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Qi H, Xu C, Yan H, et al: Comparison of icodextrin and glucose solutions for long dwell change in peritoneal dialysis: a metaanalysis of randomized managed trials. Martis L, Patel M, Giertych J, et al: Aseptic peritonitis due to peptidoglycan contamination of pharmacopoeia normal dialysis answer. Peritoneal Dialysis Adequacy 2006 Work Group: Clinical follow pointers for peritoneal adequacy: update 2006. Woywodt A, Meier M, Kaiser D, et al: In-center intermittent peritoneal dialysis: retrospective ten-year single-center expertise with thirty consecutive patients. Ortega O, Gallar P, Carreno A, et al: Peritoneal sodium mass removal in steady ambulatory peritoneal dialysis and automated peritoneal dialysis: influence on blood strain management. Peritoneal Dialysis Adequacy Work Group: Clinical apply tips for peritoneal dialysis adequacy. Harty J, Boulton H, Venning M, et al: Impact of increasing dialysis volume on adequacy targets: a prospective study. Locatelli F, Fouque D, Heimburger O, et al: Nutritional standing in dialysis patients: a European consensus. Mehrotra R: Nutritional issues in peritoneal dialysis patients: how do they differ from that of sufferers present process hemodialysis Bergstrom J, Furst P, Alvestrand A, et al: Protein and vitality intake, nitrogen stability and nitrogen losses in sufferers handled with continuous ambulatory peritoneal dialysis. Martin-Del-Campo F, Gonzalez-Espinoza L, Rojas-Campos E, et al: Conventional dietary counselling maintains dietary status of sufferers on steady ambulatory peritoneal dialysis in spite of systemic irritation and decrease of residual renal operate. Teixido-Planas J, Ortiz A, Coronel F, et al: Oral protein-energy supplements in peritoneal dialysis: a multicenter study. Koulouris S, Symeonides P, Triantafyllou K, et al: Comparison of the consequences of ramipril versus telmisartan in decreasing serum ranges of high-sensitivity C-reactive protein and oxidized low-density lipoprotein ldl cholesterol in sufferers with sort 2 diabetes mellitus. Bozkurt D, Cetin P, Sipahi S, et al: the consequences of renin-angiotensin system inhibition on regression of encapsulating peritoneal sclerosis. Oner-Iyidogan Y, Gurdol F, Kocak H, et al: Appetite-regulating hormones in persistent kidney disease patients. Stenvinkel P, Heimburger O, Paultre F, et al: Strong association between malnutrition, irritation, and atherosclerosis in persistent renal failure. Bergstrom J, Lindholm B: Malnutrition, cardiac illness, and mortality: an built-in point of view. Nakanishi I, Moutabarrik A, Okada N, et al: Interleukin-8 in persistent renal failure and dialysis patients. Shemin D, Maaz D, St Pierre D, et al: Effect of aminoglycoside use on residual renal function in peritoneal dialysis patients. Dittrich E, Puttinger H, Schillinger M, et al: Effect of radio distinction media on residual renal perform in peritoneal dialysis patients-: a potential study. Li Y, Zhang L, Gu Y, et al: Insulin resistance as a predictor of heart problems in sufferers on peritoneal dialysis. Wei M, Esbaei K, Bargman J, et al: Relationship between serum magnesium, parathyroid hormone, and vascular calcification in patients on dialysis: a literature evaluate. Tonelli M, Wiebe N, Culleton B, et al: Systematic evaluate of the scientific efficacy and security of sevelamer in dialysis sufferers. Losito A, Kalidas K, Santoni S, et al: Association of interleukin-6 -174G/C promoter polymorphism with hypertension and left ventricular hypertrophy in dialysis sufferers. Perez Fontan M, Rodriguez-Carmona A, Garcia-Naveiro R, et al: Peritonitis-related mortality in sufferers present process chronic peritoneal dialysis. Academic Subcommittee of the Steering Committee of the Network 9 Peritonitis and Catheter Survival Studies. Mehrotra R, Singh H: Peritoneal dialysis-associated peritonitis with simultaneous exit-site an infection. Bernardini J, Bender F, Florio T, et al: Randomized, double-blind trial of antibiotic exit site cream for prevention of exit website infection in peritoneal dialysis sufferers. McCormack K, Rabindranath K, Kilonzo M, et al: Systematic review of the effectiveness of stopping and treating Staphylococcus aureus carriage in decreasing peritoneal catheter-related infections. Pennell P, Rojas C, Asif A, et al: Managing metabolic complications of peritoneal dialysis. Dong J, Luo S, Xu R, et al: Clinical traits and outcomes of "silent" and "non-silent" peritonitis in patients on peritoneal dialysis. Perez-Fontan M, Lueiro F: Escherichia coli peritonitis in patients present process peritoneal dialysis: a significant issue which will worsen.

