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Dive into the research topics where Rodo O. von Vigier is active.

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Featured researches published by Rodo O. von Vigier.


Journal of The American Society of Nephrology | 2008

Src Inhibition Ameliorates Polycystic Kidney Disease

William E. Sweeney; Rodo O. von Vigier; Philip Frost; Ellis D. Avner

Despite identification of the genes responsible for autosomal dominant polycystic kidney disease (PKD) and autosomal recessive PKD (ARPKD), the precise functions of their cystoprotein products remain unknown. Recent data suggested that multimeric cystoprotein complexes initiate aberrant signaling cascades in PKD, and common components of these signaling pathways may be therapeutic targets. This study identified c-Src (pp60(c-Src)) as one such common signaling intermediate and sought to determine whether Src activity plays a role in cyst formation. With the use of the nonorthologous BPK murine model and the orthologous PCK rat model of ARPKD, greater Src activity was found to correlate with disease progression. Inhibition of Src activity with the pharmacologic inhibitor SKI-606 resulted in amelioration of renal cyst formation and biliary ductal abnormalities in both models. Furthermore, the effects of Src inhibition in PCK kidneys suggest that the ErbB2 and B-Raf/MEK/ERK pathways are involved in Src-mediated signaling in ARPKD and that this occurs without reducing elevated cAMP. These data suggest that Src inhibition may provide therapeutic benefit in PKD.


Journal of The American Society of Nephrology | 2008

CLDN16 Genotype Predicts Renal Decline in Familial Hypomagnesemia with Hypercalciuria and Nephrocalcinosis

Martin Konrad; Jianghui Hou; Stefanie Weber; Jörg Dötsch; Jameela A. Kari; Tomáš Seeman; Eberhard Kuwertz-Bröking; Amira Peco-Antic; Velibor Tasic; Katalin Dittrich; Hammad O. Alshaya; Rodo O. von Vigier; Sabina Gallati; Daniel A. Goodenough; André Schaller

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a rare autosomal recessive tubular disorder caused by CLDN16 mutations. CLDN16 encodes the renal tight junction protein claudin-16, which is important for the paracellular reabsorption of calcium and magnesium in the thick ascending limb of Henle’s loop. That FHHNC is frequently associated with progressive renal failure suggests additional roles for claudin-16 in the maintenance of tight junction integrity. An investigation of 32 patients with FHHNC and 17 different mutations was previously reported; here, the analysis is expanded to 39 additional patients and 12 new mutations. Expression studies revealed that five of the12 new mutations led to partial loss of claudin-16 function and the remaining seven led to complete loss of function. The 23 patients who had mutations resulting in complete loss of function of both alleles were significantly younger at the onset of symptoms than the 46 patients who had at least one mutant allele providing partial function (2.2 versus 5.6 years; P _ 0.01). In addition, those with complete loss of function had a more rapid decline in GFR (7.3 versus 2.9 ml/min per 1.72 m2/y; P _ 0.01), leading to 54% requiring renal replacement therapy by age 15 compared with 20% of those with residual function (P _0.05). These data suggest that residual function of claudin-16 may delay the progression of renal failure in FHHN


Pediatric Research | 2008

Ambulatory arterial stiffness index is increased in hypertensive childhood disease

Giacomo D. Simonetti; Rodo O. von Vigier; Elke Wühl; Markus G. Mohaupt

Arterial hypertension in adults is often associated with an increased arterial stiffness, which correlates with the ambulatory arterial stiffness index (AASI) as derived from ambulatory blood pressure (BP) measurements. The purpose of this study was to demonstrate whether children with diagnosed hypertension have an increased AASI as in hypertensive adults. AASI was calculated from 185 ambulatory BP measurements of 114 hypertensive and 71 normotensive, healthy children. Hypertensive children had higher AASI values compared with their normotensive healthy counterparts (0.370 ± 0.120 versus 0.204 ± 0.199, p < 0.0001). Children with longer duration of hypertension or a history of primary or secondary aortic coarctation displayed even more elevated AASI values. A receiver operator curve derived cut-off of AASI set at 0.301 distinguished (p < 0.0001) hypertensive from normotensive children with an odds ratio of 8.2, a sensitivity of 81%, and a specificity of 65%. Moreover, AASI correlated with pulse and systolic BP. In conclusion, AASI is elevated in hypertensive children and correlates with the duration and the origin of hypertension in childhood.


