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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.

Disturbed kidney function is a common complication after bone marrow transplantation. Recently, attention has been given to immune-mediated glomerular damage related to graft versus host disease (GVHD). We describe a 19-year-old woman who developed membranous glomerulonephritis after bone marrow transplantation (BMT). Six months later, she developed soft palate, skin and liver lesions considered to be chronic GVHD. Fifteen months after undergoing BMT, this patient presented with nephrotic syndrome. A renal biopsy showed membranous glomerulonephritis associated with a focal segmental glomerulosclerosis. She was started on corticosteroid treatment with good outcome.

Renal involvement in Sjogren's 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 Schirmer's 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.

Kidney disease is a rare complication in patients with the Down's syndrome. However, with increased survival, it appears that a growing number of these patients present with glomerulonephritis. Most cases have been reported as case reports and include lesions such as mesangiocapillary glomerulonephritis with hypo-complementemia, crescentic glomerulonephritis with anti-neutrophil cytoplasmic antibodies (ANCA), amyloidosis and immunotactoid glomerulopathy. We report the observation of a 38-year-old man with the Down's syndrome who presented with severe renal failure, proteinuria and microscopic hematuria evolving over two months. There was no history of congenital heart disease or urinary symptoms. Percutaneous renal biopsy revealed fibrous crescents, rupture of Bowman's capsule and peri-glomerular granuloma; there were no deposits on immunofluorescence study. Thoracic computerized tomography scan showed alveolar congestion. The patient tested negative for ANCA. At the time of reporting, the patient is on regular chronic hemodialysis. Our case illustrates a distinct entity that further expands the spectrum of renal disease known to occur in the Down's syndrome. Early detection of the renal disorders may prevent or slow down the progression.

The association between Kaposi's 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.

Anti-neutrophil cytoplasmic antibody-associated vasculitis and Goodpasture's glomerular basement membrane disease are the most common causes of diffuse alveolar hemorrhage, a life-threatening disease. Systemic lupus erythematosus and the antiphospholipid syndrome are also causes of alveolar hemorrhage. We retrospectively reviewed 15 cases of diffuse alveolar hemorrhage (DAH) associated with renal diseases. Diagnosis of DAH was based on the presence of bloody bronchoalveolar lavage fluid. There were three men and 12 women, with a mean age of 50.5 years (extremes: 24-74 years). Proteinuria and hematuria were observed, respectively, in 15 and 14 cases. Six patients revealed arterial hypertension. Crescentic glomerulonephritis was diagnosed with kidney biopsies in ten cases. The etiology of renal disease was microscopic polyangiitis (MPA) in seven cases, Wegener disease in four cases, systemic lupus erythematous in one case, cryoglobulinemia in one case, myeloma in one case and propyl-thiouracil-induced MPA in one case. Hemoptysis occurred in 14 cases. The mean serum level of hemoglobin was 7.1 g/dL (5.1-10 g/dL). The mean serum creatinine concentration was 7.07 mg/dL (2.4-13.7 mg/dL). Gas exchange was severely compromised, with an oxygenation index <80 mmHg in 14 patients and <60 mmHg in seven patients. Bronchoalveolar lavage was performed in 11 cases, and had positive findings for hemorrhage in all. Methylprednisolone pulses and cyclophosphamide were used in 14 patients. Plasmapheresis was performed in three cases. One patient received cycles of Dexamethasome-Melphalan. Three patients died as a result of DAH. The mortality rate in our study was 20%.

