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Thrombotic microangiopathy (TMA) is a group of disorders characterized by mechanical hemolytic anemia with thrombocytopenia and an ischemic organic lesion of variable and potentially fatal importance affecting mostly the kidneys and the brain with histologically a disseminated and occlusive microvasculopathy. The incidence of TMA represents 15% of acute kidney failure in oncological setting, largely due to the introduction of anti-angiogenic agents over the past decade. It may be more rarely related to cancer itself. The iatrogenic TMA can be classified into 2 types: The type I, secondary to chemotherapy (mitomycinC, gemcitabine), exposes to a chronic dose-dependent renal injury as well as an increase in morbidity and mortality; iatrogenic type II, secondary to anti-angiogenic agents', results in a dose-independent renal involvement and renal functional recovery is usual when the drug is discontinued. There is no randomized controlled trial to establish EBM-type management in TMA support. However, complement activation pathways and regulatory factors analyses allowed us to understand the mechanisms of endothelial lesions. As a result, the current trend includes the use of immunosuppressive agents in recurrent or plasmapheresis-refractory MAT.

The aim of the present review is to consider the clinical relevance of individualized blood pressure (BP) goal under treatment in hypertensive patients according to their age, comorbidities or established cardiovascular (CV) disease. Evidence from large-scale randomized trials to support a lower BP goal, as initially recommended by guidelines in high-risk hypertensive patients, were lacking. Recently, the randomized intervention SPRINT trial studied two treatment targets for systolic BP (120mm Hg versus 140mm Hg in the intensive and standard treatment group, respectively) among high-risk hypertensive patients, without diabetes and without a history of prior stroke. The trial was stopped prematurely owing to a significantly lower rate of the primary composite outcome and all-cause mortality in the intensive treatment group. Several practical questions have to be considered. First, using an automated measurement system at an office visit during the SPRINT protocol, while the patient was seated alone after 5min of quiet rest, may likely have resulted in lower BP values than would normally be obtained with the routine BP measurement. A target systolic of 120mm Hg in SRPINT trial may be thus equated to a target systolic BP of 130mm Hg in the real-world office setting. Second, careful and repeated examinations of SPRINT participants may have led to fewer adverse events (more frequent in the intensive treatment group) than that expected in the real-world setting. The safety profile of this intensive treatment approach should therefore remain a matter of concern in clinical practice, especially in elderly patients, in diabetic patients or with established CV or renal disease. Orthostatic hypotension should alert the clinician to withhold up titration. Third, beyond the question of BP goal, choice of antihypertensive medication and effective 24-h BP control are important to consider in the context of BP-lowering strategy. In particular, ambulatory BP measurements and during nighttime should be considered for an individualized hypertension care.

The incidence of tuberculosis (TB) is high in patients undergoing chronic dialysis than it is in the general population. The diagnosis of TB is often difficult and extrapulmonary involvement is predominant. This study investigates the spectrum of clinical presentations and outcome in dialysis patients during a nine-year period. TB was diagnosed in 41 patients. Anti-TB drugs, adverse effects of therapy, and outcome were noted. Thirty-eight patients (92.6%) were on hemodialysis and three were on peritoneal dialysis (7.3%). The mean age at diagnosis was 50.8 years and the male/female ratio was 1.16. Four patients had a history of pulmonary TB. Extrapulmonary involvement was observed in 32 (78 %) patients. The bacteriological confirmation was made in 41.46% and histological confirmation was made in 26.83%, and in the rest, the diagnosis was retained on the criterion presumption. Nineteen patients (46.34%) developed adverse effects of antitubercular drugs. Eight patients (19.51%) died during the study from TB or adverse effects of treatment. Low urea reduction ratio and female sex were associated with poor prognosis in our study. The clinical manifestations of TB in patients on dialysis are quite nonspecific, making timely diagnosis difficult, and delaying the initiation of curative treatment, which is a major determinant of the outcome.

