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Often underestimated or misunderstood in chronic renal failure (CRF), muscle wasting is nevertheless common and concerns about 50% of dialysis patients. The consequences of this myopathy on quality of life and outcomes of patients are unfavorable, identical to those observed in sarcopenia in elderly subjects with sarcopenia. The similarities between the two situations also concern the symptoms, the underlying muscle damages and the pathogenic mechanisms and may be partly explained by the frequently high age of ESRD patients. Skeletal muscle involvement should be systematically investigated in the IRC patient as in the elderly with sarcopenia to propose as early as possible a treatment of which physical activity and nutritional interventions are the mainstay., (Copyright © 2015 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.)

Oxidative stress is commonly observed in chronic renal failure patients resulting from an unbalance between overproduction of reactive oxygen species and impairement of defense mechanisms. Proteins appear as potential targets of uremia-induced oxidative stress and may undergo qualitative modifications. Proteins could be directly modified by reactive oxygen species which leads to amino acid oxydation and cross-linking. Proteins could be indirectly modified by reactive carbonyl compounds produced by glycoxidation and lipo-peroxidation. The resulting post-traductional modifications are known as carbonyl stress. In addition, thiols could be oxidized or could react with homocystein leading to homocysteinylation. Finally, tyrosin could be oxidized by myeloperoxidase leading to advanced oxidative protein products (AOPP). Oxidatively modified proteins are increased in chronic renal failure patients and may contribute to exacerbate the oxidative stress/inflammation syndrome. They have been involved in long term complications of uremia such as amyloidosis and accelerated atherosclerosis.

The national and international recommendations concerning the iron management in chronic kidney disease (CKD) patient are well established. All acknowledge the fact that iron needs are increased in uremic patients. This is particularly true for CKD-5 patients treated by hemodialysis (increased losses) and when treated by an erythropoetic stimulating agent (ESA). Annual iron requirements are currently estimated between 500 mg and 3000 mg per year. The biodisponibility of oral iron isreduced and side effects are quite common. The venous supplementation of iron offers today the best safety/efficacy profile. The evaluation of iron store is mandatory in CKD patient. The assessment of iron store in kidney patient relies on three major markers: transferrin saturation (Trf Sat); ferritin; percentage of hypochromic erythroid cells. Faced to iron deficiency, it is crucial to differentiate two situations: an absolute iron deficiency (Trf Sat < 20 % ; ferritin < 100 ng/ml; percentage of hypochromic cells > 10%); a functional iron deficiency (Trf Sat < 20%; ferritin > 200-500 ng/ml; percentage of hypochromic cells > 5-10%). When intravenous iron supplementation is indicated, dosing regime should be based on a slow and a reduced dosage administration to comply with manufacturer and best practice recommendations. Regular iron infusion of 50 to 100 mg per week is able to cover the basic needs for most hemodialysis patients.

Study Aim: Pancreas and kidney transplantation (PKTx) is indicated in uremic patients with insulin-dependent diabetes mellitus (IDDM). The aim of this study was to determine its long-term effect on metabolic control in order to establish the real efficacy of this treatment in diabetic patients., Patients and Method: Among a total experience of 191 pancreas and kidney transplantations, a metabolic control was performed in 80 patients who underwent PKTx in our center, with both grafts functioning for more than one year. Immunological markers of diabetes mellitus were also evaluated (ICA and GADab) in 50 patients., Results: Basal glycemia and glycosylated hemoglobin (HbA1c) levels throughout follow-up were within the normal range. Hyperinsulinemia was present throughout follow-up till the fourth year. The oral glucose tolerance test (OGTT) was normal in 82.5% of the patients beyond one year after the graft. Over time, no differences were detected on basal glucose and insulin levels and areas under the curve (AUC) of glycemia and insulinemia. During the evolution, no differences were found in the fasting insulin resistance index (FIRI), in spite of increasing body weight. ICA were + in 2 patients before graft and + in 7 after graft (14%). GADab were + in 10 patients before graft and + in 11 after graft (22%)., Conclusion: Pancreas and kidney transplantation provides without any insulin treatment and diet long-term normalization of glycemic control, assessed by HbA1c and OGTT, despite the existence of sustained hyperinsulinemia. Our results strongly suggest that pancreas and kidney transplantation is the most efficient treatment for uremic patients with insulin-dependent diabetes mellitus from a metabolic point of view.