Euphorbia paralias is known in traditional medicine as an anti-inflammatory agent, a purgative and for its local anesthetic property. To the best our knowledge, renal toxicity of this substance has not been previously reported. In this paper, we report the case of a 29-year-old male who developed renal damage following ingestion of Euphorbia paralias. He had been on follow-up for nephrotic syndrome since 1986, although irregularly, with several relapses but each responding well to steroid therapy. A kidney biopsy had not been performed earlier due to refusal by the patient. He was off steroids since April 2008 because the patient developed osteoporosis. He was admitted with general malaise and oliguria to our department in May 2009, following repeated vomiting and watery diarrhea for three days. On examination, he was edematous but had normal vital signs except for a pulse rate of 120/min. Hemoglobin was only 5.5 g/dL but with normal white cell and platelet counts. Blood biochemistry showed evidence of advanced renal failure with a serum creatinine level of 1835 μmol/L and urea at 44.6 mmol/L, sodium of 132 μmol/L and potassium at 4.3 mmol/L. He had features of nephrotic syndrome with severe hypoproteinamia and 24-h urinary protein of 10.45 g. Ultrasonography revealed enlarged kidneys with a reduced echogenecity of the medulla and the papillae. Subsequently, after hemodialysis with blood transfusion, a kidney biopsy was performed that showed focal segmental glomerulosclerosis associated with an acute tubular injury. On intensive interrogation, the patient gave a history of ingesting boiled Euphorbia paralias as a native treatment for edema, ten days prior to the onset of the current illness. A diagnosis of acute renal failure (ARF) resulting from the possible nephrotoxic effect of Euphorbia paralias poisoning was made. He was treated with intermittent hemodialysis and corticosteroids. Serum creatinine values improved after 48 days. At six months following the intoxication, serum creatinine of the patient was 240 μmol/L. In cases of unexplained ARF, a toxic mechanism should always be considered and acute renal failure caused by Euphorbia paralias should be included as a cause if renal toxicity is suspected in those places where it is being used as a native medicine.

We will study the epidemiologic, clinical, biological, therapeutic, prognostic characteristics and predictive factors of development of nephropathy in ankylosing spondylitis patients. We retrospectively reviewed the medical record of 32 cases with renal involvement among 212 cases of ankylosing spondylitis followed in our service during the period spread out between 1978 and 2006. The renal involvement occurred in all patients a mean of 12 years after the clinical onset of the rheumatic disease. Thirty-two patients presented one or more signs of renal involvement: microscopic hematuria in 22 patients, proteinuria in 23 patients, nephrotic syndrome in 11 patients and decreased renal function in 24 patients (75%). Secondary renal amyloidosis (13 patients), which corresponds to a prevalence of 6,1% and tubulointerstitial nephropathy (7 patients) were the most common cause of renal involvement in ankylosing spondylitis followed by IgA nephropathy (4 patients). Seventeen patients evolved to the end stage renal disease after an average time of 29.8 ± 46 months. The average follow-up of the patients was 4,4 years. By comparing the 32 patients presenting a SPA and renal disease to 88 with SPA and without nephropathy, we detected the predictive factors of occurred of nephropathy: tobacco, intense inflammatory syndrome, sacroileite stage 3 or 4 and presence of column bamboo. The finding of 75% of the patients presented a renal failure at the time of the diagnosis of renal involvement suggests that evidence of renal abnormality involvement should be actively sought in this disease., (Copyright © 2011 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.)

A 41-year-old man was admitted for evaluation of nephrotic syndrome associated with microhematuria, hypertension, and moderate renal failure. In serum and urine samples, monoclonal IgG-lambda was detected. Bone marrow examination showed normal representation of all cell lines with normal range of plasma cells. Renal biopsy demonstrated diabetes-like nodular glomerulosclerosis. Immunofluorescence failed to demonstrate the presence of kappa or lambda light chains in the kidney. Electron microcopy showed granular electron-dense deposits along the glomerular basement membranes and in the mesangial nodules. The patient was diagnosed as having light-chain deposition disease (LCDD) without evidence of plasma cell dyscrasia. This report was designed to stress the significant challenges that remain in the diagnosis of LCDD-related glomerulopathy. The salient morphological features that help in making an accurate diagnosis are discussed.

Wegener's granulomatosis (WG) is a necrotizing granulomatous vasculitis involving the nose, paranasal sinuses, lungs, and kidneys. Ocular involvement can occur in about 50% of cases. There are very few reports of WG with orbital inflammation and exorbitism. We report a case of a female patient who presented with exorbitism related to orbital inflammation secondary to WG, with renal involvement. A 29-year-old woman with a previous history of recurrent pan-sinusitis presented with bilateral exophthalmos and renal failure with rapidly progressive glomerulonephritis. Computed tomography showed extensive bilateral soft tissue in the retro-orbital area. Immunologic tests showed the presence of type-C anti-neutrophil cytoplasmic antibodies and renal biopsy revealed pauci immune crescentic glomerulonephritis. The patient was treated with corticosteroids and pulses of cyclophosphamide followed by azathioprine and trimethoprim-sulfamethoxazole. After a follow-up of 10 months, the renal outcome was favorable with improvement of renal function but there was persistence of exorbitism and loss of visual function. Our case suggests that WG should be considered in the differential diagnosis of persistent bilateral exophthalmos. Prompt recognition of this early manifestation is important for the institution of early treatment.

