Daniela Lopes

Analysis of Ultrafiltration Failure Diagnosed at the Initiation of Peritoneal Dialysis with the Help of Peritoneal Equilibration Tests with Complete Drainage at Sixty Minutes. A Longitudinal Study.

♦ Background: Ultrafiltration failure (UFF) diagnosed at the initiation of peritoneal dialysis (PD) has been insufficiently characterized. In particular, few longitudinal studies have analyzed the time course of water transport in patients with this complication. ♦ Objective: To investigate the time course of peritoneal water transport during the first year on PD in patients presenting UFF since the initiation of this therapy (study group). ♦ Method: Prospective, observational, single-center design. We analyzed, at baseline and after 1 year of follow-up, peritoneal water transport in 19 patients incident on PD with UFF. We used incident patients without UFF as a control group. Water transport was characterized with the help of 3.86/4.25% dextrose-based peritoneal equilibration tests (PETs) with complete drainage at 60 minutes. ♦ Results: The study group revealed a disorder of water transport affecting both small-pore ultrafiltration (SPUF) (p = 0.054 vs incident without UFF) and free water transport (FWT) (p = 0.001). After 1 year of follow-up, FWT displayed a general increasing trend in the study group (mean variation 48.9 mL, 95% confidence interval [CI] 15.5, 82.2, p = 0.012), while the behavior of SPUF was less predictable (−4.8 mL, 95% CI −61.4, 71.1, p = 0.85). These changes were not observed in incident patients without UFF. Neither initial clinical characteristics, baseline PET-derived parameters, or suffering peritoneal infections during the first year predicted the time course of the capacity of UF in the study group. Recovery from incident UFF was apparently linked to improvement of SPUF. ♦ Conclusions: Patients with UFF at the start of PD suffer a disorder of peritoneal water transport affecting both FWT and SPUF. Free water transport increases systematically in these patients after 1 year of follow-up. The evolution of SPUF is less predictable, and improvement of this parameter marks reversibility of this complication.

Inhibition of Gastric Acid Secretion by H2 Receptor Antagonists Associates a Definite Risk of Enteric Peritonitis and Infectious Mortality in Patients Treated with Peritoneal Dialysis

Background Evidences linking treatment with inhibitors of gastric acid secretion (IGAS) and an increased risk of serious infections are inconclusive, both in the population at large and in the particular case of patients with chronic kidney disease. We have undertaken an investigation to disclose associations between treatment with IGAS and infectious outcomes, in patients undergoing chronic Peritoneal Dialysis (PD). Method Observational, historic cohort, single center design. Six hundred and ninety-one patients incident on PD were scrutinized for an association among treatment with IGAS (H2 antagonists H2A or proton pump inhibitors PPI) (main study variable), on one side, and the risks of enteric peritoneal infection (main outcome), overall peritoneal infection, and general and infectious mortality (secondary outcomes). We applied a three-step multivariate approach, based on classic Cox models (baseline variables), time-dependent analyses and, when appropriate, competing risk analyses. Main results The clinical characteristics of patients treated with H2A, PPI or none of these were significantly different. Multivariate analyses disclosed a consistently increased risk of enteric peritonitis in patients treated with IGAS (RR 1.65, 95% CI 1.08–2.55, p = 0.018, Cox). Stratified analysis indicated that patients treated with H2A, rather than those on PPI, supported the burden of this risk. Similar findings applied for the risk of infectious mortality. On the contrary, we were not able to detect any association among the study variables, on one side, and the general risks of peritonitis or mortality, on the other. Conclusions Treatment with IGAS associates increased incidences of enteric peritonitis and infectious mortality, among patients on chronic PD. The association is clear in the case of H2A but less consistent in the case of PPI. Our results support the convenience of preferring PPI to H2A, for gastric acid inhibition in PD patients.

New combined CFH/MCP mutations and a rare clinical course in atypical haemolytic uraemic syndrome

Atypical haemolytic uraemic syndrome (aHUS) is a rare, life-threatening, chronic, genetic disease due to uncontrolled alternative pathway complement activation. In this report, we discuss the case of a heterozygous carrier of a mutation on both factor H and membrane cofactor protein, who persistently presents haemolytic anaemia without need for blood transfusions, normal platelet count, normal renal function and no signs or symptoms of organ injury due to thrombotic microangiopathy 4 years after the diagnosis of aHUS.

Cutaneous involvement in haemolytic uraemic syndrome

A 35-year-old woman was admitted to our hospital with severe hypertension, oedema and renal failure. Twelve months earlier, she had a pregnancy, which was complicated by preeclampsia. A successful Caesarean was performed in the 29th week of gestation (Figures 1 and 2). After the birth, she remained with poorly controlled hypertension and proteinuria exceeding 1 g/day. Six months later, she began to have fatigue, headaches, severe hypertension and facial and pedal oedema. There was no fever, neurologic abnormalities or diarrhoeal prodrome. She was pale and hydrated and blood pressure was 151/103 mmHg. Laboratory screening revealed haemoglobin 4.65 mmol/L (7.5 g/dL), urea 182 mg/dL, creatinine 65 mmol/L (6.46 mg/dL), platelets 46 × 109/L, increased reticulocyte count and schistocytes in peripheral blood. Proteinuria value was 4.9 g/24 h and urinary sediment revealed 5–10 red blood cells/HPF. The remaining study showed lactic dehydrogenase 1669 U/L, normal liver enzymes, total bilirubin 14mg/L, direct bilirubin 4.4mg/L, haptoglobin <0.2 mg/dL and negative Coombs test. All immunologic tests and viral screening were normal. A diagnosis of atypical haemolytic uraemic syndrome (aHUS) was established, and she started daily plasmapheresis with haemodialysis. After 6 months, haematological parameters normalized but she never recovered renal function and remained on dialysis. Seven months later, she had a relapse of the aHUS and needed plasmapheresis during 6 months. After 4 months, she complained of three painful leg skin lesions which progressed to ulcers, with some necrotic areas of the base and edges. One month later, she again developed uncontrolled hypertension and relapse of the haemolytic activity. Immunologic studies including antiphospholipid antibodies remained normal. Skin biopsy showed fibrin thrombi in the small blood vessels, with discrete inflammatory infiltrate of lymphocytes and plasma cells. A new relapse of aHUS was then diagnosed and she was once again treated with plasmapheresis, with resolution of haematological and cutaneous disorders after 11 weeks. aHUS is a rare, systemic, life-threatening disease [1, 2], caused by dysregulation of the alternative pathway of complement [3]. Although being extremely rare, we should be mindful of skin involvement in aHUS and establish this association in a timely manner which would lead to an early diagnosis and correct treatment, avoiding wasted time and costs [2].