ஜர்னல் ஆஃப் நெப்ராலஜி & தெரபியூட்டிக்ஸ்

Nephrotic syndrome complicated by necrotizing fasciitis is rare. Necrotizing fasciitis is a skin and soft tissue infection with a rapid progression and difficult diagnosis. Moreover, the early presentation of necrotizing fasciitis is similar to that of cellulitis. Serratia marcescens is a rare pathogenic cause of necrotizing fasciitis, even in skin and soft tissue infection. We present a patient with nephrotic syndrome complicated by necrotizing fasciitis caused by Serratia marcescens. A 49-year-old Chinese woman presented with minimal change disease and nephritic syndrome. She was admitted for pain in her right leg, for which she received cefazolin and clindamycin. However, 3 days later, a sanguineous bulla developed over her left calf, and she developed septic shock. After an emergency fasciotomy and broad-spectrum antibiotic administration, this patient died 12 h after fasciotomy. The blood culture and deep tissue culture collected during surgery both yielded Serratia marcescens. This unusual case reminds physicians that gramnegative bacilli can be pathogenic in soft tissue, especially in immunocompromised patients.

Secondary Focal Segmental Glomerulosclerosis (FSGS) from thrombotic microangiopathies including Antiphospholipid Antibody Syndrome (APS), is well documented. We present a case with clinical features of APS but consistently negative serologies, suggesting ‘Seronegative APS (SNAPS)’. The patient was evaluated at the Division of Nephrology, University of Connecticut Health Center for progressive Chronic Kidney Disease (CKD). A renal biopsy exhibited thrombotic microangiopathy and associated FSGS.

Systemic thrombophilia can be primary or secondary and has an extensive list of differential diagnoses. Distinct clinical features and serologic markers characterize a particular etiology. Antiphospholipid Syndrome (APS) is the most common acquired thrombophilia. Serologic evidence of APS is the presence of commonly recognized antibodies to phospholipids in this syndrome i.e. anticardiolipin (aCL) antibodies, Lupus Anticoagulant (LA) and β2-glycoprotein 1 (β2GPI) antibodies. Rarely a patient with classic clinical features of APS does not exhibit any of the above antibodies, suggesting ‘Seronegative APS (SNAPS)’.

Background: Variety of growth factors and cytokines are involved in the process of bone turnover. Evidences are showing that alterations in OPG/RANK/RANKL system form the basis of many metabolic diseases. So, we evaluated the relationship between OPG and RANKL levels, to establish a possible relationship with other bone markers and coronary artery calcification.
Methods: Patients with chronic kidney disease and patients during the first year after transplantation had coronary artery scan and their blood was analyzed for serum bone markers. The following serum markers were measured: OPG, RANKL, BAP, TRAP5b and iPTH.
Results: All measured bone markers values increased with the disease progression and return to normal values during the first year after transplantation. Serum values of OPG, BAP, TRAP5b and iPTH are influenced by gender, age and dialysis duration. There is a significant negative correlation between PTH and OPG, and positive between PTH, BAP and TRAP5b values. No correlation between OPG and sRANKL, or OPG/sRANKL levels with other tested markers was found. In multivariate analysis of CACS revealed that OPG is significantly correlated with calcification in entire study population. Conclusions: This study shows that increased bone turnover markers are present in chronic kidney disease but mainly depending on gender, age and dialysis duration. The effects of those factors are overridden by glucocorticoids effect in transplanted patients. The correlation of OPG with arterial calcification presents it as a possible calcification marker. This is the first study on bone metabolism that covered Chronic Kidney Disease (CKD) patients, both predialysed and hemodialysed, as well as kidney transplant recipients. Results of our study demonstrate that serum levels of all investigated bone markers as well as calcification of coronary arteries are increased during CKD, with highest measured values in HD population.

The incidence and prevalence of End-Stage Renal Disease (ESRD) secondary to Diabetic Nephropathy (DN) have been progressively increasing, reaching pandemic proportions over the past 20 years. Diabetes mellitus is responsible for more than 40% of all cases of ESRD in the United States. Despite that, the treatment of DN is still suboptimal. Both the elderly and diabetic populations are among the fastest growing categories. While several guidelines are available for management of DN in the general population, elderly patients have unique characteristics that may require adaptation of the general therapeutic guidelines used for the general population. Current therapy directed at delaying the progression of DN in elderly includes optimal glycemic and blood pressure control, proteinuria/albuminuria reduction, interruption of the renin-angiotensin-aldosterone system through the use of angiotensin converting enzyme inhibitors and angiotensin type-1 receptor blockers, along with dietary modification and cholesterol lowering agents. This review highlights the available standard therapeutic approaches to manage progressive DN in elderly.

End Stage Renal Disease (ESRD) is a life threatening condition with high mortality despite advances in supportive care. Several epidemiologic studies have demonstrated an association between gonadal abnormalities and ESRD.

Introduction: The quality of Blood Pressure (BP) control remains poor among patients with Chronic Kidney Diseases (CKD). It is therefore crucial to develop therapeutic strategies enabling improvement in BP control in order to retard the progression of the underlying renal diseases. The cornerstones of therapy include the use of effective and well tolerated drugs and a good drug adherence. In this pilot study conducted in ambulant routine care we evaluated the potential clinical benefits of implementing a Telemonitoring System (TMS) in parallel to an anticipated change of treatment in hypertensive CKD patients with uncontrolled hypertension and/or adverse reactions due to the current antihypertensive treatment.

Methods: This is an observational study conducted by 13 Swiss nephrologists in patients with CKD stage III-IV and a BP >130/80 mmHg under treatment with an antihypertensive drug. A validated, automated TMS for home BP and Heart Rate (HR) monitoring and an electronic scale to measure Body Weight (BW) and a modem to transfer the measured parameters to a central database were provided to each patient. The protocol included a run-in phase and a drug titration phase of 1 month each and a 2 month maintenance phase. During the titration phase, the calcium antagonist lercanidipine could be introduced and up titrated in case of uncontrolled BP.

Results: The use of a TMS in conjunction with the introduction of lercanidipine resulted in a significant reduction of office systolic and diastolic BP of respectively -10 ± 21 mmHg (p=0.028) and -5.0 ± 11 mmHg (p=0.049). Home BP revealed a parallel significant reduction of -3 ± 1.4 mmHg systolic (p=0.043) and -3 ± 1.2 mmHg (p=0.021) diastolic, respectively. The fall in BP was associated with a slight but significant increase in serum creatinine and decrease in Estimated Glomerular Filtration Rate (eGFR).

Conclusion: The results of this observational pilot study suggest that a telemonitoring system enabling to follow home BP may be useful to improve BP control in hypertensive patients with CKD. However, a prospective randomized control study would be needed to assess the real added benefits of this strategy. Administration of lercanidipine in CKD patients was effective and well tolerated.