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Valentini J, Grotto D, Paniz C, et al: the affect of the hemodialysis treatment time underneath oxidative stress biomarkers in continual renal failure sufferers. Bohler J, Schollmeyer P, Dressel B, et al: Reduction of granulocyte activation during hemodialysis with regional citrate anticoagula- 1911. Ono K, Ueki K, Inose K, et al: Plasma levels of myeloperoxidase and elastase are differentially regulated by hemodialysis membranes and anticoagulants. Caimi G, Carollo C, Montana M, et al: Nitric oxide metabolites, leukocyte activation markers and oxidative status in dialyzed topics. Takeshita K, Susuki C, Itoh S, et al: Preventive effect of alphatocopherol and glycyrrhizin in opposition to platelet-neutrophil advanced formation induced by hemodialysis membranes. Merino A, Portoles J, Selgas R, et al: Effect of various dialysis modalities on microinflammatory standing and endothelial injury. Filiopoulos V, Hadjiyannakos D, Takouli L, et al: Inflammation and oxidative stress in end-stage renal illness sufferers handled with hemodialysis or peritoneal dialysis. Costa E, Rocha S, Rocha-Pereira P, et al: Neutrophil activation and resistance to recombinant human erythropoietin therapy in hemodialysis patients. Witko-Sarsat V, Friedlander M, Capeillere-Blandin C, et al: Advanced oxidation protein merchandise as a novel marker of oxidative stress in uremia. Pihlstrom H, Mjoen G, Marz W, et al: Neopterin is related to cardiovascular occasions and all-cause mortality in renal transplant patients. Caimi G, Carollo C, Montana M, et al: Elastase, myeloperoxidase, nitric oxide metabolites and oxidative status in subjects with scientific secure persistent renal failure on conservative remedy. Cohen-Mazor M, Sela S, Mazor R, et al: Are primed polymorphonuclear leukocytes contributors to the excessive heparanase ranges in hemodialysis sufferers Dounousi E, Koliousi E, Papagianni A, et al: Mononuclear leukocyte apoptosis and inflammatory markers in sufferers with persistent kidney illness. Ruiz P, Gomez F, Schreiber A: Impaired function of macrophage Fc gamma receptors in end-stage renal disease. Zaza G, Pontrelli P, Pertosa G, et al: Dialysis-related systemic microinflammation is associated with particular genomic patterns. Granata S, Zaza G, Simone S, et al: Mitochondrial dysregulation and oxidative stress in patients with persistent kidney illness. Ferretti G, Bacchetti T, Masciangelo S, et al: Lipid peroxidation in hemodialysis patients: effect of vitamin C supplementation. Zaza G, Granata S, Sallustio F, et al: Pharmacogenomics: a new paradigm to personalize therapies in nephrology sufferers. Chatenoud L, Dugas B, Beaurain G, et al: Presence of preactivated T cells in hemodialyzed patients: their attainable position in altered immunity. Thus, alterations in signal-feedback mechanisms and in production, transport, metabolism, elimination, and protein binding of hormones happen somewhat commonly in circumstances affecting the kidney. The objective of this chapter is to overview particular endocrine abnormalities that manifest as a consequence of kidney disease. Later evidence suggests that fructose not solely induces metabolic syndrome, hyperuricemia, and weight gain15 but in addition exerts direct antagonistic effects on renal tubular cells. Animal fashions of insulin deficiency suggest that the impact of insulin on protein turnover is mediated by way of the activation of the ubiquitin proteasome pathway. In a later analysis of new users of oral hypoglycemic treatment monotherapy in patients with type 2 diabetes mellitus, larger risk of mortality was associated with glibenclamide, glipizide, and rosiglitazone than with metformin. A cross-sectional analysis confirmed considerably larger (>38%) cardiovascular and all-cause mortality in rosiglitazone users,51 according to a systematic evaluation of trials in patients with type 2 diabetes mellitus that confirmed increased risk of myocardial infarction and a borderline elevated threat of dying from cardiovascular causes. Thus, a decline of kidney function is accompanied by a attribute disturbance in thyroid physiology (Table 58. Medications that are capable of suppress thyroid hormone metabolism embody corticosteroids, amiodarone, propranolol, and lithium. Free and complete thyroxine (T4) concentrations could also be regular or slightly lowered, mainly as a outcome of impaired hormone binding to serum provider proteins. Such finding differentiates the uremic affected person from sufferers with different persistent illnesses. In addition, bioavailability and cell uptake of thyroid hormones could also be partially blunted in uremia, resulting in a state of thyroid resistance. In normal rat hepatocytes, treatment with serum from uremic patients lowered T4 uptake by 30%.