Hereditary complete C4 deficiency has until now been reported in 30 cases only. A disturbed clearance of immune- complexes probably predisposes these individuals to systemic lupus erythematosus, other immune- complex diseases and recurrent microbial infections. We present here a 20- year- old female with hereditary complete C4 deficiency. Renal biopsy demonstrated renal AA amyloidosis. This unique case further substantiates that deficiency of classical pathway components predisposes to the development of recurrent microbial infections and that the patients may develop AA amyloidosis. Furthermore, in clinical practice, the nephrotic syndrome occurring in a patient with hereditary complete complement C4 deficiency should lead to the suspicion of renal AA amyloidosis.

Microscopic polyangiitis is a systemic necrotizing vasculitis of the small vessels. Its typical clinical manifestations are rapidly progressive glomerulonephritis and alveolar hemorrhage. We describe a 30-year-old woman with rapidly progressive glomerulonephritis. Seven years later, she presented with partial loss of motor and sensory function in both lower limbs with sphincter dysfunction. This is the first reported case of epidural inflammation ascribed to microscopic polyangiitis. Possible mechanisms include auto-immune disease.

Brown tumors are unusual but serious complications of renal osteodystrophy. We retrospectively studied 12 patients presenting with chronic renal failure and brown tumor related to secondary hyperparathyroidism. Eleven patients were on chronic hemodialysis. The median duration between renal failure and end stage renal failure was 36 months (range: 12-190 months) and the median duration in dialysis for 11 cases: 92 months (range: 72-252 months). The bone pain was noted in all cases (100%), pathological fracture in one case (8%) and a palpable bone tumor in 10 cases (83%). Elevated serum calcium (> 2.35 mmol/L) was noted in four cases (33%), elevated serum Phosphate (> 1.78 mmol/L) in ten cases (80%), elevated serum alkaline phosphate (> 290 UI/L) in all cases and intact PTH was > 300 pg/mL in all cases with a serum median rate at 1475 pg/mL (range: 682-3687 pg/L). Subtotal parathyroidectomy was performed in all cases with a resultant decrease in size of brown tumors. We report here patient with CKD with unusual frequency and variable locations. This may be attributed to the lack of the new calcium free phosphate binders and calcimimetics.

To evaluate the contribution of electron microscopy to the final diagnosis of glomerulopathies, the authors established a prospective study during the first semester of 2006. A total of 52 kidney biopsies were performed with 3 samples for light microscopy, immunofluorescence, and electron microscopy. Among these renal biopsies, only 20 were examined with electron microscopy because the diagnosis made on the basis of conventional methods had remained unclear or doubtful. In 18 cases, electron microscopy was undertaken for the investigation of primary kidney disease. The 2 remaining cases were transplant biopsies. In this series of 20 patients, there were 3 children with an average age of 9 years and 17 adults with an average age of 35.5 years. Fifteen patients (75%) were nephrotic. The study revealed that electron microscopy was essential for diagnosis in 8 cases (40%) and was helpful in 12 cases (60%). In conclusion, the results showed that the ultrastructural study provides essential or helpful information in many cases of glomerular diseases, and therefore electron microscopy should be considered an important tool of diagnostic renal pathology. As was recommended, it is important to reserve renal tissue for ultrastructural study unless electron microscopy can be routinely used in all biopsies. Thus, this technique could be performed wherever a renal biopsy has to be ultrastructurally evaluated.

Cardiovascular diseases are a major cause of morbidity and mortality in patients with end-stage renal disease (ESRD). The aim of our investigation was the evaluation of an extensive cardiovascular profile in hemodialysis (HD) and peritoneal dialysis (PD) patients. We studied 74 patients with ESRD (38 males, 36 females), maintained either on chronic HD (n= 50) or chronic PD (n= 24) and age and sex matched 20 healthy subjects as controls. The lipid profile, homocysteine (Hcy) and C reactive protein (CRP) were measured. When compared to a healthy population, HD patients displayed a marked atherogenic profile, as attested by increased levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein-cholesterol (LDL-C), apolipoprotein A (Apo A), CRP, Hcy and lower concentrations of high-density lipoprotein-cholesterol (HDL-C), Apo B, albumin (ALB). A significant difference was noted concerning the rates of Apo B, HDL-C, TC, ALB and Hcy. Same biological disorders that those found at HD patients were noted in these PD patients. One also noted lower concentration in Apo A. there were a significant difference with the reference group concerning the rates of albumin, Apo A, HDL-Cl and Hcy. When compared to PD patients, HD patients had significantly decreased concentration of LDL-C. The peculiar metabolic changes observed in the present study confirm the marked tendency of patients with impaired renal function for developing cardiovascular diseases, irrespectively of the type of dialysis. We suggest including uremia-related risk factors in the panel for evaluation of cardiovascular risk in dialysis patients.