Autosomal-dominant polycystic kidney disease (ADPKD) is a systemic disorder associated with various extrarenal complications. There is little information regarding the occurrence and distribution of cardiovascular abnormalities during the course of ADPKD. The major cardiovascular complications of ADPKD include valvulopathies and vascular ectasia. Aneurysm of the atrial septum (ASA) is a very rare manifestation in ADPKD. A 37-year-old woman who was diagnosed with ADPKD was admitted to our hospital for advanced renal failure. Pelvic computed tomography revealed multiple variable-sized cysts in both kidneys. Trans-thoracic echocardiography showed ASA while the patient was completely asymptomatic.

Obstetric cortical renal necrosis is a serious complication that can lead to chronic renal failure and the need for chronic dialysis. The aim of renal cortical necrosis therapy is to restore hemodynamic stability, institute early dialytic therapy, and treat the underlying cause of the disease. Most cases of renal cortical necrosis do not recover a normal renal function despite intensive care. We describe the course of a patient who was diagnosed with acute renal cortical necrosis in pregnancy treated with hemodialysis for three years but then she recovered her renal function.

Anaplastic lymphoma kinase 1 (ALK-1) is a member of the insulin receptor tyrosine kinase family. In clinical practice, three small molecule inhibitors of ALK-1 are used, namely crizotinib, ceritinib and alectinib. Several more agents are in active pre-clinical and clinical studies. Crizotinib is approved for the treatment of advanced ALK-positive non-small cell lung cancer (NSCLC). According to the package insert and published literature, treatment with crizotinib appears to be associated with kidney failure as well as an increased risk for the development and progression of renal cysts. In addition, this agent is associated with development of peripheral edema and rare electrolyte disorders. This review focuses on the adverse renal effects of Crizotinib in clinical practice.

Resume L’intro du lenalidomide dans l’arsenal therapeutique de tumeurs malignes a represente une etape importante dans la gestion du myelome multiple. Cependant, son utilisation est associee a plusieurs effets toxiques dont l’atteinte renale. Cet article fait le point sur la pharmacocinetique de la molecule, ses principaux effets indesirables renaux et propose des recommandations pour l’ajustement de la posologie chez les patients atteints d’insuffisance renale sous-jacente.

The arteriovenous fistula (AVF) is the vascular access of the first choice for hemodialysis (HD). Studies on patency of AVF and its affecting factors reveal a high risk for access failure. The aim of this study was to assess the primary and secondary AVF patency and their determinant factors. It was a retrospective, descriptive study conducted in the HD facility of the Nephrology Department in Rabta University Hospital. We included AVF created before December 2009 in end-stage renal disease (ESRD) patients. The end of the follow-up was fixed in December 2013. We included 126 AVFs created in 111 patients; 22.5% were aged >65 years, 39.6% were diabetic, 68.5% were hypertensive, and 26.1% had peripheral vascular disease. The primary patency rates were 78% at one year and 42% at five years. The secondary patency rates were 80% at one year and 69% at five years. Multivariate analysis revealed that the factors affecting the primary patency of AVF were: the use of jugular catheter for longer than three months (odds ratio (OR):1.91, P = 0.044) and a C-reactive protein >5 mg/L (OR: 1.7, P = 0.049). Aging (>65 years) (OR: 2.46, P = 0.042), referral time to a nephrologist

Fluoroquinolones are usually well tolerated with a minimum of serious adverse effects; renal toxicity is uncommon. Apart from the renal side effects of ciprofloxacin, we aimed to highlight the renal impact of a ciprofloxacin overdose, and thus conducted a prospective study in the Department of Nephrology at La Rabta Hospital between 2010 and 2015. The cohort database was continually updated until the inclusion of five patients who were subjected to an overdose and who were initially admitted to the medical intensive care unit and then transferred to our department for acute renal failure (ARF) due to ciprofloxacin ingestion requiring urgent hemodialysis. All patients developed ARF after 12–36 h of ingestion. Renal ultrasound was normal in all cases. Twenty-four-hour proteinuria was present but not significant in one case, while microscopic hematuria was present in one case. Treatment consisted of supportive therapy and extrarenal purification by conventional intermittent hemodialysis. Four patients recovered normal renal function within 3 weeks and the remaining patient eventually had chronic kidney failure.

