Diabetic nephropathy came to one of the first places among the causes of terminal renal failure. Diabetic patients in Europe and the United States are now about half among those undergoing hemodialysis. Direct toxicity of elevated glucose concentrations for the nephron structures with concomitant lipid metabolism disorders (frequent lipid deposition in the kidneys) and subsequent sclerotic changes in mesangium cells, together with deposits of circulating immune complexes underlie renal parenchyma lesions in diabetes.

In recent years, attention has been drawn to the role of “vascular endothelial growth factor” as a multifunctional cytokine, known as vascular permeability factor, in development of micro- and macrovascular complications in diabetes and, in particular, diabetic nephropathy. If immune complex glomerulonephritis is typical for Type 1 diabetes, then atherosclerotic nephroangiosclerosis – for Type 2 diabetes. Due to increase in vascular permeability during nephropathy, the earliest signal for the development of such a pathology is the detection of microalbuminuria (concentration - 30-200 mg / l, or excretion at a rate of 20-200 μg / min), which can be found in 29-41% of diabetics with the disease duration of more than 5-7 years. 70% of diabetics with microalbuminuria suffer from arterial hypertension, which strengthens the link between diabetes and nephropathy.

A normal level of glycaemia can be maintained, but this does not prevent the accumulation of secondary toxic metabolites that damage the walls of the blood vessels, and there are no medications to prevent the progressive course of these complications. Most of these pathological large-molecular substances, such as circulating immune complexes, glycoproteins, lipids, endothelin, antibodies to insulin and others are not excreted by the kidneys and can only be removed using plasmapheresis, which is essentially the only way to correct these complications - elimination of secondary metabolic disorders. And you need to start this not waiting for the terminal renal failure development, but already at the first signs of the kidney damage. Membrane plasmapheresis on the Russian Hemofenix device with a small volume of filling allows it to be performed even on an outpatient basis, including in children, and that expands the possibilities of its use in almost any medical institution, even of the municipal level. This is especially important, given the huge number of patients in need of this treatment.

Abstract .  At present, COPD is considered as a disease with a systemic manifestation [1,2]. One of the most important extrapulmonary effects of COPD is renal dysfunction [3], which exacerbates the general background of the course and prognosis of the disease.                  

Purpose. To study risk factors, as well as the contribution of systemic effects of chronic obstructive pulmonary disease to the development of renal pathology.                           

 Materials and methods. We studied 121 patients with stage I – IV COPD among a man (n = 74) and a woman (n = 47), the average age was 58.5 years. All subjects were divided into 4 clinical and control groups. The concentration level of interleukin 6 (IL-6), tumor necrosis factor alpha (TNF alpha) was determined. Statistically significant results were considered level p <0.05.    Results. In patients with COPD, 3 or more risk factors for the development of CKD have been identified. It was found that as the level of forced expiratory volume per second (FEV1) decreases, the average values of mycroalbuminuria (MAU) and cystatin C increase (table 1). The total frequency of cases of chronic kidney disease CKD (S1) at all stages of COPD in determining GFR by creatinine was 41.6%, S2–57.2%, S3 - 0.41%. When determining GFR using cystatin C, the frequency of stage S1 of CKD was 17.7%, S2 - 43.7%, S3 - 36.4% and S4 - 1.04%.

Table 1.

The results of the laboratory-anamnestic indicators of patients,

suffering from COPD (x ± m)

Note: * - p <0.05 Between the COPD stage and the control group. M – men; F - women; BMI - body mass index. GFR - glomerular filtration rate.

Serum levels of IL-6, TNF alpha, C-reactive protein (CRP) tended to increase with increasing severity of COPD. The correlation analysis revealed a positive relationship between the level of cystatin C and IL-6, CRP, and the MAU indicator positively correlated with IL-6, TNF alpha.

Output. Thus, a patient with COPD has many risk factors for developing renal dysfunction; systemic inflammation in COPD makes a major contribution to the formation of renal dysfunction.