Objective: The dietary intake was investigated and food sources were identified among Tunisian ethnic groups from Jerba Island in the south of Tunisia., Methods: Ninety-four subjects of moderate socioeconomic status (47 Berbers and 47 Arabs) aged 32 to 64 y completed a 1-mo qualitative food-frequency questionnaire and a single 24-h dietary recall, and dietary intakes and demographic status were observed from 2006 to 2007., Results: The prevalence of overweight and obesity was not significantly associated with Arab men compared with Berber men. Therefore, obesity was significantly associated with Berber women (P<0.001). Height was significantly different between Arab and Berber women (P<0.001). There were no significant differences in energy intake between men and women. Protein intake was not significantly different between ethnic groups. Milk and dairy products in the Berber group were significantly different from the Arab group. Intakes of calcium, zinc, iron, and folate were below recommended nutrient intakes in men and women in the two ethnic groups. Vitamin E intake was greater in Berbers than in Arabs (P<0.01)., Conclusion: Ethnicity was significantly associated with dietary intakes in the two ethnic groups of Jerba Island.

The dissecting aortic aneurysm (DAA) is a rare pathology that may result in fatal outcome. We report follow up of three cases of DAA patients undergoing maintenance hemo-dialysis who were managed conservatively.

Acute rejection episodes (AREs) are a major determinant of renal allograft survival. The incorporation of new immunosuppressive agents explains, at least partially, the improvement seen in the results of transplantation in recent years. The objectives of this study are to analyze the incidence and severity of AREs, their risk factors and their influence on graft and patient survival. We retrospectively studied 280 kidney transplants performed in adults at the Charles Nicolle Hospital, Tunis, between 1986 and 2004. The diagnosis of ARE was based on clinical data and response to treatment. Allograft biopsies were performed in ten cases. The treatment of AREs consisted of pulse methylprednisolone and anti-thymocyte globulin. There were 186 males (66.4%) and 94 females (33.6%), and their mean age was 31 +/- 8.9 years. Overall, the 280 study patients experienced a total of 113 AREs. Of them, 85 had only one ARE, 28 had two to three and none had more than three AREs. A total of 68 AREs were completely re-versible, 42 were partially reversible while three could not be reversed with treatment. The mean inci-dence of AREs was 40.4%. The incidence was > 45% between 1986 and 1997, decreased to 20.5% between 1998 and 2000 and to 9% between 2001 and 2004. Graft survival rates in patients with and without AREs were respectively 91% and 93% at three years, 82% and 90% at five years and 73% and 83% at 10 years. We found a decrease in the incidence of AREs in recent years in our study patients, and this was related to the introduction of sensitized cross-match and the newer immunosuppressive agents, particularly MMF. Additionally, AREs had a deleterious impact on late graft survival in our study population.

Calpaïn 10 (CAPN10) is the first diabetes gene to be identified through a genome scan followed by positional cloning, encoding the cysteine protease, the calpaïn 10 encodes for a ubiquitously expressed protease implicated in the two fundamental pathophysiological aspects of T2DM insulinoresistance and insulinosecretion. Many investigators, but not all, have subsequently found association between calpaïn 10 polymorphism and type 2 diabetes (T2DM) as well as insulin action and insulin secretion. The aim of this study was to determine whether there is an association between specific polymorphism SNP19 in CAPN10 gene and T2DM in two ethnic groups from Djerba Island. Overall, 162 patients with type 2 of diabetes and 110 healthy volunteers who served as controls for genetic characterization with no family history of diabetes were included in the present study. They consisted of 159 women and 113 men. Their mean +/- SD age was 56,47 +/- 11,86 years. All subjects were genotyped according to SNP 19 polymorphism in CAPN10 gene with PCR method to perform case-control study. After adjusting for gender and age, we found an association with a high risk of T2DM in Djerba Island only in Arab sub-group.