Ageing does not spare the kidneys but, remarkably, renal impairment is virtually asymptomatic as homaeostasis remains ensured. Nevertheless, in routine practice physicians must take into account the "physiological" renal insufficiency of the elderly. In old people with chronic renal impairment the diagnostic and therapeutic approaches are special, owing to the age-related risks attached to both paraclinical examinations and treatments. Yet in certain subjects treatment can be remarkably effective and prevent the progression to terminal uraemia, and this justifies the detection and exploration of renal insufficiency in elderly patients. In the last few years, iterative dialysis programmes have been made available to third or even fourth age patients who had reached the so-called end-stage renal failure. The results are encouraging, but there are still purely medical questions concerning the measures to be taken in priority and the numerous organization problems to be solved for optimal management of these patients.

The recent availability of Recombinant Human Erythropoietin (EPO) has radically stirred-up diagnosis and therapeutical approach of anemia in dialysis patients. By correcting anemia in a dose related manner in virtually all dialysis patients, clinical use of EPO has confirmed its remarkable efficiency. Correction of anemia marked by a rapid improvement in "well being" of patients is also objectively associated with the correction of most of the debilatating multiple organs dysfunction due to the uremic state. Hypertension is one of the more frequent and worrying complication associated with EPO therapy. Optimal use of EPO, integrating administration route and frequency of injections, will reduce the EPO doses needed and minimize cost and side-effects incidence. EPO represents a major advance in the treatment of chronic uremia. EPO opens a new therapeutic era offering for the first time a substitute to a kidney endocrine failure.

Various neurological complications may occur in patients under haemodialysis for end-stage chronic renal failure. Their frequency has clearly been reduced by improvements in the modalities and techniques of dialysis. Some of these complications are related to uremia and/or to the accumulation of endogenous toxic substances the nature of which has not been elucidated (e.g. uraemic encephalopathy, polyneuropathy), while others are directly due to the haemodialysis itself (e.g. dialysis disequilibrium syndrome, aluminum encephalopathy).

Twenty men and 23 women aged from 18 to 65 years, who had been under maintenance haemodialysis for 2 to 16 years and whose haematocrit had been below 30 percent for at least 3 months received recombinant human erythropoietin intravenously at the end of each session for one year. Anaemia was corrected in all patients, the delay in response to each dosage variation being about 4 weeks. The necessary maintenance dosage ranged from 96 to 240 u/kg/week. The number of leucocytes increased significantly until the 4th month, from 5880 +/- 1760 to 6600 +/- 1920 per cubic mm (P less than 0.01). During treatment, pre-dialysis blood creatinine concentrations and potassium and phosphate levels rose, while blood calcium levels fell significantly from 2.45 +/- 0.16 to 2.36 +/- 0.19 mmol/l (P less than 0.01). A nonsignificant increase in systolic and diastolic pressures was also observed, from 129 +/- 16 to 134 +/- 18 mmHg (P = 0.06) and from 75 +/- 9 to 78 +/- 10 mmHg (P = 0.07) respectively. Eight patients (18 percent) required antihypertensive drugs or a higher dose of those previously prescribed. There were 7 cases of vascular thrombosis on pre-existing stenosis, and the dosage of heparin during dialysis had to be increased in most patients. This study confirms that erythropoietin plays a major role in the genesis of the anaemia associated with renal failure. The absence of severe complications in this series was probably due to the criteria of inclusion in the study.

