Intensive haemodialysis using PMMA dialyser does not increase renal response rate in multiple myeloma patients with acute kidney injury.

BACKGROUND: Intensive haemodialysis (IHD) in addition to bortezomib-based chemotherapy might be efficient to rapidly decrease serum immunoglobulin-free light chains removal in patients with multiple myeloma (MM) and to improve renal prognosis and survival. METHODS: The aim of this retrospective multi-centre study was to compare the efficacy (renal recovery rate) of IHD and of standard haemodialysis (SHD) in patients with MM and dialysis-dependent acute kidney injury (AKI), concomitantly treated with bortezomib-based chemotherapy. RESULTS: We selected 41 patients with MM and dialysis-dependent AKI, most likely due to myeloma cast nephropathy (MCN), and who were treated in eight French hospitals between January 2007 and June 2011. Patients were classified in two groups according to dialysis regimen: IHD [n = 21, with a mean of 11.3 dialysis sessions all with poly(methyl methacrylate) (PMMA) membranes for 13.2 days] and SHD (n = 20 patients, mostly three times per week, 31% with PMMA membrane). The main outcome was dialysis-independence at 3 months. At 3 months, 15 patients could stop dialysis: 8 (38.1%) in the IHD and 7 (35%) in the SHD group (P = 1). Moreover, 14 (56%) of the 25 patients who did show haematological response and only one of the 16 patients who did not were dialysis-independent (P = 0.002) at 3 months. CONCLUSIONS: The results of this retrospective study did not show any clear renal benefit of IHD in patients with MM and MCN compared with SHD. Conversely, they underline the importance of the haematological response to chemotherapy for the renal response and patient prognosis.

[Is cancer incidence different between type 2 diabetes patients compared to non-diabetics in hemodialysis? A study from the REIN registry]. / Patients en hémodialyse : l'incidence de cancer est-elle différente entre les diabétiques de type 2 comparés aux non-diabétiques ? Une étude du registre REIN.

BACKGROUND AND OBJECTIVES: In France, diabetes mellitus is now the second cause of end stage renal disease. In a large previous French national study, we observed that dialyzed diabetics have a significant lower risk of death by cancer. This first study was focused on cancer death but did not investigate cancer incidence. In this context, the aim of this second study was to compare the incidence of cancer in diabetic dialyzed patients compared to non-diabetic dialyzed patients in a French region. METHODS: This epidemiologic multicentric study included 588 diabetic and non-diabetic patients starting hemodialysis between 2002 and 2007 in Bretagne. Data were issued from REIN registry and cancer incidence were individually collected from medical records. Diabetics and non-diabetics were matched one by one on age, sex and year of dialysis initiation. RESULTS: During the follow-up, we observed 28 cancers (9.4%) in diabetic patients and 26 cancers (8.9%) in non-diabetics patients. The cumulative incidence to develop a cancer 2 years after the dialysis start was approximately 6% in both diabetics and non-diabetics patients. In univariate Fine and Gray analysis, BMI, hemoglobin, statin use had P-value<0.2. However, in the adjusted model, these variables were not significantly associated with cancer incidence. CONCLUSION: This study lead on a little number of dialyzed patients did not show any significant difference on cancer incidence between diabetic and non-diabetic patients after hemodialysis start.

Warfarin-related nephropathy induced by three different vitamin K antagonists: analysis of 13 biopsy-proven cases.

Background: Acute kidney injury (AKI) with renal tubular obstruction by red blood cell casts (RBCC) has been described in patients treated with warfarin and is known as warfarin-related nephropathy (WRN). Methods: To determine whether other vitamin K antagonists (VKA) cause WRN, we retrospectively collected and analyzed the clinical and histological data of 13 patients treated with different VKA (seven with fluindione, four with warfarin and two with acenocoumarol) in seven French hospitals. Results: They all developed gross hematuria following overanticoagulation complicated by severe AKI (median serum creatinine concentration = 693 µmol/L). Histological analysis of the kidney biopsies highlighted the presence of intratubular RBCC and acute tubular necrosis in all patients and of an underlying kidney disease in 12 patients. WRN was suspected in patients treated with warfarin; however, the initial diagnosis was incorrect in six of the nine patients treated with other VKA. Nine patients progressed to chronic kidney disease, one fully recovered renal function, two died and one still needs dialysis. Conclusions: This is the first report of AKI caused by fluindione. In agreement with the recent publication on AKI in two patients treated with dabigatran, we suggest that the term 'anticoagulant-related nephropathy' is more appropriate than WRN. Gross hematuria in patients with an underlying kidney disease and treated with VKA requires rapid control of the international normalized ratio and renal function monitoring.

The PROPKD Score: A New Algorithm to Predict Renal Survival in Autosomal Dominant Polycystic Kidney Disease.

The course of autosomal dominant polycystic kidney disease (ADPKD) varies among individuals, with some reaching ESRD before 40 years of age and others never requiring RRT. In this study, we developed a prognostic model to predict renal outcomes in patients with ADPKD on the basis of genetic and clinical data. We conducted a cross-sectional study of 1341 patients from the Genkyst cohort and evaluated the influence of clinical and genetic factors on renal survival. Multivariate survival analysis identified four variables that were significantly associated with age at ESRD onset, and a scoring system from 0 to 9 was developed as follows: being male: 1 point; hypertension before 35 years of age: 2 points; first urologic event before 35 years of age: 2 points; PKD2 mutation: 0 points; nontruncating PKD1 mutation: 2 points; and truncating PKD1 mutation: 4 points. Three risk categories were subsequently defined as low risk (0-3 points), intermediate risk (4-6 points), and high risk (7-9 points) of progression to ESRD, with corresponding median ages for ESRD onset of 70.6, 56.9, and 49 years, respectively. Whereas a score ≤3 eliminates evolution to ESRD before 60 years of age with a negative predictive value of 81.4%, a score >6 forecasts ESRD onset before 60 years of age with a positive predictive value of 90.9%. This new prognostic score accurately predicts renal outcomes in patients with ADPKD and may enable the personalization of therapeutic management of ADPKD.