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.

Gastrointestinal (GI) hemorrhage is a frequent and sometimes life-threatening complication of end-stage renal failure. Angiodysplasia (AD), vascular malformation, is the most common cause of recurrent lower-intestinal hemorrhage in patients with renal failure. We report four chronic hemodialysis patients with AD. All patients presented with severe anemia requiring transfusion. GI hemorrhage ceased spontaneously in three cases and after treatment with argon plasma coagulation in another. Diagnosis of AD is usually challenging, since its cause is still unknown, and its clinical presentation is variable. Lesions are multiple in 40-75% of cases, often located in the stomach and duodenum but can affect the colon and the jejunum. Diagnosis is improved by endoscopy which has a much higher sensitivity compared to angiography. Capsular endoscopy may reveal the hemorrhage site in the small intestine when regular endoscopy fails, and therapeutic intervention usually include argon plasma coagulation.

We conducted a prospective study in hemodialysis patients to assess the safety and efficacy of sevelamer, a non-absorbable phosphate binding polymer free of calcium and aluminum, in lowering serum phosphorus, serum intact parathyroid hormone, and serum lipids. Phosphate binders were discontinued during a two-week washout period. We considered the patients with serum phosphorus levels more than 1.8 mmol/l during the washout period eligible for treatment. Sevelamer was administered to 29 hemodialysis patients for eight weeks. Sevelamer reduced the mean serum phosphorus levels to 1.8 mmol/l by the end of the eight-week treatment period (p < 0.0001). Two weeks after the completion of the sevelamer study the mean serum phosphorus levels increased to 2.09 mmol/l (p < 0.02). Mean serum calcium levels did not significantly change during sevelamer trial. Mean serum intact parathyroid hormone declined from 501 pg/ml at the start of the study to 425 pg/l at the end of the eight week treatment period (p = 0.05). In addition, sevelamer reduced the mean serum total cholesterol levels from 5.22 mmol/l to 4.26 mmol/l (p < 0.0001), and the mean serum low density lipoprotein cholesterol from 3.56 mmol/l to 2.79 mmol/l (p < 0.0001) at the end of the study. However, the mean serum levels of high density lipoprotein and triglycerides did not change during the study period. We conclude that sevelamer can control serum phosphorus and reduce the level of intact parathyroid hormone and cholesterol without inducing hypercalcemia or other side effects.

Sarcoidosis is a systemic disease characterized by chronic granulomatous inflammation. Chronic kidney disease (CKD) was reported in less than 1% of patients of sarcoidosis. The prevalence of tubulo-interstitial nephritis (TIN) in sarcoidosis varies from 7 to 27%. In this retrospective study, we present 15 patients with interstitial or glomerular renal involvement secondary to sarcoidosis diagnosed in our center from 1975 to 2006. Patients were 13 (96.6%) females and two males with a mean age of 56.5 years. CKD was present in 14(93.3%) patients, proteinuria in 13(96.6%), and nephrotic syndrome in one. Pulmonary involvement was present in 10 (66.6%) patients. Renal biopsy performed in 12 (80%) patients revealed TIN lesions in 10 (66.6%) patients, extracapillary proliferative glomerulonephritis (GN) in one, and membranous GN type 2 in another. Corticosteroid therapy using prednisolone 0.5 to 1 mg/kg per day was used in 12(80%) patients. Ten (66.6%) patients were followed up for a mean period of 25 months (ranged from 2 to 48 months). The outcome was favorable with 7 (46.6%) patients improved their renal function, 6 (40%) remained with a moderate CKD, one normalized his renal function, and one died suddenly after 2 months of initiating the treatment corticosteroids. We conclude that corticosteroid treatment is efficient in TIN and variably efficient in GN. Patients with sarcoidosis may cause advanced renal failure, which renders it a serious nephrological condition.