American Journal of Hypertension | 2002

Effectiveness and safety of the angiotensin II antagonist irbesartan in children with chronic kidney diseases

Lorenzo M.D. Franscini; Rodo O. von Vigier; Roger Pfister; Carmen Casaulta-Aebischer; Emilio Fossali; Mario G. Bianchetti

BACKGROUND Studies in adults with chronic kidney diseases demonstrate that the orally available angiotensin II antagonist irbesartan reduces arterial pressure and pathological proteinuria, mostly with an excellent tolerability profile. Little information is available on irbesartan in childhood. METHODS A total of 44 pediatric outpatients with chronic kidney disease (27 male and 17, aged 3.7 to 18 years, median 10 years) were given irbesartan once a day during 18 weeks for arterial hypertension (N = 23), proteinuria (N = 8), or both (N = 13). RESULTS In patients with hypertension, the use of irbesartan 4.1 (3.1-5.3) mg/kg body weight daily (median and interquartile range) was associated with a decrease (P <.005) in arterial pressure by 17 (13-22)/10 (7-12) mm Hg. In patients with overt proteinuria the urinary protein excretion decreased (P <.01) during treatment with irbesartan (2.9 [2.0-4.8] mg/kg body weight) by 52 (0-75) mg/[m(2) x h]), whereas plasma albumin increased (P <.05) by 4 (1-5) g/L. The frequency of abdominal pain, constipation, cough, diarrhea, dizziness, edema, fatigue, headache, insomnia, myalgia, orthostasis, and rash was similar before and with irbesartan. Plasma sodium slightly decreased, whereas plasma potassium increased, with irbesartan (P <.01). CONCLUSIONS In pediatric patients with chronic kidney diseases, irbesartan given once a day for 18 weeks significantly reduces arterial pressure and proteinuria, with an excellent tolerability and side effect profile.


Nephron | 2002

Maintenance Hemodialysis and Circulating Ionized Magnesium

Anita C. Truttmann; Rita Faraone; Rodo O. von Vigier; Jean Marc Nuoffer; Roger Pfister; Mario G. Bianchetti

Background: Circulating magnesium exists in the bound and in the free ionized form, that is biologically active. In kidney disease the relationship between ionized and total circulating magnesium is often altered. Little information is available on the influence of hemodialysis on the relationship between ionized and total circulating magnesium in end-stage kidney disease. Methods: Plasma total and ionized magnesium and the plasma ionized magnesium fraction were assessed before and after hemodialysis (dialysate magnesium content 0.75 mmol/l) in 46 patients with end-stage kidney disease and in a control group of 25 healthy subjects. Results: In patients plasma total (from 1.19 [1.05–1.33] to 1.10 [1.02–1.16] mmol/l; median and interquartile range) and ionized (from 0.71 [0.66–0.78] to 0.65 [0.63–0.69] mmol/l) magnesium significantly decreased during dialysis (control subjects: 0.82 [0.80–0.92], respectively, 0.57 [0.54–0.59] mmol/l). The plasma ionized magnesium fraction was significantly lower in patients both before (0.61 [0.58–0.64)] and after (0.60 [0.56–0.62]) hemodialysis than in controls (0.68 [0.65–0.70]). Conclusion: The study demonstrates a tendency towards a reduced circulating ionized magnesium fraction in end-stage kidney disease that is not corrected by hemodialysis.