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.

The aim of this study is to evaluate the features of visceral leishmaniasis (VL) in adults with nephropathy, who were not infected with the human immunodeficiency virus. This is a retrospective study of 14 adults hospitalized between 2000 and 2014, with VL and renal involvement. Clinical, biological, and therapeutic data were collected from the patients' medical files. Eleven women and three men, most of whom were from the North of the country, with a mean age of 40.5 years were studied. Lupus was present in five cases, the Sicca syndrome in three cases, diabetes in one case, renal failure on dialysis in two cases, and there were three renal transplant recipients. Major clinical symptoms were fever and weakness in all cases. Enlargement of the spleen was present in eight cases and hepatomegaly in six cases. Biologic inflammatory syndrome and anemia were present in all cases, and pancytopenia was present in seven cases. Renal insufficiency was noted in all cases. Diagnosis of VL was confirmed by bone marrow examination or serology. Treatment consisted of antimoniate in 10 cases and amphotericin B in four cases. Seven deaths were recorded. Clinical symptoms of VL are atypical in patients with nephropathy and therefore, the diagnosis should be suspected in such patients because VL is still endemic in our country.

Various adverse reactions may occur after intravesical bacillus Calmette-Guérin (BCG) therapy. Although the virulence of attenuated BCG is low, serious complications such as bacterial cystitis, bladder contractures, granulomatous prostatitis, epididymitis, orchitis, and systemic reactions such as fever and malaise have been described. Disseminated granulomatosis such as hepatitis and pneumonitis have also been described, but are rare. We report here the case of a 67-year-old patient who presented with renal granulomatosis with polyangiitis following intravesical BCG therapy for superficial bladder tumor. The biological evaluation revealed the presence of perinuclear anti-neutrophil cytoplasmic antibodies with specificity for antimyeloperoxidase. Renal biopsy specimen revealed pauci-immune crescentic glomerulonephritis with segmental glomerular necrosis, presence of granulomas and no evidence of any caseating necrosis. He received antituberculosis drugs in addition to corticosteroids and cyclophosphamide without any improvement of the renal function.

A patient is admitted in hospital to explore a nephrotic proteinuria associated with milky urine. This is explained by a chyluria (presence of lymphatic fluid in the urines), which is due to a pyelolymphatic fistula probably linked to a lymphatic filariasis. Usually, the diagnosis of chyluria can be confirmed by the presence of urinary chylomicrons. The presence of an urinary-lymphatic fistula can be proved by different techniques (cystoscopy, retrograde pyelography, uroscanner, lymphoscintigraphy). The main cause of chyluria is parasitic infections (filarial infection, echinococcus, cysticercosis), but other causes can be found, such as granulomatosis, neoplasia, lymphatic malformations, or sequela of surgery or traumatism. Chyluria is one of the causes of post-nephronic nephrotic proteinuria. Depending on the impact of the chyluria for the patient, there will either be no treatment, or a treatment by sclerotherapy or surgery.