Introduction:

Renal replacement therapy( RRT ) with the OXIRIS filter is used in sepsis septic shock with AKI , but few clinical studies compare the adsorbing effect of Oxiris filter on the inflammatory mediators to RRT.

The aim of this study is 1- to confirm whether oxiris decreases cytokines and procalcitonin in sepsis septic shock . 2- This effect is superior to RRT . 3- This translates in a better cardio renal response.

Methods:

A  coohort study and a  propensity  –  matched analysys included 73 patients admitted to three Intensive Care   ( Aurelia Hospital , European Hospital , Tor Vergata – Rome ) with a diagnosis of septic shock . 50 patients were submitted to RRT with oxiris filter and 23 patients to RRT without adsorbing filters . Il 6 , Procalcitonin EAA , the cardiorenal indices and SOFA score were compared before ( T0 ) and at the end of the treatments ( T1 ) .All data are expressed as mean ±SD. ANOVA one way was used to compare the changes of the variables in the time. P< 0,05 was considered statistically significant.

Results:

Of 50 patients submitted to RRT with the oXiris filter 32 could be matched to 22 septic patients who received RRT. IL6  Procalcitonin  and Endotoxin ( EAA) decreased in the Oxiris ( p< 0,01 ) but not in the RRT group . MAP increased ( p< 0,01 ) and noradrenaline dosage decreased in oxiris group ( p< 0,01) , but non in RRT group. Also PaO2/FIO2 ratio , diuresis , SOFA improved only in the in the oxiris group (p<0,05 ).

Conclusion:

In sepsis / septic shock patients with AKI  , CVVHDF with oXirs improves the cardio - renal function and the clinical course . The study confirms that RRT with oXiris filter may be useful in  AKI with sepsis / septic shock when other convective / diffusive techinques fail.

Introduction:

Hypercalcemia is defined by total calcemia greater than 2.6mol/1, the etiologies are dominated by parathyroid adenoma and cancers. Hypercalcemia can be seen during most granulomatosis, sarcoidosis being the most common cause, but can also occur during tuberculosis, HODGKIN disease, non-Hodgkin's lymphoma.

The diagnosis of granulomatosis as the cause of hypercalcemia is often difficult.

Patients and methods:

This is an observational case control study performed in a patient with appropriate severe PTHi hypercalcemia.

This is the 67-year-old  man, electrician by profession, with lymph node tuberculosis in 1989 treated and declared cured, presenting with stage 3 chronic kidney disease on interstitial tubulo nephropathy who consults for impairment of the general condition.

He presents a global dehydration with a polyuropolydipsic syndrome, vomiting with obstinate constipation, dorso lumbar rachialgies with functional impotence of the two lower limbs.

At ECG: diffuse shortening of the QT space.

Results:

Biology: Urea :1,8g/l, creatinine: 21mg/l, Cl à 24 ml /min/1, 73m2

Hemoglobin:5, 9g/dl, Blood smear: without anomalies, EEP: hypo albuminemia, hyper alpha1, alpha2 and beta globulin .

Corrected calcemia :3,6mmol/l, albuminemia: 22g/l

Phosphoremia: 1mmol/l    PTHi :8, 7pg/l

25(OH)vitD: 9 ,7micromol/l     1,25 (OH)2vitD: 47ng/l

CPK: 100 UI               LDH: 240 UI

the intradermal reaction (IDR) to  the tuberculin: Phlyctenular reaction

Morphology:

Standard chest X-ray: paravertebral spindle D8 –D10.

CT scan of the dorso lumbar spine: dorso lumbar spondylodiscitis evoking a specific infectious disease such as tuberculosis with necrotized cervico-mediastinal lymphadenopathy.

Abdominal pelvic ultrasound: renal micro lithiasis with splenic macro calcifications. Left foot X-ray: vascular calcifications.

Pathological anatomy:

Bone marrow biopsy puncture: discret granulocytosis.

Lymph node biopsy: granuloma epithelio giganto cell with caseous necrosis.