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Arryhani M, El Youbi R, Sqalli T: Pregnancy-related acute kidney damage: expertise of the nephrology unit at the University Hospital of Fez, Morocco. World Health Organization: World well being report 2008: major well being care-now more than ever. Agarwal A, Soni A, Ciechanowsky M, et al: Hyponatremia in sufferers with the acquired immunodeficiency syndrome. In Ronco C, Bellomo R, Brendolan A, editors: Sepsis, kidney and multiple organ dysfunction, Basel, Switzerland, 2004, Karger, pp 44�52. Motaouakkil S, Charra B, Hachimi A, et al: [Rhabdomyolysis and paraphenylene-diamine poisoning. Experience of the nephrology department, Central University Hospital Ibn Rochd, Casablanca. Arryhani M, El Youbi R, Sqalli T: Pregnancy-related acute kidney injury: experience of the Nephrology Unit at the University Hospital of Fez, Morocco. Ezekiel L, Naicker S, Wadee S, et al: the finish result of renal alternative therapy in an intensive care unit in South Africa. Machemehl T, Hsu P, Pahad H, et al: Haemodialysis for posttraumatic acute renal failure- factors predicting consequence. Verroust P, Ben-Maiz H, Morel-Maroger L, et al: A scientific and immunopathological research of 304 cases of glomerulonephritis in Tunisia. Tewodros W, Muhe L, Daniel E, et al: A one-year examine of streptococcal infections and their issues among Ethiopian youngsters. Ben Maiz H, Abderrahim E, Ben Moussa F, et al: [Epidemiology of glomerular illnesses in Tunisia from 1975 to 2005. Lasry F, Mikou N, Oumlil M, et al: [Is the age of acute postinfectious glomerulonephritis decreasing in Morocco Levy M, Chen N: Worldwide perspective of hepatitis B�associated glomerulonephritis within the 80s. Wiggelinkhuizen J, Sinclair-Smith C: Membranous glomerulonephropathy in childhood. Connor M, Rheeder P, Bryer A, et al: the South African stroke threat generally apply examine. Combined report on upkeep dialysis and transplantation within the Republic of South Africa. Anochie I, Eke F, Okpere A: Childhood nephrotic syndrome: change in pattern and response to steroids. Pakasa M, Mangani N, Dikassa L: Focal and segmental glomerulosclerosis in nephrotic syndrome: a brand new profile of grownup nephrotic syndrome in Zaire. Bhimma R, Adhikari M, Asharam K: Steroid-resistant nephrotic syndrome: the affect of race on cyclophosphamide sensitivity. Wadee S, Tikly M, Hopley M: Causes and predictors of dying in South Africans with systemic lupus erythematosus. Ben Ma�z H, Abderrahim E, Ben Moussa F, et al: Epidemiology of glomerular diseases in Tunisia from 1975 to 2005. World Health Organization: World well being report 1998-life within the twenty first century: a vision for all. Afifi A, El Setouhy M, El Sharkawy M, et al: Diabetic nephropathy as a explanation for end-stage renal illness in Egypt: a six-year study. Abderrahim E, Zouaghi K, Hedri H, et al: Renal replacement remedy for diabetic end-stage renal illness. Katz I: Kidney and kidney-related continual ailments in South Africa and chronic illness intervention program experiences. The term Near and Middle East is a historical, Eurocentric, and Western time period that was used to describe a geographic region whose boundary is imprecise and whose inside borders are continuously changing due to political and historical evolution. Casualties, displacement, and migration are significant consequences of such disasters and adversely affect the socioeconomic stratum and health status of a country. Malarial kidney injury is often a consequence of several hemodynamic, immune, and metabolic disturbances, which may also be accompanied by central nervous system sequelae and by fluid and electrolyte alterations. In several publications, investigators have described and analyzed the elements which have had major implications for kidney involvement and outcomes in survivors who sustained crush syndrome in catastrophic earthquakes in Turkey and Iran. These issues can happen within hours of the initial damage and may result in early lack of limb or life.