Drug-induced acute interstitial nephritis (AIN) is an established cause of acute kidney injury (AKI). Antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs) are the most frequent offending drugs [1]. Only a few vitamin K antagonist-induced AIN cases have been reported. Some publications describe AIN associated with fluindione (Previscan®), an anticoagulant of the antivitamin K family, derived from indanedione, exclusively marketed in France. We present an additional case of AIN secondary to fluindione and review the available literature. A 70-year-old woman was hospitalized for AKI. Her treatment list included amlodipine and atenolol. In December 2007, the serum creatinine (SCr) level was 70 μmol/L and an asymptomatic atrial fibrillation was detected. Fluindione was hence initiated. SCr rose to 220 μmol/L (04/08). On admission, her SCr level had reached 3.4 mg/dL and fluindione was stopped. Blood pressure was 110/ 80 mmHg, and neither cutaneous rash nor peripheral lymphadenopathy was found. Laboratory tests showed SCr 299.2 μmol/L, proteinuria 2 g/24 h (1 g albumin and low-molecular-weight proteins, each) and negative urine sediment. A renal ultrasound revealed reduced-sized (10 cm) kidneys without obstructive uropathy. Immunological analyses were negative. A transjugular renal biopsy was performed. The renal biopsy included 11 glomeruli; 5 were sclerotic and 6 were normal. A diffuse infiltrate of lymphocytes, eosinophils and monocytes was found in the interstitium associated with severe tubulitis (Figure ​(Figure1).1). Immunostains demonstrated CD3-positive lymphoid cells in the interstitium (Figure ​(Figure2)2) compared to CD20 immunohistochemical staining (Figure ​(Figure3).3). Immunofluorescence was negative. Electron microscopy was not performed. The diagnosis of fluindione-induced AIN (FI-AIN) was made. Despite withdrawal of the offending agent replaced by acenocoumarol, and oral corticosteroid therapy (1 mg/kg/day), renal function did not return to baseline values after 1 month (SCr, 259.6 μmol/L) but improved to 199.8 μmol/L 6 months later. Fig. 1 Renal biopsy specimen showing expansion of the renal interstitium by large lymphocyte inflammatory cell aggregates and severe tubulitis. Masson's trichrome stain; original magnification ×40. Fig. 2 Immunophenotyping analysis showing positive CD3 + T cells. Original magnification ×400. Fig. 3 Immunophenotyping analysis showing few CD20 + lymphocytes. Original magnification ×400. About 15% of the renal biopsies performed on patients with AKI demonstrate drug-induced AIN as the cause of the renal insufficiency. Only 13% of these patients showed the classic triad of rash, fever and eosinophilia. Discontinuation of the offending drug remains the first therapeutic step. Nevertheless, a considerable part of the affected patients may develop ESRD (23.4%). An important clinical prognostic factor is the average duration of the renal dysfunction; a cut-off point of 2–3 weeks seems relatively determining [1–3]. Few cases of vitamin K antagonist-induced AIN have been reported with warfarin, phenindione and fluindione [4]. Hypersensitivity reactions occur in 0.2–2% of cases [5]. Review of the literature revealed 16 biopsy-proven FI-AIN [5–11], including this case (Table ​(Table1).1). AKI appeared 7.5 ± 6.9 weeks (range 2–20) after introducing the offending drug. The average baseline SCr was (102.08 ± 35.2; range 62.5–149.6 μmol/L) obtained 7.5 ± 4.6 (range 0.5–16) months before the onset of FI-AIN. Fifty percent of patients showed proteinuria (0.3–19.7 g/24 h) associated with microscopic haematuria (12.5%) and leukocyturia (12.5%). The highest SCr reached between 135.52 and 824.56 μmol/L with a mean of 425.04 ± 243.76 μmol/L. Two patients (12.5%) required several sessions of haemodialysis [9]. Thirty-one percent (5/16) presented the classical triad of drug-induced AIN: fever, maculopapular rash and eosinophilia. The renal biopsy was obtained in 14 out of the 16 patients. In all cases, a diffuse inflammatory infiltrate composed of lymphocytes, eosinophils, monocytes and plasma cells invading the interstitial compartment was observed. Fluindione was withdrawn in all patients. Eleven patients (68.75%) were treated with steroids. Steroid doses and the duration of treatment were not uniform. The most common scheme consisted of oral prednisone (0.5–1 mg/kg/day) tapering off over 8–12 weeks. Intravenous pulses of methylprednisolone (250–500 mg daily for 3 days) were occasionally used. In 3 out of these 11 steroid-treated patients (27.3%), SCr never reached baseline values. The five patients who did not receive steroids had a complete recovery of baseline renal function 10 days to 3 weeks after withdrawal of the offending drug. However, the largest study to date by Gonzalez et al. demonstrated the beneficial effects of steroids for the treatment of drug-induced AIN, especially when initiated soon after withdrawal of the offending agent [1]. Table 1 Characteristics of patients with fluindione-induced acute interstitial nephritis

