K. Zouaghi

Malignant hypertension-associated thrombotic microangiopathy following cocaine use

Cocaine is one of the most commonly used illicit drugs with distribution and consumption throughout the world. Acute renal failure associated with rhabdomyolysis, direct vasoconstriction and hemodynamic alteration is well described in patients with cocaine intoxication. Cocaine use is associated with high blood pressure and may rarely induce malignant hypertension associated with thrombotic microangiopathy. We report the case of a patient who developed malignant hypertension associated with thrombotic microangiopathy after chronic consumption of cocaine. A kidney biopsy revealed thrombotic microangiopathy with fibrinoid necrosis of arterioles and glomerular tufts. He required dialysis sessions. Cocaine-mediated endothelial injury and platelet activation may play important pathogenetic roles in cocaine abusers who develop malignant hypertension associated with thrombotic microangiopathy. Clinicians need to be aware of this rare feature of cocaine intoxication.

Osteomalacia complicating renal tubular acidosis in association with Sjogren's syndrome

Renal involvement in Sjogrens syndrome (SS) is not uncommon and may precede other complaints. Tubulointerstitial nephritis is the most common renal disease in SS and may lead to renal tubular acidosis (RTA), which in turn may cause osteomalacia. Nevertheless, osteomalacia rarely occurs as the first manifestation of a renal tubule disorder due to SS. We herewith describe a 43-year-old woman who was admitted to our hospital for weakness, lumbago and inability to walk. X-ray of the long bones showed extensive demineralization of the bones. Laboratory investigations revealed chronic kidney disease with serum creatinine of 2.3 mg/dL and creatinine clearance of 40 mL/min, hypokalemia (3.2 mmol/L), hypophosphatemia (0.4 mmol/L), hypocalcemia (2.14 mmol/L) and hyperchloremic metabolic acidosis (chlorine: 114 mmol/L; alkaline reserve: 14 mmol/L). The serum alkaline phosphatase levels were elevated. The serum levels of 25-hydroxyvitamin D and 1,25-dihydroxy vitamin D were low and borderline low, respectively, and the parathyroid hormone level was 70 pg/L. Urinalysis showed inappropriate alkaline urine (urinary PH: 7), glycosuria with normal blood glucose, phosphaturia and uricosuria. These values indicated the presence of both distal and proximal RTA. Our patient reported dryness of the mouth and eyes and Schirmers test showed xerophthalmia. An accessory salivary gland biopsy showed changes corresponding to stage IV of Chisholm and Masson score. Kidney biopsy showed diffuse and severe tubulo-interstitial nephritis with dense lymphoplasmocyte infiltrates. Sicca syndrome and renal interstitial infiltrates indicated SS as the underlying cause of the RTA and osteomalacia. The patient received alkalinization, vitamin D (Sterogyl ®), calcium supplements and steroids in an initial dose of 1 mg/kg/day, tapered to 10 mg daily. The prognosis was favorable and the serum creatinine level was 1.7 mg/dL, calcium was 2.2 mmol/L and serum phosphate was 0.9 mmol/L.

Therapeutic efficacy of a biosimilar epoetin alfa in hemodialysis patients

Anemia is a frequent complication in patients with chronic kidney disease. However, human recombinant erythropoietin (rHu-EPO) has revolutionized the management of anemia in chronically dialyzed patients. Epomax ® is a new rHu-EPO alfa manufactured in Tunisia (Medis Laboratories). The aim of this study was to evaluate the efficacy and tolerance of Epomax ® in chronic hemodialysis (HD) patients in a phase-III, multicenter, clinical trial. Fiftythree HD patients (mean age 47.7 ± 13 years) who received a stable dose of rHu-EPO (Hemax ® , a rHu-EPO alfa manufactured by Biosidus Laboratories) subcutaneously were switched to Epomax ® via the same route of administration. At baseline, the mean systolic pressure was 132 ± 18 mm Hg and the mean diastolic pressure was 79 ± 8 mm Hg. The mean blood hemoglobin was 10.2 g/dL and the median ferritin level was 667 ng/mL. After a follow-up of 43 days, the mean blood hemoglobin was 10.5 g/dL under the effect of Epomax ® . There was no significant difference in the mean hemoglobin levels between the treatments with both drugs. Few adverse events were reported during the study. We conclude that Epomax ® was effective at maintaining the hemoglobin levels at target concentrations and was well tolerated in HD patients.

Molecular basis of complement factor I deficiency in Tunisian atypical hemolytic and uremic syndrome Patients: CFI deficiency in Tunisian atypical hemolytic and uremic syndrome patients

The aim of the present study was to characterize the molecular basis of complement factor I deficiency in Tunisian atypical haemolytic and uremic syndrome patients with low factor I levels.