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In this study, 459 subjects with a systolic blood strain lower than one hundred sixty mm Hg and diastolic blood pressure of 80 to ninety five mm Hg had been randomly assigned to totally different diets. Subsequently, topics have been randomly assigned to considered one of three diets for eight weeks: (1) the control diet, rich in fruits and vegetables; (2) a mixed diet, rich in fruits and vegetables, with restricted dairy merchandise; and (3) a food plan with reduced content material of saturated and complete fat. For all three groups, sodium intake and body weight had been maintained at constant ranges. Compared to the management diet, the mean reductions in systolic and diastolic blood pressures associated with the mix food plan have been 5. For the 133 subjects who have been hypertensive, the results were extra pronounced; systolic and diastolic pressures were lowered by 11. This is recommended as a outcome of a food plan restricted in potassium and sodium is difficult to achieve. Patients with Nephrotic Syndrome Patients with hypercholesterolemia, edema, and more than three g urinary protein/day. Similarly, these adaptive metabolic responses happen when the food plan is restricted to solely zero. There is a significant correlation between the amount of dietary protein and leucine oxidation throughout fasting and feeding, showing the adaptive response to dietary protein adjustments. Unfortunately, some of the published studies are of low methodologic high quality because they were retrospective research with solely a small number of sufferers or serious design flaws. Instead, outcomes in reported trials were based mostly on estimating differences in changes in serum creatinine levels or the diploma of proteinuria. There are various sorts of phosphate anions, and the proportions of those anions rely critically on the blood pH and different elements, making the interpretation of the plasma phosphates advanced. Therefore, sufferers and physicians concentrate on regulating the quantity of phosphorus within the food regimen, although all physiologically essential reactions are primarily based on phosphate metabolism. The consumption of phosphates is linked to dietary protein by a predictable relationship-approximately 1 g of protein contains thirteen mg of phosphate-and, consequently, variations within the quantity of protein eaten will predictably change phosphorus intake. The serum phosphorus degree, due to this fact, is influenced by the quantity of protein within the food regimen as properly as processes that regulate phosphate metabolism, together with the intestinal absorption of dietary phosphates, excretion of phosphates by renal tubules, and modifications in bone metabolism. Over a 16-year interval of observation, it was found that wholesome adults with serum phosphate concentrations above 3. This increase in threat was additionally current when variations in the calcium-phosphate product had been examined. It was also discovered that an increase within the serum phosphorus stage was related to a faster price of lack of kidney operate (P < zero. One essential level is the contribution of protein structure to phosphorus metabolism. Although dietary phosphorus is strongly linked to dietary protein, phosphorus can be sure in bigger molecules, such as phytates, in vegetable proteins. Therefore, phosphorus from vegetable protein is less readily absorbed in contrast with phosphorus from animal protein. Study subjects obtained two 800-mg/day phosphorus diets, one from vegetable sources and one from casein. Until recently, there was a sustained, industry-wide trend to add inorganic phosphorus throughout meals processing. Specifically, the important thing to achieving a aim of maintaining serum phosphate ranges inside the inhabitants reference vary must embody a phosphorus-restricted food regimen. At first look, these results indicate a unfavorable intervention, but there are caveats to this conclusion. It was ascribed to a physiologic reduction in glomerular hemodynamics, which is a well-documented effect of dietary protein restriction. Initially, there was no protective effect of intensive insulin remedy on the progression of kidney illness. Importantly, the authors discovered no alteration in body composition or dietary indices (principally, serum albumin) in either group. When the outcomes were evaluated utilizing an intention to deal with evaluation, thirteen patients assigned to zero. Di Iorio and associates evaluated how a really low protein intake supplemented with ketoacids may have an effect on the effectivity of erythropoietin remedy in 20 patients over 2 years. In those assigned to the very lowprotein food regimen plus ketoacids, only 2 patients needed to start dialysis in comparability with 7 topics in the greater dietary protein group (P < 0.