Pediatric Nephrology | 2006

Non-lethal fetal toxicity of the angiotensin receptor blocker candesartan

Giacomo D. Simonetti; Thomas Baumann; Jana M. Pachlopnik; Rodo O. von Vigier; Mario G. Bianchetti

Angiotensin receptor blockers are potent antihypertensive drugs with very few side effects [1, 2]. No association has been documented between use of angiotensin receptor blockers during the first trimester of gestation and congenital defects. However, there are several reports of malformations and physiologic disturbances, mostly with lethal outcome, in infants exposed to these drugs during the second and third trimesters, as recently reviewed [3, 4]. We report the adverse long-term sequelae noted in an infant following maternal treatment with an angiotensin receptor blocker. A 39-year old woman on treatment with candesartan cilexetil 16 mg once a day [5] for mild essential hypertension became pregnant but the drug was not discontinued. At 31 weeks a male boy weighing 1.65 kg was delivered by cesarian section. The physical examination disclosed climb contractures, skull hypoplasia with microcephaly (head circumference 0.265 m) and moderately underdeveloped calvarial bones. The child developed immediate respiratory distress (treated with oxygen, exogenous surfactant and mechanical respiratory support), arterial hypotension (treated with dopamine and epinephrine), and moderate oliguria (creatinine up to 281 μmol/l, urea up to 15.6 mmol/l and a pathologically increased urinary protein to creatinine ratio of 739 mg/mmol; upper reference 50). His conditions improved during the second week of postnatal life. However, a tendency towards arterial hypertension (mean blood pressure 75–80 mm Hg; upper reference 68) was noted, requiring treatment with the calcium channel blocker amlodipine once a day during 6 weeks. Routine chromosome analysis revealed a normal male karyotype. The boy is currently 34 months of age. Body weight is 11.1 kg (−2.8 SDS), length 0.901 m (−1.5 SDS), head circumference 0.481 m (−2 SDS) and blood pressure slightly elevated (approximately 110/70 mm Hg; upper reference 106/66) and the calvarial bones normally developed. His cognitive and especially his linguistic development are moderately retarded. The physical examination is otherwise normal. Plasma creatinine (36 μmol/l) and urea (6.0 mmol/l) are normal. The urinary protein to creatinine ratio is slightly increased (29 mg/mmol, upper reference 20). Renal ultrasound study demonstrates rather small hyperechogenic kidneys and loss of corticomedullary differentiation. In conclusion during pregnancy the use of drugs that block the renin–angiotensin–aldosterone system, namely angiotensin receptor blockers [3, 4] and converting enzyme inhibitors [4, 6], is strongly cautioned against. Infants surviving the exposition to these agents during the second and third trimesters tend to a chronic kidney disease and a developmental delay. A corresponding long-term follow up is warranted. Giacomo D. Simonetti is currently supported by a scholarship of the Ettore e Valeria Rossi Foundation.


Pediatric Nephrology | 2010

Gout in pediatric renal transplant recipients

Johannes Trück; Guido F. Laube; Rodo O. von Vigier; Philippe Goetschel

Clinical gout has rarely been described after pediatric renal transplantation (RTx), although asymptomatic hyperuricemia is common in these patients. We describe three male pediatric patients who presented with gouty arthritis 7–8.5 years following RTx. Since receiving allopurinol, all patients had been free of gouty symptoms. To prevent severe bone marrow depletion, the dosage of azathioprine, an immunosupressant drug, was reduced by 50% to prevent interaction with allopurinol. Because atypical presentation of gout can occur, a high index of suspicion is needed to allow appropriate diagnosis of this disease in patients with skeletal pain after RTx.


Pediatric Nephrology | 2007

Severe anemia caused by the angiotensin receptor blocker irbesartan after renal transplantation