Hyperosmolar diabetic coma is characterised by extreme hyperglycaemia and dehydration. Hypernatremia often contributes additionally to plasma hyperosmolarity. The pathogenesis of these component abnormalities is considered. The explanation of the absence of hyperketonaemia is examined in the light of recent experimental and clinical data. At the beginning of the development of the syndrome, high peripheral plasma insulin probably explains the lack of ketosis via inhibition of lipolysis. Later, when hyperosmolar coma is established, peripheral insulinopenia but an "insulinised" liver may coexist. This would favour metabolism of free fatty acids along nonketogenic pathways.

The authors review the literature on the effects of the nervous system on the kidney in 3 stages: 1) Historical stage when the role of the renal nerve supply was overetimated by Claude Bernard. 2) Intermediate stage between the two wars with a clinical description of uremic encephalits or acute delirium. From the experimental point of view was demonstrated the inessential character of the nerve supply for the survival of the kidney. 3) Modern stage: from the clinical point of view one may distinguish functional nephropathies including those of nervous origin. The latter are due to metabolic or vascular mechanisms which are intricated to various degrees. Problems of regulation are raised in man by certain findings.

The clinical signs of 2 arteriovenous fistulas are discussed and compared with the literature. Arteriovenous fistulas following percutaneous kidney bioposies are very frequent. Most of them are not to be treated. In contrast to the common spontaneous closure of these fistulas in the kidney periphery, central arteriovenous fistulas should be operated always by partial resection.

The authors report a case of delayed diagnosis of intraperitoneal rupture of the bladder, and describe the wide variety of signs and symptoms observed in these cases. They emphasize the diagnostic value of biological test results, and discuss a case in which cicatrization without sequelae was obtained without operative intervention.

Following effective long-term antihypertensive therapy, hemodialysis could be discontinued in 4 patients with malignant hypertension in view of improved renal function. Diagnoses included nephroangiosclerosis (2 cases), scleroderma and chronic glomerulonephritis. All patients had symptoms of hypertension or renal disease for at least one year prior to initiation of hemodialysis treatment. At the outset, blood pressure averaged 249 +/- 43/150 +/- 22 mm Hg (mean +/- SD) and all patients had grade IV hypertensive retinopathy. After 1 to 20 months strict blood pressure control, renal function had improved to such a degree that hemodialysis could be discontinued. One year later, blood pressure averaged 138 +/- 20/89 +/- 6 mm Hg and serum creatinine 3,2 +/- 1,2 mg/100 ml. These data suggest that in hypertensive patients with chronic renal failure, strict control of blood pressure is of the utmost importance whatever the severity and nature of the underlying renal disease.

In chronic uremic patient, two kinds of digestive troubles can occur: gastric or duodenal lesions secondary to an abnormal gastro-intestinal hormone excretion, and drug-induced disorders. Most of these manifestations were missed by usual barium meal and the use of routine endoscopic check-up can be particularly useful. We performed 70 gastroscopies in 67 chronic hemodialyze patients. Examinations were practiced immediately before dialysis with only a light sedation. We observed 39 lesions: 3 drug-induced gastritis, 15 erosive or pseudopolypoid inflammations of the polyric antrum, 2 gastric ulcers, 5 duodenal ulcers (two of them were linear), 2 peptic oesophagitis and 34 p. cent of our patients had marked duodenitis, most of these digestive abnormalities could be missed or overdiagnosed by using routine barium meal. In presence of the number and the therapeutic importance of these disorders, we think that a gastroscopy should be prescribed in three indications: uremic patients before the beginning of an hemodialyze treatment, chronic hemodialyze patients with unexplained anemia, check-up before renal transplantation where ulcerations are a major contra-indication. In such situations, gastroscopy seems an important progress for the management of this particular group of patients.

The determination of blood amino-acids by column chromatography has been carried out on 53 patients, 17 with acute myeloid leukemia, 22 with chronic myeloid leukemia. A comparison was made with 25 normal subjects. These determination has shown a significant increase in glycin, cystin and a non significant increase of tryptophan. A positive relationship may exist between uricemia and content of glycin and glutamin, both amino-acids which are messengers of uric acid. A positive correlation has been found between glycin tryptophan and the number of myeloblasts.