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This strategy can probably remove the source of the infection (the biofilm) whereas allowing catheter salvage. The use of antibiotic locks, in conjunction with systemic antibiotics, has been shown to eradicate infection and salvage the catheter in about two thirds of patients. At our institution, implementation of an antibiotic lock protocol has dramatically decreased the frequency of catheter exchanges brought on by an infection. Strict sterile method, topical local anesthesia (1% lidocaine), and acutely aware sedation are offered. The catheter cuff located near the exit website within the subcutaneous tissue is dissected, and the catheter is pulled out, forsaking the wire. A new, permanent hemodialysis catheter is then prepped and advanced over the wire into place. The intraperitoneal portion of the catheter may be straight, coiled, or T-fluted or with a silicone disc. The coiled catheter design additionally decreases ache throughout infusion and is much less more doubtless to migrate. The inside cuff should be inserted in the stomach wall musculature (rectus muscle) to prevent leaks. The outer cuff should be located within the subcutaneous tissue to create a useless house in between the two cuffs, which is assumed to stop the migration of infections coming from the exit site. The subcutaneous tract and exit site should face downward and laterally to keep away from exit website infection. Providing sufficient time for healing helps avoid leaks, which might enhance the danger of infection and are discouraging to sufferers. The decrease incidence of cuff extrusion enhances the survival of swan neck catheters. The presternal exit site modification has been proven to decrease the incidence of peritonitis and exit website an infection. They advocated using the presternal catheters in obese sufferers, sufferers with ostomies, and youngsters wearing diapers and/or with fecal incontinence. Conscious sedation is run with midazolam hydrochloride and fentanyl citrate. A nurse obtains important signs and administers aware sedation through the process. The insertion website is chosen to be 2 cm to the left or proper and beneath the umbilicus. Under ultrasound steering, the needle penetrates through the pores and skin, subcutaneous tissue, outer fascia of rectus muscle, muscle fibers, inner fascia, and parietal layer of peritoneum. Radiocontrast, three to 5 mL, is injected into the peritoneal cavity beneath fluoroscopic guidance to ensure the correct location; a radiologic sample of outer bowel delineation is indicative of excellent placement. A 2-cm incision is made on the skin, and the subcutaneous tissue is digitally dissected as much as the rectus muscle. A collection of dilators (8-, 12-, and 14-Fr) are passed over a stiff guidewire, and an 18-Fr peel-away sheath is positioned. A double-cuff, swan neck, Tenckhoff peritoneal dialysis catheter is introduced over the stiff guidewire into the peritoneal cavity. A tunnel is created with an exit web site located distally, laterally, and under the initial incision, with the outer cuff buried in the subcutaneous tissue. It has the identical preliminary preparation as for the fluoroscopic or ultrasound technique. The scope is once more eliminated, and the peritoneal catheter is introduced via the catheter with the help of a chrome steel stylette. The outcomes of a kidney biopsy are useful in guiding medical therapy and providing a prognosis. The aim of a kidney biopsy should be to maximize the yield of sufficient tissue while minimizing the risk of complications. Percutaneous kidney biopsies have advanced from a blind process to a real-time, ultrasound-guided needle biopsy. Cozens and coworkers238 retrospectively compared a 15-gauge, Tru-Cut renal biopsy with ultrasound localization and marking to the utilization of an 18-gauge, spring-loaded gun renal biopsy beneath real-time ultrasound guidance. They reported a 79% yield of enough renal tissue with the blind technique (15 gauge) as compared with 93% with real-time ultrasound guidance (18 gauge).