Subcutis calcinosis caused by injection of calcium-containing heparin in a chronic kidney injury patient

Subcutis calcinosis, characterized by abnormal calcium deposits in the skin, is a rare complication of using calcium-containing heparin occurring in patients with advanced renal failure. We report the case of an 83-year-old female, a known case of chronic kidney disease (CKD) for four years with recent worsening of renal failure requiring hospitalization and hemodialysis. She developed subcutis calcinosis following injection of calcium-containing heparin. Biochemical tests showed serum parathormone level at 400 pg/dL, hypercalcemia, elevated calcium-phosphate product and monoclonal gammopathy related to multiple myeloma. She developed firm subcutaneous nodules in the abdomen and the thighs, the injection sites of Calciparin ® (calcium nadroparin) that was given as a preventive measure against deep vein thrombosis. The diagnosis of subcutis calcinosis was confirmed by the histological examination showing calcium deposit in the dermis and hypodermis. These lesions completely disappeared after discontinuing calcium nadroparin injections. Subcutis calcinosis caused by injections of calcium-containing heparin is rare, and, to the best our knowledge, not more than 12 cases have been reported in the literature. Pathogenesis is not well established but is attributed to the calcium disorders usually seen in advanced renal failure. Diagnosis is confirmed by histological tests. Outcome is mostly favorable. The main differential diagnosis is calciphylaxis, which has a poor prognosis. Even though rarely reported, we should be aware that CKD patients with elevated calcium-phosphorus product can develop subcutis calcinosis induced by calcium-containing heparin. When it occurs, fortunately and unlike calciphylaxis, outcome is favorable.

Kaposi's sarcoma with HHV8 infection and ANCA-associated vasculitis in a hemodialysis patient

The association between Kaposis sarcoma (KS) and human herpes virus eight (HHV-8) infection is rarely reported in hemodialysis (HD) patients. We report here the rare association of KS, HHV-8 and hepatitis C virus (HCV) infection as well as syphilis in a HD patient. We report the case of a 72-year-old woman who presented with microscopic polyangiitis with alveolar hemorrhage and pauci-immune necrosing and crescentic glomerulonephritis as well as renal failure requiring HD. Biological tests showed positive HCV and syphilis tests. The patient was treated by HD and intravenous pulse, followed by oral corticosteroids and six cyclophosphamide monthly pulses with remission of the alveolar hemorrhage, but without renal functional recovery as the patient remained HD dependent. Five months after the first treatment administration, she developed extensive purpuric lesions on her lower limbs, abdomen face and neck. A skin biopsy showed KS. The HHV-8 test was positive, with positive polymerase chain reaction-HHV8 in the serum and skin. After immunosuppression withdrawal, the KS skin lesions regressed rapidly without relapse after 12 months of follow-up, but alveolar hemorrhage relapsed after 16 months of follow-up. Our case showed that the immunosuppressed state related to multiple factors such as aging, vasculitis, HHV-8, HCV, syphilis, immunosuppressive therapy and HD may all have contributed to the development of KS in our patient.

Phéochromocytome surrénalien chez un insuffisant rénal chronique en dialyse péritonéale

Pheochromocytoma is a rare tumor responsible for paroxysmal hypertension which is difficult to control. Diagnosis is important because it represents a curable form of hypertension. Few cases of pheochromocytoma patients with end-stage renal failure were reported in the literature. These cases are specially responsible for diagnosis and therapeutic problems. We report here a case of an end-stage renal failure patient who has pheochromocytoma, he was treated by automated peritoneal dialysis. The patient is a 47-year-old man who has an IgA glomerulonephritis. On peritoneal dialysis, his blood pressure level remains high despite four antihypertensive drugs association and adequate dialysis. Furthermore, the patient suffered from headaches, sweats and palpitations. This leads to suspect pheochromocytoma. Thus, urinary excretion rates of metanephrines and normetanephrines were high. Radiographic diagnosis tests were negative but MIBG scintigraphy was able to localise the tumor in the left suprarenal gland. He had coelioscopic left adrenalectomy without complications, microscopic studies showed an hyperplasia of the adrenal medulla. Soon after surgery his blood pressure was well controlled by one antihypertensive drug. We conclude that refractory hypertension, as a possible diagnosis, is uncommon in peritoneal dialysis patients. Pheochromocytoma must be eliminated by careful evaluation.

Infections chez les insuffisants rénaux hémodialysés chroniques: étude de 125 cas

Introduction : l’infection est une cause majeure de morbi-mortalite chez les hemodialyses chroniques. Notre objectif etait de determiner leurs caracteristiques clinico-biologiques, bacteriologiques et evolutives.