Renal involvement with amyloidosis is common but causes patient survival to be poor, rarely reaching 5 years. In this study, we retrospectively reviewed clinical and biological characteristics as well as treatments and outcomes of patients with renal amyloidosis followed for more than 5 years. Between 1975 and 2003, 485 patients were diagnosed with renal amyloidosis including only 12 patients who were followed more than 5 years. The six men and six women of mean age 42.4 years (range 18 to 66 years) displayed renal signs of lower limb edema in all cases; hypertension in four cases, proteinuria on urinalysis in all cases with microscopic hematuria in five cases. Biological tests showed nephrotic syndrome in 11 patients, normal renal function in nine patients, and renal failure in three patients whose mean creatinine was 481.6 micromol/L (range 294 to 726). The amyloidosis was AA type in 11 cases and non-AA in one case. An etiologic survey revealed spondylarthropathy in one patient, pulmonary tuberculosis in two patients, chronic bronchitis in three patients, hepatic hydatic cyst in one patient, Mediterranean familial fever in two patients, Crohn's disease in one patient, Hodgkin's lymphoma in one patient, and multiple myeloma in one patient. Specific treatment was initiated with colchicine in seven patients. At a 110-month mean follow-up (range 53 to 153 months), remission of nephrotic syndrome was observed in four cases, progression to chronic renal failure in two patients, and to end-stage renal failure in five cases (range 53 to 196 months), with stabilization of renal function in seven patients. In conclusion, primary amyloid disease should be optimally suppressed in patients with renal involvement. The role of this treatment in remission of renal amyloidosis is not well established. This efficacy of the treatment has been demonstrated in some patients with improved survival.

A 63-year-old woman presented with severe volume depletion and pre-renal azotemia. She had xerostomia, xerophthalmia and cervical lymhadenopathy. Urine examination revealed proteinuria, hematuria and glycosuria. Laboratory studies, after volume repletion, revealed hyper-gammaglobulinemia. Renal biopsy showed interstitial nephropathy and salivary-gland biopsy showed glandular atrophy and diffuse fibrosis. Diagnosis of leishmaniasis was established by bone marrow examination and serology. The patient was treated with pentavalent antimonial (Glucantime) with an excellent response. The treatment, however, had to be interrupted because of transient nephrotoxicity. After a break of four weeks, the antimonial was reinstituted with no more side effects. Both the sicca syndrome and the nephropathy responded very well to the treatment at nine months follow-up. In this case the presentation of visceral leishmaniasis was atypical, probably because of the partially suppressed immunity. The clue to the diagnosis was the polyclonal hypergammaglobulinemia.

Fifty-eight patients on maintenance hemodialysis in a dialysis unit at Tunis, Tunisia were tested for anti-hepatitis C virus (anti-HCV) antibodies by second generation ELISA test, and for HCV-RNA by nested reverse transcriptase polymerase chain reaction (RT-PCR) of 5' non-coding region. Specificity of the antibodies was confirmed by immunoblot test. HCV genotype was defined using INNO-LIPA test. Twenty-seven out of 58 patients (46.5%) were reactive by ELISA. Transaminase levels were assessed over a six-month period and showed normal average values. Fourteen of the 27 anti-HCV positive patients (51%) were positive by RT-PCR. Type 1b HCV genotype was the most prevalent, seen in all the dialysis patients and one patient in addition, was co-infected with genotype 4. There was a significant correlation between the duration on dialysis (over five years) and the prevalence of anti-HCV-positive patients (P< 0.005) while no correlation existed between the number of blood transfusions and the presence of anti-HCV antibodies. The present study illustrates the high prevalence of HCV infection among Tunisian dialysis patients (51%) and indicates that the spread may be nosocomial rather than transfusion-related.

Effective surgical treatment was carried out in 67 patients who were selected from a population of 336 subjects with renovascular hypertension. Split renal function studies and estimation of plasma renin activity in both renal veins were made to demonstrate the functional significance of the stenosis. The degree of disturbance of these tests did not correlate with the preoperative blood pressure level. The percentage decrease in postoperative blood pressure was directly related to the preoperative blood pressure (P less than 0.01). In 23 postoperative patients followed yearly for 5 years, the blood pressure increased progressively and was positively correlated with the duration of follow up (P less than 0.02). Patients with renovascular hypertension had a lower frequency of blood group 0 and a higher frequency of blood group A than did normotensive controls. The results of the study suggest that, in renovascular hypertension, the antihypertensive effect of surgical treatment is not exclusively related to the physiological consequence of the stenosis and that nonspecific factors, possibly of genetic origin, may determine the blood pressure response after surgical treatment.