Discussion:

Urea – creatinine dissociation and acute worsening on a chronic background are secondary to dehydration induced by vomiting and polyuropolydipsic syndrome due to this hypercalcemia.

It is severe hypercalcemia(3.6mmol/l) with appropriate PTHi.The low value of vitamin D signs a deficient state and eliminates the intoxication with vitamin D .The renal production of 1 alpha hydroxylase has collapsed and the calcitriolemia is supposed to be low  by deficiency in its precursor (25(OH) vitamin D).A normal value of calcitriol suggests the extra renal production of 1 alpha hydroxylase .Lymphadenopathy with fistulization, tuberculin IDR, POTT sickness suggests a tuberculous origin which is confirmed by the anatomopathological study. Hypercalcemia is secondary to tuberculous granulomatosis. It is chronic (renal lithiasis, vascular and splenic calcifications): well tolerated at some point, aggravated and maintained by prolonged bed rest.

Conclusion:

The diagnosis of hypercalcemia secondary to granulomatosis would be easy to evoke in a patient known for granulomatosis or has suggestive symptoms with appropriate PTH hypercalcemia, without hypophosphatemia and hypercalcitriolemia.

In front of any tuberculosis or other granulomatosis, screening for hypercalcemia (asymptomatic in most cases) is systematic.

Kidney transplantation is the preferred treatment for endstage renal failure. Unfortunately, donor organ shortages prevent many individuals receiving a renal transplant and there is a need to increase the pool of appropriate donors. The presence of acute kidney injury (AKI) in deceased donors has traditionally been a relative contraindication to renal transplantation, even though renal recovery may be favorable in the absence of chronic renal disease.

Methods: We undertook an 8 years retrospective observational study of potential deceased organ donors with AKI requiring renal replacement therapy (RRT). We evaluated the rate of successful transplantation as well as short term and outcomes at a median of 19.5 (13.0–52.7) months after donation.

Results: Amongst 1058 consented potential organ donors, 39 patients had AKI requiring RRT, of which 19 became donors (13 not medically suitable, 7 did not proceed to donation). The median (interquartile range (IQR)) donor age was 41 (34–50) years and norepinephrine, epinephrine and vasopressin were given to 18, 14 and 9 donors, respectively. From the 38 donated kidneys 34 were transplanted. The median (IQR) age of recipients was 53 (42.8–58.5) years and they were dialysis free in a median (IQR) of 5.5 (2.3–10.8) days. Only minor abnormalities were found at 3 and 6 months renal biopsies, and two patients experienced graft failure in the first 12 months.

Conclusion: Amongst deceased donors with AKI receiving RRT and vasoactive medications outcomes of renal transplantation seems acceptable in the absence of pre-existing renal failure and other donor co-morbidity. Such patients may be an important additional source of kidney donation

Despite the understanding of the problem of treatment CKD-MBD, success in the treatment of this pathology is very modest. This was primarily due to the absent of effective drugs to achieve target biochemical parameters. Recently, new phosphate binders containing iron and calcimimetics have become available for treatment of CKD-MBD. The aim of the study was to assess the effect of new drugs on CKD-MBD targets, including FGF-23, Klotho, PTH, P, Ca and others. We got a good effect from the use of a combination of calcimimetics and phosphate binders containing iron. Only an assessment of the changes in all disease markers under the influence of new drugs gave us the opportunity to improve approaches to treating CKD-MBD.

Conclusions.  Based on our own research results, we can conclude that in the treatment of CKD -MBD we must use new highly effective drugs to achieve the target parameters, including FGF 23 and  Klotho.

Background: Acute gastroenteritis (AGE) is the most common pediatric illness, which results in significant morbidity in children and it’s associated with electrolyte disturbance that some of them can be dangerous.

Materials and methods: A prospective cross-sectional study of 473 children with gastroenteritis that admitted in children medical hospital emergency ward. They were treated for gastroenteritis such as oral rehydration therapy, anti-emetics and probiotics and fluid intravenous treatment. Electrolytes and urea, creatinine of all patients were checked and recorded in the data form.