Hypertension (HTN) in chronic kidney disease (CKD) is influenced by blood pressure (BP) and the progression of CKD, including hemodialysis and renal transplantation. To date, the efficacy of antihypertensive drug strategies has chiefly been assessed by measuring steady-state systolic, diastolic and mean arterial pressures (MAP). However, recently elucidated features of the BP curve have highlighted other important goals, that is, the specific roles of pulse pressure (PP), arterial stiffness, pulse wave velocity (PWV) and wave reflections as potentially deleterious factors affecting the progression of HTN and CKD. Pharmacological strategies to date have included progressive withdrawal of alpha-blocking agents; efficacy of beta-blockers for coronary prevention; use of angiotensin blockade in HTN with glomerular injury, using angiotensin-converting enzyme inhibition or receptor blockade, as mono but never double-blockade, to avoid major complications; development of combination therapies with diuretics and/or calcium channel blockers. Nowadays, most clinical trials show that SBP, DBP and MAP-lowering is an effective strategy, although results no longer show preference for any specific drug class.Studies of arterial stiffness in CKD have become crucial. In older individuals, PWV is considerably elevated. The 'stiffness gradient' disappears or is inverted (normally, aortic PWV is lower than brachial PWV). Despite BP-lowering, PP is insufficiently dampened, thus promoting microcirculatory damage, progression of arterial calcifications and disturbed wave reflections, which all increase the risk of mortality. In the absence of effective hemodialysis or graft, increased arterial stiffness is therefore a major cardiovascular risk factor in CKD.

Objectifs La nephropathie a IgA (NIgA) est une des glomerulonephrites les plus communes caracterisee par le depot d'IgA dans le mesangium glomerulaire. Elle progresse vers l'insuffisance renale (IR) terminale dans 10 a 30 % des cas apres 20 ans d'evolution. Methodes Il s'agit d'une etude retrospective incluant 41 patients presentant un NIgA colliges sur une periode de sept ans (2007–2015). Les donnees cliniques et para cliniques ont ete recueillies a partir des observations medicales. Resultats Quarante et un patients avaient une NIgA, avec predominance masculine (sex-ratio a 0,63). L'âge moyen de nos patients au moment du diagnostic etait de 33 ans ± 14 ans. Il s'agit d'une maladie de Berger chez 24 patients (58,5 %), d'un purpura rhumatoide dans 4 cas (9,7 %) et d'une nephropathie a IgA secondaire dans 13 cas (31,7 %). L'hematurie microscopique etait retrouvee dans tous les cas alors que l'hematurie macroscopique recidivante etait notee que dans 17 cas (41 %). Une HTA etait presente dans 50 % des cas. La creatinemie moyenne etait de 36,4 mg/l (17–72 mg/l). Une insuffisance renale etait objectivee dans 51,2 % des cas et un syndrome nephrotique etait note dans 65 % des cas. L'evolution vers L'IR terminale etait retrouvee dans 17 % des cas. L'etude en immunofluorescence a revele une fixation mesangiale d'IgA dans tous les cas. Des lesions de microangiopathie thrombotique (MAT) etaient presentes dans 11 cas (26,8 %). Une fibrose interstitielle etait retrouvee dans 16 cas (39 %) alors qu'une atteinte vasculaire a type d'arteriosclerose a ete mise en evidence sur 5 biopsies renales (12 %). L'analyse statistique a permis de retenir 5 facteurs pronostic correles avec la survenue d'IR terminale : La creatinine initiale (p = 0,006), l'HTA (p = 0,02), l'atrophie tubulaire (p = 0,04), la fibrose interstitielle (p = 0,03) et la sclerose glomerulaire (p = 0,01). L'HTA etait fortement correlee a la presence d'une sclerose glomerulaire (p = 0,005) et d'une MAT (p = 0,01). Conclusion La severite de la sclerose et de la fibrose des arterioles renales est assez bien correlee a la presence de l'HTA et a l'importance de la sclerose glomerulaire. Les lesions vasculaires ont ete fortement incriminees dans l'apparition et la progression de l'insuffisance renale selon plusieurs etudes. Par sa frequence et sa gravite a long terme, la nephropathie a Ig A constitue une preoccupation majeure, d'autant qu'il n'existe pas actuellement de traitement curatif. L'insuffisance renale initiale et l'HTA sont les principaux facteurs pronostiques de la nephropathie a IgA. La prise en charge se base sur le diagnostic precoce d'ou l'interet du depistage.