Prévalence de l’infection a cytomégalovirus chez les receveurs de reins

Introduction : l’infection a Cytomegalovirus (CMV) chez le patient transplante renal peut mettre en jeu le pronostic vital mais aussi la survie du greffon vu l’augmentation du risque de rejet aigu d’ou l’interet d’une prophylaxie. Methodes : nous rapportons une serie de 61 patients transplantes du rein et mis sous prophylaxie anti –CMV et nous etudions la prevalence de l’infection a CMV dans notre serie. Resultats : la prophylaxie anti–CMV proposee dans notre serie est la Valaciclovir (Zelitrex*) des J1 de greffe renale pendant 3mois si le profil CMV est D+ /R+ ou D-/R+ ou D-/R- et pendant 6 mois si D+/R. Nous realisons la serologie CMV a J1, J7 post greffe renale ainsi qu’au 3 eme mois, 6 eme et 12 eme mois apres la transplantation renale. Pendant la periode de l’etude qui s’etend de Decembre 2011 a Juin 2016, nous avons collige 2 cas d’infection a CMV soit 5%. Comme 1 ere observation; Il s’agissait d’un patient âge de 43 ans transplante renal par un donneur vivant apparente. Le profil CMV etait D+/R+. Apres la transplantation renale le patient a ete mis sous traitement prophylactique par Valaciclovir pris pendant 25 jours puis arrete par le patient. Il presentait 30 jours apres l’arret du Valaciclovir, une diarrhee avec fievre et a la biologie une leucopenie, une CRP elevee et une creatinine a 1,3 mg/dl. Une PCR CMV en temps reel est fortement positive. Le traitement par Ganciclovir a ete instaure avec evolution favorable et PCR CMV negative. A J21 de Ganciclovir on a note une aggravation de la leuco-neutropenie. Apres 12 jours d’arret de Ganciclovir, le taux de globules blancs est revenu a la normale spontanement. La deuxieme observation etait porte sur une Patiente A.N âgee de 41 ans, transplantee renale a partir d’un donneur vivant apparente et un statut serologique D+/R+ mise sous prophylaxie par Valaciclovir pendant 90 jours. Elle a presente une insuffisance renale aigue (IRA) (creatinine passant de 176 µmol/l a 316 µmol/l) a 3 mois post transplantation renale. La biopsie du greffon a montre un rejet aigue humoral Borderline et elle etait mise sous Rituximab et Immunoglobulines intra-veineuses. L’evolution etait marquee par la stagnation de la creatinine. Devant l’IRA, la leucopenie et la thrombopenie une PCR CMV a ete pratiquee revenue positive, et la patiente a ete traitee par Cymevan pendant 21 jours. L’evolution a ete marquee par la normalisation du bilan hematologique et l’amelioration de la fonction renale (creatinine = 132 μmol/l). Dans notre centre, nous preconisons la prophylaxie anti-CMV systematique par Valaciclovir. Le 1er cas d’infection a CMV que nous avons note est survenu chez un patient qui n’avait pas pris le Valaciclovir. Chez la deuxieme patiente, l’infection a CMV est survenue a l’arret de la prophylaxie dans un contexte de forte immunosuppression pour un rejet humoral. Conclusion : le faible effectif et le recul court dans notre etude ne permettent pas de conclure. Des etudes plus larges seront d’un grand apport.

PProbable fièvre bilieuse hémoglobinurie secondaire à la prise d’un traitement antipaludéen préventif

Introduction : l’hemolyse aigue compliquee d’une insuffisance renale aigue, en particulier la fievre bilieuse hemoglobinurique (FBH), est une complication rare mais grave, consecutive a la prise d’antipaludiques. La FBH se voit actuellement au cours du traitement curatif ou preventif d’un paludisme. Methodes : Mr SK âge de 40 ans sans antecedents pathologiques a sejourne en Afrique (Gabon et Mali) pendant une semaine, ou il a pris le Quinimax comme un traitement antipaludien preventif en deux prises. Une heure apres la deuxieme prise medicamenteuse il presente des vomissements, douleurs abdominales et 3 episodes d’hematurie. L’examen clinique etait sans particularite, les bandelettes urinaires ont montre une faible proteinurie sans hematurie, la biologie a montre une insuffisance renale aigue et une perturbation transitoire du bilan hepatique sans signes d’hemolyse. La goutte epaisse n’a pas montre la presence de Plasmodium falciparium. La ponction biopsie renale a montre une necrose tubulaire aigue. Le diagnostic le plus probable etait une hepatonephrite d’origine immuno allergique, mais l’evolution rapidement favorable etait contre. Resultats : le Quinimax ne peut provoquer une necrose tubulaire aigue que par le biais d’une hemolyse intra vasculaire, un tableau qui peut se voir au cours de la fievre bilieuse hemoglobinurique (FBH). Notre patient a developpe une necrose tubulaire aigue sans stigmates d’hemolyse ni d’infection par le Plasmodium falciparium. Conclusion : notre observation pose la problematique des hemolyses aigues intra vasculaires au cours des traitements antipaludiques. Elle peut se manifester par une hemoglobinurie avec une insuffisance renale aigue au cours du traitement curatif et preventif d’un paludisme et impose l’arret de tout traitement des l’apparition d’un ictere ou d’urines colorees.