Giacomo D. Simonetti; Mario G. Bianchetti; Martin Konrad; Rodo O. von Vigier

Renal transplant recipients are often anemic in the early post-engraftment period because of preexisting anemia exacerbated by perioperative blood loss [1]. Six or more months after transplantation, anemia is slightly less common, and mostly occurs in the setting of chronic allograft nephropathy associated with reduced glomerular filtration rate [1]. We report the first pediatric case of anemia after renal transplantation caused by the use of irbesartan, a drug that inhibits the renin-angiotensin II-aldosterone system by blocking the type 1 of angiotensin II receptors [2–5]. A 12-year-old boy with a history of congenital nephrotic syndrome of the Finnish type and poor renal function (GFR estimated 25 ml/min/1.73 m, urinary protein/creatinine ratio 48 mg/mmol) 7 years after a cadaveric transplantation was on treatment with the immunosuppressants mycophenolate and sirolimus. This rather unusual immunosuppressive regimen had been started 2 years earlier because of resistant arterial hypertension and chronic nephropathy while on therapy with cyclosporine A, azathioprine and prednisone. The chronic antihypertensive regimen included the calcium-channel blocker amlodipine (0.16 mg/kg body weight once a day), the β-blocker metoprolol (1.7 mg/kg body weight once a day) and irbesartan (up to 10 mg/kg body weight once a day). An important hyporegenerative normocytic anemia (hemoglobin 63 g/l) was noted, which was not associated with either acute or chronic infections, including testing for Parvovirus B19 infection, and failed to improve on parenteral iron and recombinant human erythropoietin (at the beginning 170 IU/kg weekly, increased during anemia up to 230 IU/kg weekly). Finally, hemoglobin increased up to 119 g/l within 4 weeks after withdrawing irbesartan (Fig. 1). Drugs that inhibit the renin-angiotensin II-aldosterone system modestly decrease hemoglobin and circulating erythropoietin [1]. Like converting enzyme inhibitors, angiotensin II receptors blockers may produce anemia either by direct inhibition of erythropoietin or insulin-like growth factor-1 production, or via an indirect mechanism that improves renal perfusion and subsequently decreases oxygen consumption. Furthermore, a negative effect on hematopoiesis at the bone-marrow level has also been suggested, since angiotensin II type 1 receptors have been identified on erythroid progenitors [6]. The effect on hemoglobin is usually of limited clinical relevance, and should not stand in the way of use of these agents for their cardioprotective and renoprotective effects [1, 2]. The present report confirms that there may be “susceptible” patients for whom hemoglobin levels decrease significantly on drugs that inhibit the renin-angiotensin II-aldosterone system [1]. Thus, in selected cases, some thought could be given to engineering a “drug holiday” to test whether hemoglobin level increases after discontinuation, as previously reported in a child with nephrotic syndrome on treatment with the converting enzyme inhibitor enalapril [7]. Pediatr Nephrol (2007) 22:756–757 DOI 10.1007/s00467-006-0400-3


Nephron | 2000

Congenital Hypohaptoglobinemia in Childhood Hemolytic Uremic Syndrome

Sabine A. Zehnder Schlapbach; Gert Printzen; Rodo O. von Vigier; Mario G. Bianchetti

Accessible online at: www.karger.com/journals/nef Dear Sir, Circulating haptoglobin combines with free hemoglobin forming a complex. When haptoglobin combines with free circulating hemoglobin, the complex is rapidly cleared, while free haptoglobin has a long circulation time [1]. Thus levels of circulating haptoglobin of !300 mg/l are typical of hemolytic states [1]. The large molecular mass of the haptoglobin-hemoglobin complex limits the glomerular excretion of large amounts hemoglobin preventing renal damage caused by intratubular accumulation of heme pigments [1]. Since hemoglobinuria and renal damage tend to occur when free circulating hemoglobin is elevated, therapy with human haptoglobin products has been advised to preserve the kidney from the injury caused by severe hemolysis [2, 3]. A subset of the pediatric patients who recover from acute hemolytic uremic syndrome have late sequelae such as hypertension, pathological proteinuria and decreased renal function. Consequently, these patients receive follow-up care for many years [4, 5].


Nephrology Dialysis Transplantation | 2000

Hypomagnesaemia–hypercalciuria–nephrocalcinosis: a report of nine cases and a review

Vincenzo Benigno; Claudia S. Canonica; Alberto Bettinelli; Rodo O. von Vigier; Anita C. Truttmann; Mario G. Bianchetti

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Martin Konrad

Boston Children's Hospital

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Christoph Rudin

Boston Children's Hospital

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