Objectifs La granulomatose renale est une infiltration inflammatoire de l’interstitium renal. Elle realise un tableau de nephropathie tubulo-interstitielle dans la plupart des cas. L’hypertension arterielle complique exceptionnellement cette atteinte. Methodes Nous rapportons une observation d’une granulomatose renale compliquee d’hypertension arterielle maligne et d’insuffisance renale aigue. Resultats Nous rapportons le cas de la patiente A. S âgee de 18 ans, sans antecedents notables, hospitalisee pour prise en charge d’une sarcoidose sys-temique. Le diagnostic de sarcoidose a ete retenu devant : une atteinte pulmonaire avec au lavage broncho alveolaire un rapport CD4/CD8 = 1,2 et a la TDM thoracique des adenomegalies mediastinales, une atteinte neurologique avec cliniquement une paralysie faciale peripherique et a l’IRM cerebrale un hypersignal de la substance blanche cadrant avec une neurosarcoidose, une hepatomegalie, une atteinte cutanee a type d’erytheme noueux et a la biologie une lymphopenie. Dans les suites du traitement cor-ticoide, la patiente a presente des chiffres tensionnels eleves a 190/120 mmHg. Le bilan etiologique de cette hypertension arterielle etait negatif : pas de stenose a l’echographie doppler des arteres renales, pas de coarctation de l’aorte a l’angioscanner thoracique, le dosage des derives methoxyles etait normal, la cortisolemie etait normale et le rapport renine/aldosterone etait celui d’un hyperaldosteronisme secondaire. L’imagerie renale (echographie et scanner) a mis en evidence un aspect macronodulaire du rein gauche. L’histologie renale a revele une granulomatose gigantocellulaire centree par une necrose caseeuse comprimant les structures renales. Le diagnostic de tuberculose a ete retenu et un traitement antituberculeux etait alors instaure avec degression de la corticotherapie. Le diagnostic d’hypertension arterielle maligne compliquant la granulomatose renale etait retenu devant le retentissement multi visceral de l’HTA (œdeme papillaire, insuffisance renale rapidement progressive) et l’hyperaldosteronisme secondaire. La patiente a ete mise sous 5 antihypertenseurs (inhibiteur calcique, antialdosterone, un ARA II, un betabloquant et un alphabloquant). L’evolution etait marquee par l’amelioration de l’etat general, l’equilibration des chiffres tensionnels mais persistance d’une insuffisance renale avancee necessitant le recours a l’hemodialyse apres un delai de 16 mois. Conclusion Si les manifestations pulmonaires conduisent aisement au diagnostic de tuberculose, les atteintes renales sont plus rares. Il importe de ne pas les meconnaitre, car elles sont potentiellement graves.