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Galdo T, Gonzalez F, Espinoza M, et al: Impact of being pregnant on the function of transplanted kidneys. Le Ray C, Coulomb A, Elefant E, et al: Mycophenolate mofetil in pregnancy after renal transplantation: a case of major fetal Malformations. Krotz S, Fajardo J, Ghandi S, et al: Hypertensive illness in twin pregnancies: a review. The first part reviews the pharmacology of nondiuretic antihypertensive drugs to present clinicians with a whole overview of tips on how to use these therapies safely in practice (Table 50. The first part also discusses individual drug lessons and highlights the category mechanisms of action, members, renal effects, and efficacy and safety. The half-life is 2 hours; with long-term administration, the hemodynamic effects are maintained for three to eight hours. The elimination half-life increases markedly in patients with creatinine clearances of less than 20 mL/min/1. In such patients, the initial dosages ought to be decreased, and smaller increments should be used for titration. The first antihypertensive drug, hydralazine, was a nonspecific vasodilator found within the Nineteen Fifties. This was followed by blockade of calcium channels on vascular smooth muscle cells, the calcium channel blockers in the 1960s, and blockade of postsynaptic -adrenoceptors on peripheral sympathetic neurons, the alpha blockers within the late 1970s. After absorption, cilazapril is rapidly de-esterified in the liver to its energetic metabolite, cilazaprilat. Enalapril undergoes biotransformation within the liver into the active compound, enalaprilat (see Table 50. The initial antihypertensive response occurs in 1 hour, peaks at 6 hours, and lasts for 24 hours (see Table 50. Moexipril is quickly transformed within the liver to moexiprilat, which is 1000 times more potent than the parent compound. The dosage ought to be lowered by 75% and 50% in patients with creatinine clearances of less than 50 and less than 10 mL/min/1. The onset of motion happens in 1 hour, and the height response occurs in 2 hours and lasts for twenty-four hours. Quinapril is extensively metabolized in the liver into the energetic metabolite, quinaprilat (see Table 50. Renal excretion by means of filtration and lively tubular secretion accounts for 50% of the clearance. Ramipril is well absorbed from the gastrointestinal tract; peak concentrations are achieved in 1 to 2 hours (see Table 50. Ramipril is extensively metabolized within the liver into the lively metabolite, ramiprilat. The dosage ought to be lowered by 50% to 75% in sufferers with a creatinine clearance of less than 50 mL/min/1. The peak serum concentrations of trandolaprilat happen inside 2 to 12 hours; the period of action is 24 hours, however it may be so long as 6 weeks. The mechanism liable for this effect is the direct inhibition of proximal, and probably distal, tubule sodium reabsorption. However, the upkeep of normal sodium excretion at decrease arterial pressures correlates with elevated excretion in the setting of hypertension. Several mechanisms account for the discount in urinary protein excretion, together with the following: a decrease in glomerular capillary hydrostatic strain; a lower in mesangial uptake and clearance of macromolecules; and improved glomerular basement membrane perm-selectivity. The sulfhydryl group of captopril is thought to invoke an immune complex�mediated nephropathy similar to that which occurs with penicillamine administration. African Americans with hypertension have been discovered to reply less nicely to decrease dosages than whites, however higher dosages are equally efficient. The trial was stopped prematurely due to antagonistic events (hyperkalemia and hypotension).

