystis jiroveci pneumonia. With this medication, not only the pneumonia was cured, but also a sustained remission of the nephrotic syndrome occurred. This case suggests a possible therapeutic role of high-dose TMP-SMX in membranous glomerulonephritis. We will discuss the possible mechanism.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

R. Jimbo, Y. Ubara, T. Tagami, Y. Higa, T. Suwabe, S. Nakanishi, Y. Sogawa, K. Nomura, H. Kadoguchi, J. Hoshino, N. Sawa, H. Katori, F. Takemoto, S. Hara, S. Hara, K. Ohashi and K. Takaichi

¹Nephrology Center, ²Health Care Center, ³Department of Pathology, Toranomon Hospital, Tokyo, Japan
Antineutrophil cytoplasmic antibody- (ANCA) associated glomerulonephritis usually shows histopathologic features of pauciimmune crescentic glomerulonephritis and occurs late in life. We report a 14-year-old Japanese girl presenting with proteinuria, hematuria and mildly elevated serum creatinine. A renal biopsy specimen demonstrated crescentic glomerulonephritis, immunofluorescence showed mesangial IgA staining. Electron microscopic examination disclosed paramesangial deposits. Serum ANCA against myeloperoxidase(MPO) were detected at high titers. Myeloperoxidase-ANCA-related nephritis accompanied by IgA nephropathy is considered rare in childhood and teen years. Yet, if ANCA assays and detailed electron microscopic examination of renal specimens were performed routinely in patients with rapidly progressive glomerulonephritis, the diagnosis might be more frequent in young patients.Correspondence to:
Dr. Y. Ubara Nephrology Center Toranomon Hospital Kajigaya 1-3-1 Kajigaya, Takatsu Kawasaki, 213-0015, Japan
Email: ubara@toranomon.gr.jp

Abstract

I. Pela and D. Seracini

Department of Pediatrics, Pediatric Nephrology, University of Florence, Italy
The hyperammonemia in distal renal tubular acidosis, previously only described in two cases, is considered an unusual occurrence. After the report published in 2005, we observed plasma ammonia levels above normal range during metabolic decompensation in two other consecutive pediatric patients suffering from distal renal tubular acidosis. The ammonia plasma levels returned to normal range after treatment with sodium bicarbonate and potassium salt. In distal renal tubular acidosis, hyperammonemia is probably the result of an imbalance between the increased ammonia synthesis, in response to metabolic acidosis, and the impaired ammonia excretion, typical of distal renal tubular acidosis. According to this physiopathological mechanism, our observation shows that hyperammonemia is not an uncommon finding in distal renal tubular acidosis, and should be included among differential diagnosis of hyperammonemia in infants and children.Correspondence to:
I. Pela, MD Associate Professor Pediatric Nephrology Department of Pediatrics Via Luca Giordano 13 50132 Florence, Italy
Email: ivana.pela@unifi.it

Abstract

J. Granese, K. Brightbill, P. Osborne, C.E. Cox and L.W. Gaber

¹Department of Pathology and Laboratory Medicine and ²Department of Urology, University of Tennessee Health Science Center, Memphis, TN, USA
Analgesic nephropathy results from chronic abuse of non-narcotic analgesics, most frequently with the use of phenacetin and mixed analgesic preparations. Renal papillary necrosis and chronic interstitial nephritis with progressive scarring are characteristic of the histopathology of analgesic nephropathy. Typically, papillary necrosis in these patients is bilateral and affects almost all renal papillae. This report describes a case of severe analgesic nephropathy that discriminantly affected a unilateral non-functioning kidney and spared the contralateral normally developed kidney. The patient herein consumed therapeutic doses of acetaminophen and naproxen daily and for several years. We estimated the cumulative doses of acetaminophen and naproxen used by the patient during that period to be approximately 1.0 and 0.4 kg, respectively. The cumulative dose of acetaminophen is at the threshold of doses that were traditionally associated with an increased risk for end-stage kidney failure. Simultaneous intake of both analgesics could have had a synergetic adverse effect on renal function. This case also demonstrates that preexisting renal insufficiency is prerequisite to the development of analgesic nephropathy. Conversely, kidneys with normal function are resistant to the chronic nephrotoxicity associated with habitual analgesic use. Correspondence to:
L.W. Gaber, MD, Professor and Head Department of Pathology and Laboratory Medicine University of Tennessee Health Science Center 930 Madison Avenue Memphis, TN 38163, USA
Email: lgaber@utmem.edu

Abstract

I. Ohsawa, H. Ohi, T. Maruyama, H. Hamada and Y. Tomino

¹Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, ²Kasukabe Kisen Hospital, Kasukabe, Saitama, Japan
A 57-year-old-woman, who was treated with regular maintenance hemodialysis (HD), newly contracted rheumatoid arthritis (RA). Oral predonisolone was effective for alleviating her arthralgia but the RA activity became steroid-dependent. For treatment of poorly controlled synovitis leukocytapheresis (LCAP) showed excellent efficacy in the treatment of her joint pain. No serious adverse effects were observed. Serological markers such as CRP, serum amyloid A, matrix metalloproteinase 3 and peripheral blood lymphocyte count fluctuated with her clinical symptoms. We recommend LCAP as candidate therapy for steroid-dependent patients with RA who are on maintenance HD.Correspondence to:
Y. Tomino, MD Division of Nephrology Department of Internal Medicine Juntendo University School of Medicine 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan
Email: yasu@med.juntendo.ac.jp

Abstract

S. Gupta and G. Woodrow

Renal Unit, Leeds General Infirmary, Leeds, United Kingdom
Encapsulating peritoneal sclerosis remains a serious complication of peritoneal dialysis. Prolonged duration on dialysis and severe episodes of peritonitis are the two most important risk factors for developing the condition. Here we describe a patient who developed a fulminant form of encapsulating peritoneal sclerosis soon after suffering from an episode of fungal peritonitis. There was clinical evidence of ongoing inflammation and gross malnutrition. Signs of chronic intestinal stasis were present on radiological imaging. There was concern in this situation that symptoms could partly relate to ongoing peritoneal sepsis, which could be worsened by immunosuppressives such as steroids. Tamoxifen was used without steroids in our patient with prompt resolution of stasis symptoms and withdrawal of artificial nutrition support. To our knowledge tamoxifen has never been previously used alone, in this scenario. We propose that tamoxifen might be a safer alternative to use in this clinical setting where there is concern about presence of ongoing sepsis, than corticosteroids and immunosuppressive agents.Correspondence to:
Dr. G. Woodrow, MD, FRCP Consultant Renal Physician Renal Unit, Leeds General Infirmary Great George Street Leeds LS1 3EX, England, UK
Email: graham.woodrow@leedsth.nhs.uk

Abstract

K. Kisters, B. Gremmler, F. Tokmak, M. Cziborra, C. Funke and M. Hausberg

¹Medical Clinic I, St. Anna Hospital Herne, ²Medicaal Clinic, Marienhospital Bottrop, ³Ruhr University Bochum, ⁴Medical University Policlinic M
Correspondence to:
Prof. Dr. med. K. Kisters Med. Clinic I, St. Anna Hospital Hospitalstra
Email: kisters@annahospital.de

Abstract

A.D. Tsakok

A.D. Tsakok Mathematical Center London, UK
Correspondence to:
A.D. Tsakok A.D. Tsakok Mathematical Center 46 Leighton Gdns. London NW10 3PT, UK

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Volume 68, No. 2/2007(August)