Objectifs Au cours du lupus erythemateux systemique (LES), l'hypertension arterielle (HTA) est une manifestation frequente de mecanisme multifactoriel. On se propose de determiner le profil anatomo-clinique de l'HTA chez les patients ayant une nephropathie lupique (NL). Methodes Il s'agit d'une etude retrospective portant sur 42 patients suivis pour LES colliges sur une periode de 7 ans (2007–2015). Nous avons etudie leurs caracteristiques cliniques, biologiques, histologiques et evolutives. On a recherche l'hypertension arterielle definie par une elevation de la pression arterielle systolique > 140 mmHg et/ou de la pression arterielle diastolique > 90 mmHg et on a etudie ses differentes caracteristiques ainsi que son traitement. Resultats Il s'agit de 38 femmes et 4 hommes soit un sex ratio H/F a 0,1. L'âge moyen au moment du diagnostic de la maladie lupique de 41,2 ans (18–59 ans). 25 patients soit 59 % etaient hypertendus. L'âge moyen d'apparition de l'HTA etait de 45,3 ans. Le delai moyen de diagnostic de l'HTA par rapport a celui du LES etait de 15,2 mois. Tous les patients hypertendus avaient une Nephropathie lupique confirmee histologiquement (classe III: 9 cas, classe IV: 12 cas, classe II: 1 cas, classe V : 4 cas). Des lesions de microangiopathie thrombotique (MAT) etaient notees dans 3 cas (7 %) compliquees d'HTA maligne. Un syndrome des antiphopholipides (SAPL) a ete retrouve dans 11 cas (26 %). Trois patients (7 %) ont presente une HTA secondaire a la corticotherapie apres un delai moyen de 10 mois (5–34 mois). Le traitement etait base essentiellement sur les inhibiteurs de l'enzyme de conversion (IEC), soit en monotherapie, soit en association avec les diuretiques ou les inhibiteurs calciques ou plus rarement les centraux. La duree de suivi moyenne etait de 52 mois (15 jours-72 mois). Le taux de survie a 5 ans etait de 84,5 %. L'evolution etait marquee par la survenue d'accidents vasculaires cerebraux associes a l'HTA et a un SAPL dans 5 cas. On a deplore 6 deces. Les causes de deces etaient dominees par les complications thrombo-emboliques. Conclusion La frequence de l'HTA (59 %) est superieure a celle rapportee dans la litterature. Elle est plus frequente et plus severe en cas de lesions glomerulaires proliferatives et/ou de lesions de MA. Le traitement de l'HTA repose sur l'utilisation des IEC souvent en bitherapie.

Objectifs La stenose de l'artere renale (SAR) est souvent associee a une maladie atheromateuse diffuse et, en consequence, a une morbidite et une mortalite cardiovasculaires accrues. Le nombre de revascularisations de l'artere renale a considerablement augmente ces dernieres annees. Mais les succes rapportes par cette procedure, par rapport a un traitement medical seul, semblent modestes tant sur le controle de la pression arterielle que sur la progression de l'insuffisance renale. Methodes C'est une etude retrospective portant sur 14 patients colliges sur une periode de sept ans (2007–2015). Les donnees cliniques et para cliniques ont ete recueillies a partir des observations medicales. Nous avons elimines les dossiers ou il n'y a pas eu de confirmation radiographique de SAR. Resultats Quatorze patients etaient porteurs de stenoses des arteres renales. Une HTA etait objectivee dans 10 cas (71,4 %). Une retinopathie hypertensive etait retrouvee dans 5 cas (35 %). A la biologie, on a note une insuffisance renale dans 7 cas (50 %) avec une creatinemie moyenne de 21 mg/l. Le doppler des arteres renales a mis en evidence une SAR dans tous les cas. On a confirme le diagnostic par une angiographie renale dans deux cas, un angioscanner dans 4 cas et une angio-IRM dans 5 cas. Le seuil stenotique significatif avec une reduction du diametre > 60 % a ete retrouve dans 71 % des cas. La scintigraphie renale avec le test au captopril etait pratiquee dans 3 cas (21 %). Sur le plan therapeutique, le traitement medicale comportant les regles hygieno-dietetiques, le traitement antihypertenseur, l'utilisation d'antiagregants plaquettaires et de statines etait la regle dans tous les cas sans recours a un geste de revascularisation dans 6 cas (42,8 %). Une revascularisation par angioplastie endoluminale a ete pratiquee dans 5 cas (35 %) avec une evolution vers l'IR terminale dans 3 cas (60 %). L'analyse univariee a defini les parametres correles avec les SAR : la pression arterielle systolique (p = 0,03), la pression pulsee (p = 0,005), l'âge (p 50 ans (p = 0,02), le tabagisme (p = 0,003) et l'hyperuricemie (p = 0,01) Conclusion La stenose des arteres renales est une maladie heterogene et multi-factorielle de diagnostic anatomique aise mais dont la prise en charge varie considerablement selon les particularites anatomique de la stenose, la severite de l'HTA et le retentissement renal.