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Harambat J, Fargue S, Acquaviva C, et al: Genotype-phenotype correlation in main hyperoxaluria kind 1: the p. Topaloglu R, Vilboux T, Coskun T, et al: Genetic basis of cystinosis in Turkish sufferers: a single-center expertise. Vivante A, Lotan D, Pode-Shakked N, et al: Familial autosomal recessive renal tubular acidosis: significance of early prognosis. Aleem A: Renal abnormalities in patients with sickle cell illness: a single heart report from Saudi Arabia. Eliakim M, Levy M, Ehrenfeld M: Recurrent polyserositis (familial Mediterranean fever), Amsterdam, 1981, Elsevier-North Holland Biomedical Press. Mohammadnejad L, Farajnia S: Mediterranean fever gene evaluation in the Azeri Turk population with familial Mediterranean fever: evidence for brand spanking new mutations related to disease. Lotan D, Yoskovitz G, Bisceglia L, et al: A mixed approach to the molecular evaluation of cystinuria: from urinalysis to sequencing through genotyping. Sidi R, Levy-Nissenbaum E, Kreiss I, et al: Clinical manifestations in Israeli cystinuria patients and molecular evaluation of carrier rates in Libyan Jewish controls. Raas-Rothschild A: Pediatrics: implementing the promise of early intervention for Fabry illness. Bahat H, Dinour D, Ganon L, et al: Non-urate transporter 1-related renal hypouricemia and acute renal failure in an IsraeliArab family. Jahanzad I, Amoueian S, Attaranzadeh A: Familial lecithincholesterol acyltransferase deficiency. Al-Haggar M: Cystinosis as a lysosomal storage disease with a quantity of mutant alleles: phenotypic-genotypic correlations. Al-Haggar M, Bakr A, Tajima T, et al: Familial hypomagnesemia with hypercalciuria and nephrocalcinosis: uncommon clinical associations and novel claudin16 mutation in an Egyptian family. Ait-Idir D, Khilan A, Djerdjouri B, et al: Spectrum of mutations and carrier frequency of familial Mediterranean fever gene in the Algerian inhabitants. Brik R, Shinawi M, Kepten I, et al: Familial Mediterranean fever: scientific and genetic characterization in a blended pediatric inhabitants of Jewish and Arab patients. Langevitz P, Zemer D, Livneh A, et al: Protracted febrile myalgia in sufferers with familial Mediterranean fever. Mattit H, Joma M, Al-Cheikh S, et al: Familial Mediterranean fever within the Syrian population: gene mutation frequencies, provider rates and phenotype-genotype correlation. Medlej-Hashim M, Rawashdeh M, Chouery E, et al: Genetic screening of fourteen mutations in Jordanian familial Mediterranean fever patients. Settin A, El-Baz R, Abd Rasool M, et al: Clinical and molecular prognosis of familial Mediterranean fever in Egyptian kids. Shinawi M, Brik R, Berant M, et al: Familial Mediterranean fever: excessive gene frequency and heterogeneous illness amongst an IsraeliArab inhabitants. Solak M, Yildiz H, Koken R, et al: Analysis of familial Mediterranean fever gene mutations in 202 patients with familial Mediterranean fever. Sohar E, Gafni J, Pras M, et al: Familial Mediterranean fever: a survey of 470 circumstances and review of the literature. Shohat M, Magal N, Shohat T, et al: Phenotype-genotype correlation in familial Mediterranean fever: evidence for an association between Met694Val and amyloidosis. Touitou I, Sarkisian T, Medlej-Hashim M, et al: Country as the first risk factor for renal amyloidosis in familial Mediterranean fever. Tunca M, Tankurt E, Akbaylar Akpinar H, et al: the efficacy of interferon alpha on colchicine-resistant familial Mediterranean fever assaults: a pilot examine. Tweezer-Zaks N, Rabinovich E, Lidar M, et al: Interferon-alpha as a treatment modality for colchicine-resistant familial Mediterranean fever. Tunca M, Akar S, Soyturk M, et al: the impact of interferon alpha administration on acute assaults of familial Mediterranean fever: a double-blind, placebo-controlled trial. Ozgocmen S, Ozcakar L, Ardicoglu O, et al: Familial Mediterranean fever responds well to infliximab: single case experience. Belkhir R, Moulonguet-Doleris L, Hachulla E, et al: Treatment of familial Mediterranean fever with anakinra.