RESULTS: A total of 437 children interred in this study. Of these, 243 (51%) were males and 231 (49%) were females.4.4% of patients had mild dehydration and 78.7% of these had moderate dehydration and 20.8% of child had severe dehydration. Renge of serum Na was 116-156 mmol/l and mean 136.618.85. Level of serum potassium was 3-6 mmol/l with mean 4.2 0.64. According to this study prevalence of sodium disturbance was 41.6 percent in the studied group. (4% severe hyponatremia with serum Na<120 meq/L  and 23.6%  with serum Na 120 meq/L to 135 meq/L and 14% hypernatremia with serum Na> 145 meq/L).  There was 17.2% potassium disturbance in our studied group, 13% hypokalemia (serum K<3.5 mmol/L) 3.7% hyperkalemia (serum K>5.5). In conclusion, electrolyte disturbances are very common in children with acute diarrhea disease. The degree of dehydration and age less than 12 months appear to be good predictors of the occurrence of, electrolyte disturbances. Early diagnosis and management  prevent of complication.

Introduction:

Metabolic syndrome (MS) is defined by clinical dysfunctions and biochemical abnormalities, which include obesity, hypertension, dyslipidemia, and impaired glucose metabolism. Metabolic complications after renal transplantation (TR) are Frequent and deserve special attention because they represent factors of morbidity and cardiovascular mortality. In addition, it may be responsible for the appearance of proteinuria and worsening of graft function, suggesting a link with chronic kidney disease (CKD).

The aim of our work is to determine the frequency of metabolic syndrome in post-renal transplantation, its risk factors and its impact on cardiovascular morbidity and mortality as well as graft function.

Materiels and methods:

This is a descriptive retrospective study involving 115 patients who received a renal transplant followed within our unit.

Results:

16 cases of metabolic syndrome have been described in our renal transplant patients, which represents an incidence of 14% of all our patients. The mean age was 41.75 years with a sex ratio H / F of 3. 4 patients had a family history of hypertension and 3 diabetes; only 3 patients practiced a regular sport activity.

The initial nephropathy was indeterminate in 81.25%. It was a preemptive graft in 18.75%. The average duration of hemodialysis was 36.9 months.Renal transplantation was predominantly from a living donor in 81% of cases, with an average donor age of 40.8 years.As induction therapy we used a standard ATG protocol or basiluximab, tacrolimus, MMF and prednisone. One patient had delayed recovery of renal function.

During follow-up, 6 patients were overweight during the first year, 2 being obese.Hypertension was the most common factor found in 93.75% of patients, 73% of whom appeared in the 3 months after renal transplantation. Amlodipine was the most used treatment, and the evolution was favorable with good control of blood pressure.6 patients were overweight during the first year post transplantation, compared to 2 cases of obesity, HTA was established in 93.75% of patients, 73% before M3 post TR, treated with amlodipine.81.25% of the patients presented before the end of the first year a dyslipidemia and only 23% treated by the statins. De novo diabetes was described in 18.75% of our patients and 68.75% had hyperglycemia.Eight patients reported a cardiovascular event: 5 cases of compensated hypertensive heart disease, one case of labor angina with stenosis of the stented IVA artery, one case of compensated heart failure, and one case of stenosis of the renal artery.

Regarding renal function, four cases of aggravation of renal function with positive proteinuria have been described with the biopsy puncture of the graft a case of tubular epithelial nonspecific pain.

Discussion and Conclusion:

In our series the association HTA, dyslipidemia and hyperglycemia was the most frequent, 50% of our patients developed a cardiovascular event and 25% worsening of the renal function.Although the small size of our study population does not allow us to extrapolate our results, it would be interesting to stratify our transplant patients according to metabolic complications in order to establish close surveillance for at-risk patients. This would allow us to reduce the occurrence of cardiovascular complications and loss of kidney transplant.