Objectifs L’atteinte cardiaque est frequente au cours du lupus erythemateux systemique (LES), et peut concerner le tissu pericardique, myocardique, valvulaire ou les arteres coronaires. En effet, le cœur est touche dans 15 % a 82 % des cas et represente l'une des plus grandes causes de mortalite. Methodes Etude retrospective et descriptive portant sur les dossiers de patients hospitalises au Service de Nephrologie de l'Hopital la Rabta, entre 2007 et 2015 pour LES (retenu sur au moins 4 criteres sur 11 de l'ACR). Resultats La duree moyenne d’evolution du lupus etait de 11 ans. Il s’agissait de 38 femmes et de 4 hommes soit un sex-ratio de 0,1, d’âge moyen de 40 ans. Les manifestations cardiaques etaient retrouvees chez 12 patients, soit 28 % des cas. Elles etaient dominees par la pericardite lupique notee dans 7 cas, compliquee d’une tamponnade dans un cas. Une endocardite type Libman-Sacks etait retrouvee dans un cas et une myocardite dans deux cas. Deux patientes avaient presente une insuffisance coronarienne en rapport avec un syndrome des antiphospholipides. Ces manifestations etaient survenues au decours de la pathologie initiale avec une clinique peu parlante. En effet, les patients ne presentaient qu’une dyspnee stade II (5 cas) a III (2 cas). A l'electrocardiogramme, un microvoltage etait note dans 1 cas (pericardite), un trouble du rythme dans 2 cas (myocardite) et un syndrome coronarien ST moins dans deux cas. L’echographie cardiaque avait contribue au diagnostic de pericardite dans 7 cas, de myocardite dans deux cas et d’endocardite dans 1 cas. Une IRM myocardique a confirme le diagnostic de myocardite dans les deux cas. L’atteinte valvulaire etait retrouvee chez 6 de nos patients : la mitrale etait la plus touchee (4 cas). Une HTAP etait notee dans 4 cas. Le traitement etait le renforcement de la corticotherapie associe a un traitement immunosuppresseur dans tous les cas, une anticoagulation curative dans deux cas, un traitement specifique de l'atteinte coronarienne et de l'insuffisance cardiaque dans 4 cas. L’evolution etait marquee par l'amelioration clinique et radiologique dans 11 cas. Un deces est survenu dans les suites d’une insuffisance cardiaque globale. Conclusion La pericardite est la manifestation cardiaque la plus frequente au cours du LES, cependant d’autres manifestations cardiaques peuvent se rencontrer telles que l'atteinte valvulaire, la myocardite, l'atteinte coronaire et l'insuffisance cardiaque. L’atteinte myocardique est inhabituelle et constitue un signe de gravite au cours du LES.

Aortic stiffness is associated to chronic kidney disease. Although it is well established that patients with chronic kidney disease have classical and non classical risk factors correlated to a high pulse wave velocity, there is no data on the deleterious effect of high pulse wave velocity on intra renal microvasculature. The aim of this study was to explore the relationship between arterial stiffness, assessed by cfPWV and renal microvascular lesions assessed by renal biopsy. In 25 patients who went through a renal biopsy we analysed renal vascular lesions, and obtained cfPWV using a Complior device. cfPWV and age were positively correlated to the severity of vascular lesions. These results support the hypoyhesis that an elevated pulsatility in target organ microcirculation such as kidneys leads to vessel damage and contributes to worsen glomerular filtration rate.